Zinc Nutrition of Cattle: A Review1

sY~POSlU~ sity of California Press, Berkeley. (160) Watson, L. T., C. B. Ammerman, W. G. Hillis, and C. B. Hulsbrook. 1969. Ruminant utilization of inorganic manganese. J. Animal Sci., 29:175. (161) Weinman, D. E., J. R. Campbell, M. E. Tumbleson, and J. E. English. 1969. Tissue iron priorities in iron deficient calves. J. Animal Sei., 29: 175. (]62) Weintraub, L. R., M. B. Weinstein, H. J. Husen, and S. Rafal. 1968. Absorption of hemoglobin iron: the role of a heinesplitting substance in the intestinal mucosa. J. Clin. Invest., 47:531. (163) Westerfield, W. W. 1961. Effect of metalbinding agents on metalloproteins. Feder-

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ation Proc., 20 (Suppl. 10) : 158. (164) Wheby, M. S., L. G. Jones, and W. H. Crosby. 1964. Studies on iron absorption. Intestinal regulatory mechanisms. J. Clin. Invest., 43: 1433. (165) Wheby, M. S., and G. Umpierre. 1964. Effect of transferrin saturation on iron absorption in man. New England J. Med., 271: 1391- Nutrition Abstr. Rev., 35:4150. (166) Williams, R. J. P. 1961. Nature and properties of metal ions of biological interest and their coordination compounds. Federation Proe., 20 (Suppl. 10):5. (167) Wilson, J. G. 1966. Bovine functional infertility in Devon and Cornwall: response to Mn therapy. Vet. Record, 79: 562.

Zinc Nutrition of Cattle: A Review 1 W. J. MILLER

Dairy Science Department, University of Georgia, Athens Abstract

Zinc is an essential nutrient for animals, functioning largely or entirely in enzyme systems and being involved in protein synthesis, carbohydrate metabolism, and many other biochemical reactions. A severe zinc deficiency causes numerous pathological changes, including skin parakeratosis, reduced or cessation of growth, general debility, lethargy, and increased susceptibility to infection. However, the mechanism and routes by which specific enzymatic changes are responsible for the serious pathological alterations caused by the deftciency have not been elucidated. Recovery of calves from a severe zinc deficiency is rapid and dramatic. I n studies involving special and purified diets, approximately 9 ppm of zinc were adequate for normal health and performance of calves. However, in a few instances, 20 to 40 ppm zinc in practical diets were not sufficient for optimum performance, but in others, such levels were adequate. Logical biological theories are presented for these differences, but proof is lacking. Cattle have a relatively high 1Journal Series Paper no. 560, University of Georgia College of Agriculture Experiment Station, College Station, Athens. Supported in part by PHS Research Grant no. AM-07367-NTN from the National Institute of Arthritic and Metabolic Diseases.

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tolerance for zinc, with no toxic effects exhibited from diets containing 500 ppm zinc. I n some studies, higher levels of zinc caused no adverse effects. However, substantially lower levels might aggravate a borderline deficiency of some other essential element. The small intestine, especially the proximal part, is the main site of absorption and probably of zinc re-excretion. Most of the endogenous loss of zinc is by way of feces. Calves have an effective, but far from complete, homeostatic control mechanism(s) for zinc, which functions through changes in amounts of zinc absorbed from and re-excreted into the intestine. With a severe deficiency, there is only a moderate decline in zinc in some tissues, including liver, pancreas, and bone, with no change in others such as muscle and brain. Plasma zinc levels may change rapidly following dietary changes. When placed on severely deficient diets, animals are unable to mobilize sufficient zinc from body stores to meet their needs for even short periods. The percentage of dietary zinc absorbed changes considerably in response to several factors of which amount of dietary zinc has the greatest influence. Substantial excesses of zinc cause large increases of zinc content in a few tissues including liver, a moderate increase in some tissues and in milk, but no change in others including, especially, red muscle. Zinc is widely distributed in feeds with JOURNAL OF DAIRY SCIENCE VO~. 53, NO. 8

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the amount in the same feed varying considerably with production conditions. Even though a severe zinc deficiency in cattle has been observed under practical field conditions, this appears not to be a major practical problem. However, the data available are not adequate either to indicate or preclude the possibility of a relatively widespread borderline or mild zinc deficiency in cattle. Such a borderline deficiency would cause a small reduction in animal performance, but would be impossible to diagnose clinically and very difficult to measure experimentally; nevertheless, it could be important economically. Although zinc was believed to be an essential nutrient for animals much earlier, unequivocal proof was not obtained until 1934 when the deficiency was developed in the mouse and rat (33, 116, 119, 120). Even so, zinc was not recognized as being of practical importance to farm animals until 1955 (117). During the intervening time, in spite of the close similarity of the zinc-deficiency syndrome in swine and rats, widespread but undiagnosed zinc deficiency in swine (parakeratosis) caused large financial losses. Before 1955, animal nutritionists generally and firmly believed that a zinc deficiency would never occur in farm animals under practical conditions (10, 36, 118). To a considerable extent, this belief was based on logical, but in retrospect erroneous, interpolation of the work with rats during the ]930's. Developing a zinc deficiency in rats required extensive purification of the dietary ingredients to a zinc level far below that generally found in practical feedstuffs. Thus, nutritionists not only thought that zinc deficiency could not occur in farm animals under practical conditions but believed it would be very difficult to produce experimentally. Later research revealed a large species difference, with swine fed practical diets requiring much more zinc than rats fed purified diets (24, 119). Dietary constituents other than zinc greatly influence the zinc requirement of monogastric animals (2, 3, 6, 13, 30, 31, 82-84, 115, 119-121). Recently, zinc nutrition has become an active research field with several species of animals. I n addition to swine parakeratosis, other developments contributing to the wide interest and increased research in zinc are discoveries a) that reduced performance in poultry was common due to inadequate zinc (2, 3, 13, 119) ; b) that severe zinc deficiency occurred in cattle under farm conditions in Guyana, Finland, and JOUR~AI, OF DAIRY S(]IEI~CE VOL. 53, ~O. S

other areas (11, 12, 17, 18, 20, 32, 73, 77); e) of the reported zinc deficiency of humans in Egypt (105, 106, 111); d) of indications that supplemental zinc increased healing rate in healthy young men in the U.S. Air Force receiving normal diets (100, 1Ol); e) of vastly better analytical procedures for zinc determination (15a) ; and f) that radioactive zinc is an important contaminant in the food supply under several actual or potential conditions throughout wide areas of the world. Function of Zinc

Zinc appears involved in nucleic acid metabolism, protein synthesis, carbohydrate metabolism, and in other ways plays an essential role in many biochemical reactions in the body (33, 78a, 79, 119, 120, 126). It is a constituent of several metalloenzymes, including carbonic anhydrase, carboxypeptidase A and B, alcohol dehydrogenase, glutamic dehydrogenase, lactic d e h y d r o g e n a s e , D-glyceraldahyde-3-phosphate dehydrogenase, alkaline phosphate, a-mannosidase, and others (15a, 26, 33, 93a, 113, 120). I n addition, a number of metal enzyme complexes are activated by zinc. Whether zinc functions in important ways other than as enzyme activators (as structural components) does not appear to be completely clear (126). There is little doubt that much of the pathological effect of a zinc deficiency must be mediated through enzymatic changes in the animal. However, the mechanisms and routes by which specific enzymatic impairment are responsible for the pathological effects of zinc deficiency need to be elucidated (15a, 126). Zinc Deflciency Effects

The effects of a severe zinc deficiency have been well characterized in young male cattle (5, 42, 43, 45, 46, 64, 66, 67, 76, 77, 93, 104), goats (5, 68), and sheep (77, 91, 92, 98). Zinc deficiency in mature ruminants and in the female have been studied nmch less (17-19). Haaranen (17) described an "itching tall-root eczema," which was widely distributed on Finnish farms and responded to zinc administration. Dynna and Havre (11, 12, 20) have studied a widespread condition in Norway and described it as a complex zinc-copper deficiency. Zincdeficient animals consume less feed and grow at a slower rate. When fed at the same rate as normal calves, zinc-deficient ones grow more slowly (67). The reduced feed efficiency results not from lower digestibility but apparently from less efficient utilization of the digested nutrients (22, 70). Testicular growth and development are retarded. Bull calves severely zinc deficient

sYMPosiu~ from 2 to 5 months of age and subsequently fed a zinc-adequate diet exhibited normal semen production and histological appearance of testes (46, 99). This is in contrast to work with rats (39) in which a very severe zinc deficiency produced irreversible changes in the testicles, with the spermatogonia never functioning. These canes, however, were not zinc deficient for as large a proportion of the life cycle (the deficiency did not extend to puberty). Thus, a very severe deficiency which extended through puberty might have different effects in any cattle which survived such a regime. Borderline zinc deficiencies in bull calves would not adversely affect subsequent reproduction (46, 99). In female rats, severe zinc deficiency seriously impairs or prevents reproduction (27). Calves severely zinc deficient are lethargic; their wounds heal very slowly, if at all; and they are highly susceptible to nonspecific secondary infections, which often result in death (5, 35, 42, 43, 45, 62, 66, 67, 76, 77, 93). There is a rapid increase in bacteria in the mouth, which is alleviated by supplementary dietary zinc (77, 78a). Clinical signs of zinc deficiency include inflammation of the nose and mouth with submucous hemorrhages; unthrifty appearance; rough coat; stiffness of the joints, with soft edematous swelling of the feet in front of the fetlocks; cracks in the skin of coronary bands around the hooves which later become deep fissures; dry scaly skin on the ears; thickening and cracking of the skin around the nostrils; development of horny overgrowths of the nmcosa on the lips and dental pads; gnashing of the teeth; excessive salivation (often transitory); alopecia; red, scabby and wrinkled scrotal skin; and bowing hindlegs (5, 42, 43, 45, 66, 67, 76, 77, 92, 93). The skin of the neck and head of affected animals is hard and dry; the legs are tender, easily injured, and often raw and bleeding (5, 42, 43, 64, 76, 77, 91, 92, 93). Histologically, these skin changes can be identified as "parakeratosis," a term often used for the zinc-deficiency syndrome (64). Parakeratosis usually affects the scrotum, head, neck, and legs, while the skin on the remainder of the body may appear normal (5, 42, 43, 64, 76, 77, 91, 93). Mild trauma may determine the location of parakeratosis; thus, parakeratosis can probably appear on any part of the body (66, 77, 78a). Zinc-deficient rats have decreased mental ability (81). Blood carbonic anhydrase may be somewhat lower in zinc-deficient calves (43), but it is unlikely that this is a factor in the adverse effects of the deficiency on health and perfor-

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mance of cattle. There is a large reduction in serum alkaline phosphatase (17, 67). This enzyme is not greatly influenced by higher than normal levels of dietary zinc (54, 60) ; however, it is sensitive to many other factors (35, 57). The rapidity with which young calves develop severe zinc deficiency symptoms is dependent on the dietary level (77). With a very low zinc diet (1 to 2 ppm) there is an immediate sharp decline in plasma zinc, with reductions in feed intake and cessation of growth within less than one week (9, 77). Thus, with extremely low dietary zinc, animals are not able to mobilize sufficient zinc to remain normal for even a few days (9, 77). I n less severe deficiencies, the clinical symptoms may not develop for several weeks. Apparently, a zinc deficiency will develop almost as quickly in animals given a considerable excess of zinc before being fed the deficient diet as in those fed at or near requirements (77, 78a, 93). This further suggests that the calf has limited capacity for storing zinc in a form which can be mobilized rapidly to prevent deficiency symptoms. Viewed alternatively, animals apparently do not have an effective mechanism for mobilizing zinc from most of the major pools in response to needs. The response of severely zinc-deficient animals to supplemental zinc is rapid and dramatic (17, 43, 77, 79, 10B). For example, when severely zinc-deficient calves were given a diet containing 260 ppm, lethargy diminished considerably within 1 day and feed consumption increased within 2 or 3 days or less (43). The skin of these calves improved within 4 days. By 2 weeks, fine hair appeared in the bare areas. Feed intake was greatly increased in zinc-deficient rats within 4 hours after a zincsupplemented diet was offered, indicating a major nutritional defect had been quickly corrected (79). Requirements for Zinc

In studies with a special practical basal diet, mostly of beet pulp with urea as an important source of nitrogen, adding supplemental zinc to a diet with 9 ppm of zinc did not improve growth performance in Holstein bulls (59). Corroboratory studies at the Rowett Research Institute with a purified diet revealed that about 9 ppm zinc was adequate for normal growth, with 10 to 14 ppm zinc required to maintain normal plasma levels in young Holstein calves (77). I n contrast, some evidence indicates that considerably more zinc may be needed for cattle under certain circumstances (11, 12, 17, 20, 32, 45, 77, 97, 119). A very severe zinc deficiency occurred in a small perJOURNAL OF DAIRY SCIENCE ~OL. 5~, NO. 8

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eentage of cattle grazing in Guyana (32). The pasture plants contained from 18 to 42 p p m zinc. Even though other possibilities exist for these results, for some unknown reason the dietary zinc requirement may have been considerably higher for these animals than that adequate in calves fed experimental diets. Also, a zinc deficiency has been reported for field conditions in a number of places in Europe when the forage contained from 19 to 83 ppm zinc (11, 12, 17, 20, 77, 123). The zinc content of feeds reported in field cases was similar to those where no clinical problems were evident. I n two experiments at Purdue University, feedlot cattle made more rapid gains when zinc was added to diets containing 24 and 29 p p m zinc, but in two others supplemental zinc was not beneficial (97). I n other studies of practical diets with similar levels of zinc, adding zinc did not improve performance (44, 45, 54, 86, 129). Recent work in South Dakota suggests that adding zinc to a diet of corn silage (12.5 p p m zinc) and a concentrate mixture containing urea (43 p p m zinc) increased milk production (125). I n Georgia, adding zinc to a practical diet containing 44 p p m zinc did not influence cow performance for 6 weeks (60). Obviously, considerably more information is needed on zinc requirements for milk production. I t is probable that the dietary zinc requirement of cattle may vary considerably under different conditions (45, 77). I n most instances, the factors which may affect the requirements of ruminants are unknown. Differences in availability or absorption may be influenced either by the chemical form and association of the zinc or by other constituents of the diet. Dietary zinc is essential for rumen microorganisms, but presumably it is smaller than that for animals per se. However, supplemental zinc may have physiological effects on the tureen microbes which may not be directly related to the zinc requirement of the organisms (85, 107). Toxicity and Tolerance I n studying any required nutrient, it is important to know the minimum level for optimum performance, and it is essential to also determine the amounts tolerated by the animal without adverse effects and the effects of a toxic level. Data concerning zinc excess or toxicity in ruminants are meager (1, 14, 54, 60, 87-90, 119). Feeding a diet containing 1,269 ppm of zinc on a dry matter basis to lactating cows for 6 weeks did not significantly affect milk production; fat-corrected milk production; fat, solidsnot-fat, protein~ or magnesium in milk; volunJOURI~A~ OF DAIRY SCIENCE ~OL. 53, 1~0. 8

tary forage dry matter intake; body weight; blood hemoglobin; packed cell volume; blood serum lactic dehydrogenase; blood serum alkaline phosphatase; or apparent animal health (60). Growing cattle at Purdue University decreased in feed consumption and weight gains with practical diets containing 900 p p m of zinc, but no adverse effects were observed with 500 p p m of added zinc (88). I n the absence of adequate data, we cannot be sure of zinc levels which could be tolerated over a long time. However, it is improbable, with adequate amounts of other nutrients, that problems would arise in cattle receiving dietary zinc below 400 or 500 ppm. F o r most conditions, it is possible that the tolerance may be considerably higher. Even so, a level that ordinarily would cause no problems might tend to aggravate a borderline deficiency of some other essential element such as copper, iron, or calcium (121, 122). Zinc toxicity has been actively investigated in nmnogastric animals (6, 8, 15a, 34, 96, 112). Both the degree and the types of the toxicity are dependent on the other diet constituents. This appears to be, at least partially, because excessive zinc interferes with the utilization or nmtabolism of certain other minerals, including copper and iron (6, 34, 72, 112). Zinc Absorption and Excretion The small intestine is the main site of zinc absorption, with the duodenum or proximal p a r t of the small intestine being a much more active site than the lower intestine (23, 38, 41, 48, 96, 110, ]11, 122). Even though considerable scientific information has been obtained in recent years, most details of the mechanism of zinc absorption remain to be established. Absorption first involves uptake of zinc by the intestinal mueosa and transfer or transport into the blood (48, 110, 122). While this is a general phenomenon for several minerals, evidently the relative rates of these two processes vary from one mineral to another (110). Some evidence indicates a rapid absorption of dietary zinc into the intestinal mucosa with a slow transport into the blood stream (110). I n calves, the small intestine retains a considerable amount of ssZn for a long time after a single oral dose (48, 56, 63, and Miller et al., unpublished data). I t has been generally assumed that pancreatic secretion was the primary source of endogenous fecal zinc (95, 119). Substantial amounts of zinc are in the pancreatic secretion (4, 80). However, ligation of the pancreatic duct did not reduce fecal excretion appreciably in swine (95). Although direct proof is lacking, it seems

sY~OSIU~ probable that much of the zinc from pancreatic secretions may be reabsorbed further along the small intestine. Apparently, some endogenous zinc enters most or all sections of the gastrointestinal tract including the rumen and reticulum (23, 127). However, the proximal part of the small intestinal mucosa appears to be the most active route of zinc absorption, and also it is probably an important site of endogenous excretion (23, 41, 48~ 56, 58, 95). A considerable portion of the zinc excreted from the body into the small intestine may be reabsorbed further along the small intestine (23, 41). For all species studied, a high percentage of all zinc excreted from the body is through the feces with very little by way of urine (41, 48, 51, 53, 56, 58, 63, 69, 102~ 119, 120). No meaningful estimates of losses through hair and sweat are available for ruminants. Factors Affecting Absorption of Zinc and Interrelations with Other Nutrients

Until recent years~ it was widely believed that cattle could absorb only a very small percentage of dietary zinc and that this was a fairly fixed value (14, 119). However, recent work has shown that absorption of zinc varies tremendously in cattle (41, 47, 48, 51, 52, 56, 63, 69). The single most important factor affecting absorption is the zinc content of the diet. As dietary zinc is decreased, the percentage absorbed increases (48, 52, 63). With high dietary zinc, the absorption percentage is reduced (47, 48, 56, 60). However, when dietary zinc is decreased, a smaller absolute quantity is absorbed and vice versa when higher than normal zinc levels are fed. Another substantial factor affecting zinc absorption is whether the animal is clinically zinc-deficient (48, 51, 52). When fed the same diet before and during testing, zinc-deficient animals absorb a higher percentage of administered zinc. Zinc-deficient calves have a net absorption as high as 80% of an oral 65Zn dose. Both low dietary zinc and zinc deficiency reduce endogenous fecal 65Zn excretion (47, 48, 58, 63). Younger calves absorb a higher percentage of dietary zinc than older ones (41, 63). However, this age effect may be largely an indirect one rather than due to the inability of the small intestinal tissues to absorb the zinc (63). With a diet adequate in zinc (38 ppm), 2.5-month-old calves absorbed a much higher percentage of aSZn than 4.5-month-old calves (63); however, with a zinc-deficient diet (2 ppm), there was no difference in ~SZn absorption with age (63). The higher percentage absorption of young animals may be due to deposition of larger

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amounts of zinc in body tissues relative to total feed intake. When calves were fed a maintenance diet, 65Zn absorption was lower than for those fed a more normal feed intake (48). This also is believed to be caused by a relatively smaller growth increment in those tissues with which zinc deposition is associated. In monogastric animals, it is well established that several nutritional factors including Cd, Ca, Mg, P, and Cu, chelating agents such as EDTA, vitamin D, and phytic acid have much influence on zinc absorption and metabolism (2, 3, 6, 7, 15a, 24, 25, 30, 31, 72, 82, 110, 115, 119-121). At least some of the factors also affect zinc metabolism at the cellular level. The widespread parakeratosis in swine which occurred for many years was due to reduced absorption of zinc from diets which contained plant proteins, largely soybean meal, and high calcium levels (24, 117, 120). High dietary caleimn, at least in the presence of a phytic acid source, substantially reduces zinc absorption of swine, rats, and poultry (2, 3, 6, 7, 24, 72, 82). At least a pai~ of the effect of plant proteins such as soybean meal or sesame meal in reducing zinc absorption is associated with their phytic acid content (24, 72, 82). Sesame meal has a large depressing effect on zinc absorption by chicks (30, 31). With rats fed a diet containing phytate from plant protein, added zinc has an important sparing effect on dietary protein required for growth and survival (83). In calves, when an isolated soybean protein diet is delivered to the abomasum, zinc absorption is reduced, but it is not affected if the diet goes to the rumen (40). Adding phytic acid to a purified diet did not materially affect a zinc deficiency in lambs (77, 92). This is not surprising, as phytic acid presumably is broken down in the rumen. In normally fed ruminants, there is no direct evidence that phytie acid or other factors in plant proteins decrease zinc absorption. However, the higher zinc requirement indicated in a few studies of ruminants receiving practical diets may be mediated through some mechanism which reduces zinc absorption (11, 12, 17, 18, 20, 32, 73, 77, 97, 119, 123). The nature of such factors, and positive proof of their existence, is yet to be established. Adding zinc to calf diets which utilized soybean meal or sesame meal as protein source did not influence calf performance, indicating that either these did not adversely affect zinc absorption or that zinc was sufficient even with reduced absorption (44). High dietary cadmium (350 ppm) greatly reduced zinc absorption by calves (102). Cadmium, as well as being a strong antimetabolite JouR~

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for zinc (102), causes serious toxicity symptoms. Accordingly, whether the effect on zinc absorption is direct or indirect is not known. I t may be partially or largely indirect through a much smaller growth rate and deposition of tissue zinc (102, 103). Even though cadmium has several interrelations with zinc, it is metabolized differently (29, 37, 55, 61, 110, and unpublished data). Evidence for an increased zinc requirement for lactating cows with increasing dietary calcium was advanced (18). Other work under different conditions does not substantiate this report (19, 59). A high caleimn basal diet was used with calves in which 9 ppm zinc appeared to be adequate (59). By Itaaranen's formula (18), the diet (59) would have needed about 180 ppm of zinc to provide complete protection against a zinc deficiency. Supplemental zinc appeared to have a favorable effect in alleviating slightly lower gains and feed efficiency of lambs fed very high calcium-to-phosphorus ratios (15). Increasing calcium in a purified diet from 0.6 to 1.8 or 2.4% depressed plasma zinc concentrations and increased severity of epidermal lesions of zinc deficiency in young lambs but did not affect growth (75). Thus, the relationships between zinc and calcium have not been clearly established for ruminants. ~Zn Turnover Rate in Yarious Tissues

Following oral administration and subsequent absorption of SSZn, the different body tissues show very different accumulation and turnover rates. Peak levels of ~Zn are reached in the plasma within 1 to 3 days after oral dosing (48, 50, 51, 102). This is followed by a rapid though decelerating decline for 3 or 4 weeks and a subsequent very slow decrease (48, 50-52). The pattern in liver is similar, though with much higher concentrations (50-52). ~Zn accumulates very slowly in some tissues. Among these, the amount in red blood cells, muscle, and bone continues to increase for several weeks after a single oral dose (50). In zinc-deficient animals, many of the vital organs and other soft tissues have an increased affiinity for zinc relative to comparable tissues of normal animals. This is indicated in higher concentrations following dosing (as a percentage of absorbed dose) and slower turnover rates and, therefore, a longer biological half-life (50, 51). In contrast, bones of zinc-deficient calves accumulate smaller amounts of ~Zn, suggesting a lower affinity relative to other tissues but possibly Iittle change in the absolute affinity (48, 50, 52). JOURNAL OP DAIRY SOIElgCE VOL. 53, NO. 8

Zinc Content in Body Tissues

Zinc is widely distributed throughout the body, with substantial amounts at least in all those tissues which contain considerable protein or calcified material (48, 69, 119, 120). When an animal suffers serious pathological changes, previously described from zinc deficiency, a shortage of zinc must occur in certain tissues (53, 69, 71). In a number of tissues including muscle and brain, zinc remains essentially constant even when the animals are severely deficient (48, 53, 69). With a severe deficiency, the average zinc content in several tissues including hair, bone, liver, lung, kidney, spleen, pancreas, and blood plasma does decrease (48, 53, 69, 71). However, there is considerable variability among animals; therefore, in most of these tissues there is considerable overlapping between deficient and normal animals. Thus, diagnosis of a zinc deficiency in calves by zinc content of most tissues is not reliable, especially under field conditions (5, 53, 77). Mills and associates (77) have shown that repeated plasma zinc under 0.4 ppm indicates a severe deficiency. Perhaps the best indicator for diagnosing zinc defieiency is response~ in feed intake and growth after feeding supplemental zinc (5, 48, 53, 77). Increased voluntary feed intake should occur within a few days. Within a few days after animals are fed a zinc-deficient diet, the zinc content of some tissues decreases (5, 48, 53, 71, 77), with a very rapid decrease in plasma zinc within 36 hours if the diet is extremely deficient (77). The zinc content of other tissues declines more slowly. With time, when animals develop a clinical deficiency, a further reduction occurs in zinc content of some tissues (48, 53). However, in most ruminant tissues, decreases in zinc content are not large (48, 53). After sufficient time, the effect of zinc on hair is the most clearcut of any tissue studied (48, 53). Feeding large amounts of zinc greatly increases zinc content of some tissues including blood serum, pancreas, kidney, bone, hair, and liver, but has little effect on some others including nmscle (56, 89, 90, and W. J. Miller et al., unpublished data). In one experiment, when calves were given 600 ppm (apparently nontoxic level) of supplemental zinc with a practical diet for 3 weeks, pancreas zinc increased more than 1,000%, liver and kidney zinc by about 700%, and duodenal and rumenretieulum zinc considerably (W. J. Miller et al., unpublished data). Moderate increases occurred in some tissues including bone, hair, and aboma-

sY~Posm~ sum of those fed high levels of supplemental zinc. I n contrast to many tissues, zinc content in muscle did not change in calves fed high zinc levels. Zinc in Milk

Most of the zinc in milk is associated with the caseinates, some tightly and some loosely bound (94). About 12% of the zinc in milk is ultrafilterable, but little is associated with the fat or whey proteins (94). Milk usually contains about 4 ppm zinc (1, 60, 119). Cattle in India grazing on low-zinc forage, have produced milk containing only 0.8 to 1.8 p p m (28). Other reports of low-zinc milk exist (101). However, there is a paucity of controlled experimental data on the effects of feeding low-zinc diets on milk zinc content. Feeding high dietary zinc increases zinc content in milk (1, 60, 119). By increasing dietary zinc, there is a rapid decline in the dietary zinc percentage which appears in milk. Extremely high zinc contents in milk have not been reported (60). Apparently, the zinc content of milk is the same from cows fed 692 ppm as it is from cows fed 1,279 ppm of zinc (60). When high dietary zinc is fed, milk zinc does not increase as rapidly as plasma zinc, indicating that the udder is discriminating against zinc at the higher dietary and plasma levels. Zinc Content of Feeds

Zinc is widely distributed in feeds (16, 21, 65, 114, 119, 120, 124). I n general, protein-rich feeds contain more zinc than grains, with grains varying considerably, depending on conditions where they are grown (49, 65). I n contrast to the relatively high zinc content in protein sources such as soybean meal, urea contains little or no zinc (65). Likewise, gelatin and egg albumen are low in zinc. Coastal be1~nudagrass grown on clay soil in the Georgia Piedmont contained considerably more zinc than that grown on sandy soil in the Coastal Plain (49). Soil p H and other factors also affect zinc content of forages (49, 124). Often plant growth will cease before zinc content becomes extremely low (21, 124). Overall, data for zinc content of feeds are limited, with some of the older data, especially, being unreliable because of analytical problems. Postulation of the Mechanism of the Most Critical Function of Zinc

Currently, there is considerable interest among zinc nutrition researchers concerning the function of zinc which is first impaired when animals

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become deficient. Discovery of the basic biochemical mechanism first impaired would be a great achievement in animal nutrition. I n all probability this would be the same for all species of animals. The earliest observed effect of a zinc deficiency is reduced feed intake (79, 108, 109). Likewise, the first recovery response is an increased feed intake which occurs within 2 to 4 hours after zinc-deficient rats are fed supplemental zinc (108, 109). Some biochemical change within the animal must precede the changes in feed intake. Since zinc functions mostly or entirely in enzyme systems, it is generally agreed that deficiency in some enzyme activity is involved. Recovery in appetite of zinc-deficient rats occurs when the extra zinc eaten is less than 1% of the total body zinc (109). This indicates that the critical enzyme probably is one which does not have a high affinity for zinc and that the turnover rate of zinc for it is rapid. When animals are zinc deficient, the level of voluntary feed intake is reduced; furthermore, they cannot tolerate normal amounts of feed. Force feeding zinc-deficient animals results in death (78). The percentage of the diet digested does not a p p e a r to be affected by the zinc deficiency (70). However, this does not preclude the possibility that the first critical defect may be in the small intestine, as the passage rate of food through the intestine is reduced in zinc-deficient rats (108, 109). Feeding habits are changed when rats are zinc deficient, and a cyclic pattern develops (78a, 81, 128). Injecting zinc does not result in as rapid a recovery in appetite as giving dietary zinc (78). This observation combined with other data has led to the speculation that the first critical biochemical lesion in the animal is probably in the small intestine. However, other evidence suggests that this may not be true. Recent unpublished data show that 1 hour after zinc is placed in the duodenum, a substantial portion is in the liver and apparently peak blood levels are attained as soon as 30 minutes (W. J. Miller et al.). Thus, absorption and transport throughout many parts of the body can be rapid. Other unpublished data indicate that intravenously administered zinc is not metabolized in the same way as that given orally (W. J. Miller et ah). Since zinc injected into the blood probably forms differed complexes from that absorbed from the small intestine, it is possible that injected zinc may be much less available to the enzyme system, which is first critically deficient. From information available, the following working postulation is suggested. Probably, the JOURNAL OF DAIRY SCIENCE VOL. 53, NO. 8

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biochemical mechanism first impaired is a deficiency of an essential enzyme (or enzymes) which binds zinc loosely. I t appears that many other tissues of the body bind zinc with a greater affinity, so that soon after a severe deficiency in zinc intake there is a shortage of labile zinc and that this critical enzyme(s) is deficient and, conversely, as soon as sufficient zinc is given, this enzyme can obtain the zinc quickly. I t is speculated that the enzyme (or enzymes) impaired to a critical level is a crucial one in a major biochemical pathway, resulting in general effects throughout the body. The key enzyme impaired either may be involved in utilization of energy or otherwise is preventing the animal from obtaining adequate amounts of an essential component, or it may result in blockage of some essential reaction causing the accumulation of a toxic product(s). Practical Impi|cafions and Considerations Twenty years ago zinc toxicity was considered to be the only aspect of zinc nutrition of practical importance. Such toxicity was associated .with galvanized containers and acid conditions. Some of the toxicity attributed to zinc may have been caused by cadmium or other metals. The great decrease in galvanized equipment not only diminishes its contribution to any possible toxicity but also reduces content in a variety of dietary materials. Even though a severe clinical zinc deficiency has been described in cattle under field conditions in a number of locations through the world, it appears unlikely that this is a major problem. However, information currently available does not preclude the possibility of a widespread mild or borderline deficiency which is economically important. The first effects of a mild zinc deficiency would be expected to be decreased feed intake, growth, feed efficiency, milk production, resistance to infection and stress, and lower reproductive efficiency. There are still many more unknowns in zinc nutrition, especially with ruminants, than there are established facts. The amount of research data available on zinc with ruminants is only a small fraction of that with monogastric animals. Whether, in many practical diets, other constituents have an important effect on zinc availability and utilization by cattle is not known. While some of the data suggest that such factors may be important, this is not certain and their nature, if they exist, has not been established. Even though much of the information needed to make the most desirable practical recommendations is not available, practical decisions JOURNAL OF DAIR~ SCY~NCE VOId. 53, NO, 8

must be made. Accordingly, in response to numerous questions, until such time as more complete information is available, the following suggestions are offered. Zinc content of most feeds is variable, with data on most being unavailable and not readily obtainable. Further, as indicated, the zinc requirement varies considerably under different feeding conditions. Thus, it appears reasonable to add 20 to 40 p p m of supplemental zinc to the total feed intake (dry basis) of cattle diets. This level of zinc should be adequate to correct any likely borderline deficiency. While specific data are lacking concerning problems with higher levels, borderline deficiency problems with other essential elements might be aggravated with supplemental zinc levels much lower than those shown to have adverse effects under experimental conditions. Even though specific data for cattle generally are lacking concerning the availability of different zinc compounds, information from other species suggests that most of the normally used zinc compounds (when in suitable physical form for mixing) such as the oxide, carbonate, sulfate, and chloride would be satisfactory. A number of trends in animal production may have important implications in zinc nutrition of cattle. Formerly, most water pipe was galvanized, which often provided considerable zinc for animals. However, copper and plastic pipe do not contribute significant amounts of zinc to water. Unpiped water from some areas contains considerable zinc, whereas from others it contains almost none (65, 114). Some of the commercial trace-mineralized salt mixtures, which have been widely distributed, have contained an insignificant amount of zinc relative to the requirements of animals (54). Thus, it is possible that some of the experiments in which a traee-minerahzed salt supplement provided zinc, may not have been a valid test of whether added zinc would be beneficial. Since urea contains little zinc, its expanded use will decrease the zinc in rations. The performance rate of commercial cattle continues to increase. While relatively few direct data are involved, it seems almost certain that increased performance results in a higher zinc requirement for animals. Increased agronomic efficiency often involves more lime and higher soil p H which, in turn, results in lower zinc content of plants (49, 124). Many other changes which potentially could affect zinc metabolism also accompany increased agronomic efficiency. Thus, when all of the changes occurring are considered together, it is possible that borderline zinc deficiencies will become more prevalent. With the growing evidence and belief that borderline

sY~Posiu~ zinc deficiencies m a y be i m p o r t a n t in h u m a n health, it is possible t h a t the zinc c o n t e n t of a n i m a l food products, especially milk, m a y become a n item of increased public interest. References

(1) Archibald, J. G. 1944. Zinc in cows' milk. J. Dairy Sci., 27: 257. (2) Berg, L. R., G. E. Bearse, and L. H. Merrill. 1962. Effect of calcium level of the developing and laying ration on hatehability of eggs and on viability and growth rate of progeny of young pullets. Poultry Sci., 41: 1328. (3) Berg, L. R., G. E. Bearse, and L. H. Merrill. 1963. Evidence for a high zinc requirement at the onset of egg production. Poultry Sci., 42: 703. (4) Birnstingl, M., B. Stone, and V. Richards. 1956. Excretion of radioactive zinc (Zn ~) in bile, pancreatic and duodenal secretions of the dog. Amcr. J. Physiol., 186: 377. (5) Blackmon, D. M., W. J. Miller, and J. D. Morton. 1967. Zinc deficiency in ruminants: occurrence, effects, diagnosis, treatments. Vet. Med., 62: 265. (6) Bunn, C. R., and G. Matrone. 1966. Ill vivo interactions of cadmium, copper, zinc and iron in the mouse and rat. J. Nutrition, 90: 395. (7) Byrd, C. A., and G. Matrone. 1965. Investigations of chemical basis of zincealcinm-phytate interaction ir~ biological systems. Proc. Soc. Exptl. Biol. Med., 119 : 347. (8) Cotizias, G. C., D. C. Borg, and B. Selleck. 1962. Specificity of zinc pathway through the body; turnover of Zn-65 in the mouse. Amer. J. Physiol., 202:359. (9) Dreosti, I. E., S. Tao, and L. S. Hurley. 1968. Plasma zinc and leukocyte changes in weanling and p r e g n a n t rats during zinc deficiency. Proc. Soc. Exptl. Biol. Med., 128: 169. (10) Dukes, H. H. 1955. The Physiology of Domestic Animals. 7th ed. p. 668. Cornstock Publishing Associates, Ithaca, New York. (11) Dynna, O., and G. N. Havre. 1963. Interrelationship of zinc and copper in the nutrition of cattle. A complex zinc-copper deficiency. Acta Vet. Scand., 4: 197. (12) Dynna, O., and G. N. Havre. 1967. Some observations of a complex zinc-copper deficiency in cattle. Proc. I X t h Int. Grassland Congr., p. 717. (13) Edwards, H. M., Jr., W. S. Dunahoo, and H. L. Fuller. 1959. Zinc requirement studies with practical rations. Poultry Sci., 38: 436. (14) Feaster, J. P., S. L. Hansard, J. T. McCall, F. H. Skipper, and G. K. Davis. 1954. Absorption and tissue distribution of radio-

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zinc in steers fed high-zinc rations. J. Animal Sci., 13: 781. (15) Fontenot, J. P., R. F. Miller, and N. O. Price. 1964. Effects of calcium level and zinc supplementation of f a t t e n i n g lamb rations. (Abstr.) J. Animal Sci., 23: 874. (15a) Forbes, R. M. 1967. Studies of zinc metabolism. Chap. 7. Newer Methods of Nutritional Biochemistry with Applications and Interpretations. Vol. I I I . A. A. Albanese, ed. Academic Press, New York. (16) French, C. E., C. B. Smith, H. 1~. Fortmann, R. P. Pennington, G. A. Taylor, W. W. Hinish, and R. W. Swift. 1957. Survey of ten n u t r i e n t elements in Pennsylvania forage crops. I. Red clover. Pennsylvania Agr. Exp. Sta., Bull. 624. (17) Haaranen, S. 1962. The effect of zinc on itching tail root eczema in cattle. Nord. Vet. Med., 14: 265. (18) Haaranen, S. 1963. Zinc requirements of dairy cattle for removal of deficiency symptoms. Feedstuffs, 35(11) : 17. (19) Hartmans, J. 1965. The zinc supply of dairy cattle in the Netherlands. (Includes English title and summary). Verslag. Landbouwk. Onderzoek., 664. (20) Havre, G. N. 1969. The combined copperzinc deficiency in cattle. Proc. Int. Symp. Trace Element Metabolism in Animals. ( I n press.) (21) Hiatt, A. J., and H. F. Massey. 1958. Zinc levels in relation to zinc content and growth of corn. Agron. J., 50: 22. (22) Hiers, J. M., Jr., W. J. Miller, and D. M. Blackmon. 1968. ]~ffect of dietary cadmium and ethylenediaminetetraacetate on dry matter digestibility and organ weights in zinc-deficient and normal ruminants. J. Dairy Sei., 51: 205. (23) Hiers, J. M., Jr., W. J. Miller, and D. M. Blackmon. 1968. Endogenous secretion and reabsorption of ~Zine in ruminants as affected by zinc deficiency and the feeding of ethylenediaminetetraacetate or cadmium. J. Dairy Sci., 51: 730. (24) Hoekstra, W. G. 1964. Recent observations on mineral interrelationships. Federation Proc., 23: 1068. (25) Hoekstra, W. G. 1969. The complexity of dietary factors affecting zinc nutrition and metabolism in chicks and swine. Proc. Int. Symp. Trace Element Metabolism in Animals. ( I n press.) (26) Hsu, J. M., and 5. K. Anilane. 1966. Effect of zinc deficiency on zinc metalloenzymes in rats. Proc. 7th Int. Congr. Nutrition, 5 : 753. (27) Hurley, L. S., and H. Swenerton. 1966. Congenital malformations resulting from zinc deficiency in rats. Proc. Soc. Exptl. Biol. Med., 123:692. (28) Iyer, J. G. 1957. Trace element content JOUR~TAL OF DAIRY SCIENCE VOL. 53, NO. 8

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of milk in Indian cattle. Naturwissenschaften, 44: 636. Johnson, A. D., and W. J. Miller. 1970. Early actions of cadmium in the r a t and domestic fowl testis. I L Distribution of injected l~Cd. J. Reprod. Fert., 21: 395405. Lease, J. G., B. D. Barnett, E. J. Lease, and D. E. Turk. 1960. The biological unavailability to the chick of zlne in a sesame meal ration. J. Nutrition, 7 2 : 6 6 . Lease, J . G., and W. P. Williiams, J r . 1967. The effect of added magnesium on the availability of zinc with some highprotein feedstuffs. Poultry Sei., 46: 242. Legg, S. P., and L. Sears. 1960. Zinc sulphate treatment of parakeratosis in cattle. Nature, 186: 1061. 1,i, T. K. 1966. The functional role of zlne in metalloenzymes. In Zinc Metabolism. A. S. Prasad, ed. pp. 48-68. Charles C Thomas, Springfield, Illinois. Magee, A. C., and G. Matrone. 1960. Studies on growth, copper metabolism and iron metabolism of rats fed high levels of zinc. J. Nutrition, 72: 233. Martin, Y. G., W. J. Miller, and D. M. Blackmon. 1969. Wound healing, hair growth, and biochemical measures as affected by subnormal protein and energy intake in young cattle. Amer. J. Vet. Res., 30 : 355. Maynard, L. A., and J. K. Loosli. 1956. Animal Nutrition. 4th ed. p. 154. McGrawHill Book Company, New York. MeClanahan, B. J., R. O. McClellan, J. R. MeKenney, and L. K. Bustad. 1964. Milk secretion of zinc and cadmium in the ruminant. Presented Int. AEC Symp. Use of Radiosotepes in Animal Nutrition and Physiology. Prague, Czechoslovakia, Nov. 2327, 1964. Methfessel, A. H., O. Brdlik, and H. Spencer. 1969. Absorption of ~Zn from i~ rive intestinal loops in rats. (Abstr.) Federation Prec., 28: 761. Millar, M. J., M. I. Fischer, P. V. Elcoate, and C. A. Mawson. 1958. The effects of dietary zinc deficiency on the reproductive system of male rats. Canadian J. Biochem. Physiol., 36 : 557. Miller, J. K. 1967. Effect of protein source and feeding method on zinc absorption by calves. J. Nutrition, 93: 386. Miller, J. K., and R. G. Cragle. 1965. Gastrointestinal sites of absorption and endogenous secretion of zinc in dairy cattle. J. Dairy Sci., 48: 370. Miller, J. K., and W. J. Miller. 1960. Development of zinc deficiency in Holstein calves fed a purified diet. J. Dairy Sci., 43 : 1854. Miller, J. K., and W. J. Miller. 1962. EX-

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perimental zinc de~ciency and recovery in calves. J. Nutrition, 76 : 467. Miller, J. K., W. J. Miller, and C. M. Clifton. 1962. Calf response to starters of varying zlne contents. J. Dairy Sci., 45: 1536. Miller, W. J. 1964. Zinc gains importance in role it plays in animal nutrition. The Feed Bag Red Book, Reference Book of the Feed Industry. p. 9. Miller, W. J. 1967. Calfhood zinc deficiency and limited feed intake on subsequent reproduction in bulls. Feedstuffs, 39(17) : 18. Miller, W. J. 1968. Homeostatic control of zinc in ruminants. Prec. 2nd World Conf. Animal Prod. p. 444. Miller, W. J. 1969. Absorption, tissue distribution, endogenous excretion, and homeostatic control of zinc in ruminants. Amer. J. Clin. Nutrition, 22: 1323. Miller, W. J., W. E. Adams, R. Nussbanmer, R. A. McCreery, and H. F. Perkins. 1964. Zinc content of coastal bermudagrass as influenced by frequency and season of harvest, location, and level of N and lime. Agron. J., 56: 198. Miller, W. J., D. M. Blackmon, R. P. Gentry, F. M. Pate, and Y. G. Martin. 1969. ~Zinc distribution in various tissues of zinc-deficient and normal bull calves with time a f t e r single I.V. or oral dosing. Unpublished d a t a Miller, W. J., D. M. Blackmon, R. P. Gentry, W. J. Pitts, and G. W. Powell. 1967. Absorption, excretion and retention of orally administered zinc-65 in various tissues of zinc-deficient and normal goats and calves. J. Nutrition, 92: 71. Miller, W. J., D. M. Blackmon, R. P. Gentry, and G. W. Powell. 1966. Influence of zinc deficiency per se on Zn ~ absorption in ruminants. Prec. 7th Int. Congr. Nutrition, 5 : 749. Miller, W. J., D. M. Blaekmon, R. P. Gentry, G. W. Powell, and H. F. Perkins. 1966. Influence of zinc deficiency on zinc and dry matter content of ruminant tissues and on excretion of zinc. J. Dairy Sei., 49: 1446. Miller, W. J., D. M. Blackmon, J. M. Hiers, Jr., P. R. Fowler, C. M. Clifton, and R. P. Gentry. 1967. Effects of adding two forms of supplemental zinc to a practical diet on skin regeneration in Holstein heifers and evaluation of a procedure for determining rate of wound healing. J. Dairy Sci., 50: 715. Miller, W. J., D. M. Blackmon, and Y. G. Martin. 1968. ~ C a d m i u m absorption, excretion, and tissue distribution following single tracer oral and intravenous doses in young goats. J. Dairy Sci., 51: 1836. Miller, W. J., D. M. Blackmon, and E. M.

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Fate. 1970. Zinc metabolism in ruminants. Proc. Int. Symp. Trace Element Metabolism in Animals. (In press.) Miller, W. ft., D. M. Blackmon, F. M. Pate, Y . G. Martin, and J. W. Foster. 1968. Effects of vaccinations with strain 19 Brueel~a a b o ~ s , triple bacterin, or endotoxins on serum alkaline phosphatase in dairy calves, ft. Dairy Sci., 51: 1791. MilIer, W. J., D. M.Blackmon, G. W. Powell, R. P. Gentry, and ft. M. Hiers, Jr. 1966. Effects of zinc deficiency per se and of dietary zin~ on urinary and endogenous fecal excretion of ~Zn from a single intravenous dose by ruminants. J. Nutrition, 90 : 335. Miller, W. J., C. M. Clifton, and i~. W. Cameron. 1963. Zinc requirement of Holstein bull calves to nine months of age. ft. Dairy Sei., 46: 715. Miller, W. J., C. M. Clifton, P. R. Fowler, and H. F. Perkins. 1965. Influence of high levels of dietary zinc on zinc in milk, performance and biochemistry of lactating cows. J. Dairy Sci., 48: 450. Miller, W. J., B. Lampp, G. W. Powell, C. A. Salotti, and D. M. Blackmon. 1967. Influence of a high level of dietary cadmium on cadmium content in milk, excretion, and cow performance. J. Dairy Sei., 50 : 1404. Miller, W. J., Y. G. Martin, D. M. Blackmort, and P. R. Fowler. 1969. Effect of high protein diets with normal and low energy intake on wound healing, hair growth, hair and serum zinc, and serum alkaline phosphatase in dairy heifers. J. Nutrition, 98 : 411. Miller, W. J., Y. G. Martin, R. P. Gentry, and D. M. Blackmon. ]968. ~Zn and stable zinc absorption, excretion, and tissue concentrations as affected by type of diet and level of zinc in normal calves. J. Nutrition, 94: 391. Miller, W. J., and J. ]~. Miller. 1963. Photomicrographs of skin from zinc-deficient calves. J. Dairy Sci., 46: 1285. Miller, W. J., and J. K. Miller. ]963. Zinc content of certain feeds, associated materials, and water, J. Dairy Sci., 46: 581. Miller, W. J., J. D. Morton, W. J. Pitts, and C. M. Clifton. 1965. Effect of zinc deficiency and restricted feeding on wound healing in the bovine. Proc. Soc. Exptl. Biol. Med., 118: 427. Miller, W. it., W. J. Pitts, C. M. Clifton, and ft. D. Morton. 1965. Effects of zinc deficiency per se on feed efficiency, serum alkaline phosphatase, zinc in skin, behavior, greying, and other measurements in the Holstein calf. J. Dairy Sci., 48: 1329. Miller, W. ft., W. 5. Pitts, C. M. Clifton, and S. C. Schmittle. 1964. Experimentally

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(84) O'Dell, B. L., P. M. Newberne, and J. E. Savage. 1958. Significance of dietary zinc for the growing chicken. J. Nutrition, 65 : 503. (85) Oltjen, R. R., and R. E. Davis. 1965. Factors affecting the ruminal characteristics of cattle fed all-concentrate rations. J. Animal Sci., 24: 198. (86) Oltjen, R. R., R. E. Davis, and R. L. Hiner. 1965. Factors affecting performance and carcass characteristics of cattle fed allconcentrate rations. J. Animal Sci., 24: 192. (87) Ott, E. A., W. H. Smith, R. B. Harrington, and W. M. Beeson. 1966. Zinc toxicity in ruminants. I. Effect of high levels of dietary zinc on gains, feed consumption and feed efficiency of lambs. J. Animal Sei., 25 : 414. (88) Ott, E. A., W. H. Smith, R. B. Harrington, and W. M. Beeson. 1966. Zinc toxicity in ruminants. II. Effect of high levels of dietary zinc on gains, feed consumption and feed efficiency of beef cattle. J . Animal Sci., 25 : 419. (89) Ott, E. A., W. H. Smith, R. B. Harrington, H. E. Parker, and W. M. Beeson. 1966. Zinc toxicity in ruminants. IV. Physiological changes in tissues of beef cattle. J . Animal Sei., 25: 432. (90) Ott, E. A., W. H. Smith, R. B. Harrington, M. Stob, H. E. Parker, and W. M. Beeson. 1966. Zinc toxicity in ruminants. I I I . Physiological changes in tissues and alterations in rumen metabolism in lambs. J. Animal Sci., 25: 424. (91) Ott, E. A., W. H. Smith, H. E. Parker, R. B. Harrington, and W. M. Beeson. 1965. Zinc requirement of the growing lamb fed a purified diet. J. Nutrition, 87: 459. (92) Oft, E. A., W. H. Smith, M. Stob, and W. M. Beeson. 1964. Zinc deficiency syndrome in the young lamb. J. Nutrition, 82 : 41. (93) Oft, E. A., W. H. Smith, M. Stob, H. E. Parker, and W. M. Beeson. 1965. Zinc deficiency syndrome in the young calf. J. Animal Sci., 24: 735. (93a) Parisi, A. F., and B. L. Vallee. 1969. Zinc metalloenzymes: characteristics and significance in biology and medicine. Amer. J. Clin. Nutrition, 22: 1222. (94) Parkash, S., and R. Jenness. 1967. Status of zinc in cow's milk. J. Dairy Sci., 50 : 127. (95) Pekas, J. C. 1966. Zinc-65 metabolism: gastrointestinal secretion by the pig. Amer. J. Physiol., 211: 407. (96) Pekas, J. C. 1968. Zinc-65 metabolism: effect of continuous infusion of high levels of stable zinc in swine. J. Animal Sci., 27 : 1559. (97) Perry, T. W., W. M. Beeson, W. H. Smith, and M. T. Mohler. 1968. Value of zinc supplementation of natural rations for JOURI~ALoF,DAIRYSCIENCE~70L. 53, NO. 8

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fattening beef cattle. J. Animal Sci., 27 : 1674. Pierson, R. E. 1966. Zinc deficiency in young lambs. J. Amer. Vet. Med. Ass., 149 : 1279. Pitts, W. J., W. J. Miller, O. T. Fosgate, J. D. Morton, and C. M. Clifton. 1966. Effect of zinc deficiency and restricted feeding from two to five months of age on reproduction in Holstein bulls. J. Dairy Sci., 49: 995. Pories, W. J., J. H. Henze], C. G. Rob, and W. H. Strain. 1967. Acceleration of healing with zinc sulfate. Ann. Surg., 165 : 432. Pories, W. J., W. H. Strain, and C. G. Rob. 1968. Zinc deficiency, delayed healing, and chronic disease. Symp. Environmental Geochemistry in Relation to Human Health and Disease. 135th Annual Meeting, Amer. Ass. Adv. Sci., December 30. Powell, G. W., W. J. Miller, and D. M. Blackmon. 1967. Effects of dietary EDTA and cadmium on absorption, excretion, and retention of orally administered ~Zn in various tissues of zinc-deficient and normal goats and calves. J. Nutrition, 93: 203. Powell, G. W., W. J. Miller, and C. M. Clifton. 1964. Effect of cadmium on the palatability of calf starters. J. Dairy Sci., 47: 1017. Powell, G. W., W. J. Miller, J. D. Morton, and C. M. Clifton. 1964. Influence of dietary cadmium level and supplemental zinc on cadmium toxicity in the bovine. J. Nutrition, 84: 205. Prasad, A. S., ed. 1966. Zinc Metabolism. Charles C Thomas, Publisher, Springfield, Illinois. Prasad, A. S. 1967. Nutritional metabolic role of zinc. Federation Proc., 26: 172. Price, W. D., and W. H. Smith. 1968. Factors affecting zn requirement of cattle. (Abstr.) J. Animal Sci., 27: 1174. Quarterman, J. 1968. The metabolic role of zinc with special reference to carbohydrate and lipid metabolism. Rowett Ros. Inst. Rep., 24: 100. Quarterman, J., W. R. Humphries, and E. Florence. 1969. Changes in appetite and alimentary muco-substances in zinc deficiency. Proc. Int. Symp. Trace Element Metabolism in Animals. Sahagian, B. M., L Harding-Barlow, and It. M. Perry, Jr. 1967. Transmural movements of zinc, manganese, cadmium and mercury by rat small intestine. J. Nutrition, 93: 291. Sandstead, H. H. 1968. Zinc. A metal to grow on. Nutrition Today, 3 ( 1 ) : 1 2 . Settlemire, C. T., and G. Matrone. 1967. In vivo interference of zinc with ferritin iron in the rat. J. Nutrition, 92: 153.

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a-Mannosidase as a zinc-dependent enzyme. Nature, 218(5136) : 91. Sullivan, T . W . 1962. Zinc content of feed ingredients and dried egg samples. Poultry Sci., 41 : 339. Supplee, W. C. 1961. Production of zinc deficiency in turkey poults by dietary cadmium. Poultry Sci., 40:827. Todd, W. R., C. A. Elvehjem, and E. B. Hart. 1934. Zinc in the nutrition of the rat. Amer. J. Physiol., 107: 146. Tucker, H. F., and W. D. Salmon. ]955. Parakeratosis or zinc deficiency disease in the pig. Prec. Soc. Exptl. Biol. Med., 88: 613. Underwood, E. J. 1956. Trace Elements in Human and Animal Nutrition. Academic Press, New York. Underwood, E. J. 1962. Trace Elements in Human and Animal Nutrition. 2nd ed. Academic Press, New York. Yallec, B. L. 1959. Biochemistry, physiology and pathology of zinc. Physiol. Rev., 39: 443. Van Campen, D. R. 1969. Copper interference with the intestinal absorption of Zinc-65 by rats. J. Nutrition, 97: 104. Van Campen, D. R., and E. A. Mitchell. 1965. Absorption of Cu~, Zn% 1~o9°, and

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Fe n from ligated segments of the rat gastrointestinal tract. J. Nutrition, 86: 120. Van Leeuwen, J. M., and J. van der Grift. 1969. Observations on the zinc metabolism of calves. Prec. Int. Syrup. Trace :Element Metabolism in Animals. (In press.) Viets, F. G., Jr. 1966. Zinc deficiency in the soil-plant system. In Zinc Metabolism. 2nd ed. p. 90. A. S. Prasad, ed. Charles C Thomas, publisher, Springfield, Illinois. Voe]ker, H. H., N. A. Jorgensen, G. P. Mohanty, and M. J. Owens. 1969. Effect of zinc supplementation to dairy cattle rations. (Abstr.) J. Dairy Sci., 52: 929, and personal communication. Wacker, W. E. 1969. l~olecular biology of metalloenzymes. Symposium presentation at Federation meetings. Weston, R. H., and J. Kastelic. :1967. The transfer of zinc from the blood to the rumen in sheep. Australian J. Biol. Set., 20 : 975. Williams, R. B., and 5. K. Chesters. 1969. Effects of zinc deficiency on nucleic acid synthesis in the rat. Prec. Int. Syrup. Trace Element Metabolism in Animals. Wise, M. B., and E. R. Barrick. 1963. All concentrate rations for beef cattle. Prec. Maryland Nutrition Conf. p. 80.

Selenium D. E. HOGUE

Department of Animal Science Comell University, Ithaca, New York 14850 I ntroduction

Selenium has long been considered an element toxic to f a r m animals and since 1957, when Schwarz and F o l t z (22) demonstrated its effectiveness in p r e v e n t i n g liver necrosis in the rat, has been studied as a "required" element as well (7, 10, 13, 15, 20). Several recent symposia and reviews (2, 3, 5, 16, 17, 21, 24) have covered most aspects of selenium in nutrition; therefore, this p a p e r will attempt to elucidate those areas not previously covered in detail and present a general concept of seleninm's present status. Selenium toxicity. 0]son (17) has presented an excellent and brief review of selenium as a toxic factor in animal nutrition. Fie indicates that toxic effects may result f r o m continuous intake of feeds as low as 5 p p m of selenium and that the occurrence of 5 to 10 p p m in hair of animals on seleniferous-suspect feeds is an indication of possible selenium toxicity. Below

5 p p m can be considered safe and those above 10 p p m may indicate difficulty. Arsenicals in the feed will give some protection against selenium for poultry and swine. Some additional feeds or compounds are beneficial in selenium toxicity. Selenium in plants is derived f r o m the p a r e n t soil material and tends to accumulate, particularly in some plants (i.e., Astragalus). The selenium toxic areas in the United States are reasonably well identified and mapped. Selenium deficiency. Many syndromes have been shown selenium-responsive (included in a partial listing are: nutritional muscular dyst r o p h y in lambs, calves, foals, poults, chicks, etc. ; liver necrosis in rats and pigs and exudat i r e diathesis in chicks). E v e n so, many nntritionists hesitate to include selenium as a required element until its involvement in a specific reaction is demonstrated. This is partially a reflection of the times, since vitamin E (to which the aforementioned syndromes are responsive) ~OURI~TAI~OF DAIRY SCIENCE ~rOL, 53, ~O. 8