Toxicity of Mercury to Young Chickens

Toxicity of Mercury to Young Chickens 2. GROSS CHANGES IN ORGANS1'2 P. THAXTON C. R. PARKHURST

Department of Poultry Science, North Carolina State University, Raleigh, North Carolina 27607 (Received for publication May 1, 1972)

PODLTRY SCIENCE 52:

INTRODUCTION

M

ERCURY is an environmental contaminant that accumulates in certain food chains. For example, fish which may be a significant factor in poultry diets can contain mercury at levels surpassing the levels approved by F.D.A. Mercury administered per os to birds accumulates in several tissues. Kiwimae et al. (1969) showed that in chickens the liver and kidneys accumulated more mercury on a proportional basis than did the blood or skeletal muscle tissues. Similar results were found in several species of upland game birds, waterfowl, pigeons and doves, song birds, and fish-eating birds (Fimreite et al., 1970, 1971; Fimreite and Korstad, 1971). Westoo (1967) analyzed muscle tissue from several species and found that 60% or more of the mercury existed as methylmercury. This finding has been corroborated in hens by Karppanen et al. (1968) and Rissanen and Mietlinen (1968). Although the accumulation in tissues of 1

A preliminary report of part of this paper was presented at the 69th Annual Meeting of the Association of Southern Agricultural Workers, Richmond, Virginia, 1972. 2 Paper number 3749 of the Journal Series of the North Carolina State University Agricultural Experiment Station, Raleigh, North Carolina.

277-281,

1973

mercury from dietary sources, as well as that administered by injections has been studied, the effect that this metal has on the tissues and organs is not known. The purpose of this study was to extend the description of mercury toxicosis by determining the effect of graded doses of dietary mercury on the relative weights of several organs of chickens. MATERIALS AND METHODS Four trials were conducted in which 240 Vantress X Hubbard cockerels were maintained on graded doses of mercuric chloride (HgCl 2 ). Each trial was composed of six treatments with four groups of 10 chicks at each treatment. The treatments consisted of adding 0, 5, 25, 125, 250, or 500 y.g. of mercury per ml. of drinking water. The mercury was added as HgCl2 and the stated concentrations are correct for the mercury content. The HgCl2 was added to tap water and dissolved completely by continuous stirring for one hour with an automatic stirrer. The birds were housed in electrically heated metal cages throughout the experimental period. The chicks received the mercury treatments from hatching until termination at five, 14, or 16 weeks. Feed and water

277

Downloaded from http://ps.oxfordjournals.org/ by guest on May 12, 2015

ABSTRACT Mercury at a concentration of 2S0 p.p.m. or greater in the drinking water of young cockerels depressed growth at five weeks and caused a high level of mortality. The relative weights of the heart and adrenals were increased after five weeks of treatment. At this same time the relative weights of the liver, spleen, and bursa of Fabricius were decreased. Five and 14 weeks of continuous high dosage of mercury did not alter the relative total testes weight, although a significant depression was found after 16 weeks of this treatment.

278

H—

P. THAXTON AND G. R. PARKHURST 0.8 r

fc ><
O

-H-

5 25 125 " 250 500 MERCURY IN DRINKING WATER (ppm)

FIG. 1. Relative heart weight as affected by dietary mercury.

RESULTS

Significant changes in the relative weights of the heart, liver, adrenal glands, testes, spleen, and bursa of Fabricius were caused by 250 and 500 p.p.m. of mercury. The lower dose levels (5, 25, and 125 p.p.m.) did not cause significant changes in the relative sizes of the organs under study. Relative heart weights were increased significantly by 250 and 500 p.p.m. of mercury (Fig. 1). Concomitantly, the hearts of these birds were flaccid to the touch and lacked the degree of tonicity of hearts from controls and birds that received 125 p.p.m. of mercury or less. The relative weights of the livers of the birds that received 250 p.p.m. were decreased and the livers of the

0 5 25 125 250 MERCURY IN DRINKING WATER(ppm)

FIG. 2. Relative weight of the liver as affected by dietary mercury. 40r

'0

5 25 125 250 500 MERCURY IN DRINKING WATER (ppm)

FIG. 3. The effect of graded doses of dietary mercury on adrenal size.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 12, 2015

were available ad libitum in stainless steel troughs. At the time of sacrifice the birds were weighed and then sacrificed by cervical dislocation. The wet-weights of the heart, liver, adrenal glands, testes, spleen, and bursa of Fabricius were determined. Calculations of organ size relative to the body weight were made. Group means were subjected to an analysis of variance and the treatment means were compared by the method of least significant differences. Statements of significance are based on P < 0.05. Details of the procedures are given by Bruning and Kintz (1968).

controls and the birds that received the lower doses were not affected (Fig. 2). The relative weights of the combined adrenal glands were increased in a linear manner by the two highest doses of mercury (250 and 500 p.p.m.). The relative weights of the adrenals from the birds which received 500 p.p.m. were four-fold greater than the adrenals of controls (Fig. 3). The testes were not affected by any of the dose levels throughout the first five weeks or at 14 weeks (Table 1). However, it should be noted that 250 p.p.m. drastically reduced the relative weights of the combined testes at 16 weeks. The data which are relative to

279

MERCURY TOXICITY

O 3

0

5 25 125 " 2 5 0 500 MERCURY IN DRINKING W A T E R ( p p m )

TABLE 1.—A feci ofdietary mercury on the growth of the testes of broiler cockerels1'* Relative Total Testes Weighti S.E.M. (gm./lOO gm. body weight)

Dosage of Mercury (p.p.m.)

5 weeks

14 weeks

16 weeks

0 5 25 125 250 500

3.7 ±.32" (39) 3.6±.36 aa (39) 3.5±.34 a (39) 3.6±.32 a (39) 3.6±.31 a(32) 3.7±.32 ( 5)

4.6±.57 aa (38) 3.5±.42 (37) 3.9±.38 aa (38) 4.5±.50 (37) 3.4±.52 a (21)

15.2± .60"a (38) 13.8± .52 (37) 15.7± .63aa (37) 13.5± .42b (30) 4.1±.34 (18)

1 Means in columns possessing different superscripts differ significantly at P<0.05 and the number of birds representing the2 means are included in parentheses. The dosage of mercury was attained by adding HgCh to the drinking water and the concentrations are correct for the mercury content.

weeks by adding HgCl2 to the drinking water had a pronounced effect on growth and the relative weights of certain of the vital organs. It should be noted that only dose levels of mercury that exceeded 125 p.p.m. caused these changes. These higher levels of mercury are growth depressive and cause a high rate of mortality (Parkhurst and Thaxton, 1973). Apparently, 250 p.p.m. is the threshold dose for mercury toxicity in young chickens. DISCUSSION The results of this study indicate that mercury, when administered to chickens per os, causes several distinct systemic changes other than the neurological dysfunction syndrome described by Femreite

Fir,. 4. Relative weight of the spleen as affected by dietary mercury.

04

0

5 25 125 250 500 MERCURY IN DRINKING WATER (ppm)

Frc. S. Relative weight of the bursa of Fabricius as affected by dietary mercury.

FIG. 6. Gross pathological changes caused by chronic mercury toxicity.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 12, 2015

the effect of mercury on testes size are presented in Table 1. The relative weights of the spleen (Fig. 4) and the bursa of Fabricius (Fig. 5) were decreased significantly by doses of 250 p.p.m. of mercury or greater. Again doses less than 250 p.p.m. did not cause significant changes in the relative weights of the spleen and the bursa of Fabricius. Several gross pathological changes were observed at necropsy which was performed within 15 minutes after death. An illustration of these changes is presented in Figure 6. The typical changes in birds that died from chronic mercury toxicity were an obvious deposition of urates in the kidney and the connective tissues associated with skeletal muscles, extensive hemorrhage of liver tissue, and inflammation and distension of the intestine. Mercury administered to chicks for five

280

P. THAXTON AND G. R. PARKHURST

remains unanswered. It would appear that the effects of mercury are diverse and are recognizable as various independent systemic changes. In depth efforts are needed to delineate the mode of toxicity of mercury since this metal is rapidly becoming an unavoidable environmental contaminant. ACKNOWLEDGMENTS

This investigation was supported by Biomedical Science Support Grant RR07071 from the National Institute of Health. We thank Miss Linda Travis, Miss Jacque Atkins, and Mr. Larry Cogburn for technical assistance. REFERENCES Bruning, J. L., and B. L. Kintz, 1968. Computational Handbook of Statistics. Scott, Foresman, and Company, Glenview, Illinois. Femreite, N., R. W. Fyfe and J. A. Keith, 1970. Mercury contamination of Canadian prairie seed eaters and their avian predators. Canadian Field-Naturalist, 84: 269-276. Femreite, N., W. N. Holsworth, J. A. Keith, P. A. Pearce and I. M. Gruchy, 1971. Mercury in fish and fish-eating birds near sites of industrial contamination in Canada. Canadian Field-Naturalist, 85: 211-220. Femreite, N., and L. Korstad, 1971. Effects of dietary methyl mercury on red-tailed hawks. J. Wildlife Management, 35: 293-300. Karppanen, E., K. W. Henriksson and E. V. Nurmi, 1968. Effects of alkoxyalkyl mercury compounds on the health of hens and the occurrence of mercury in different organs. Ann. Agr. Fenn., Suppl. 7: 24-29. Kiwimae, A., A. Swenssen, U. Ulffvarson and G. Westoo, 1969. Methylmercury compounds in eggs from hens after oral administration of mercury compounds. J. Agr. Food Chem. 17: 1014-1016. Parkhurst, C. R., and P. Thaxton, 1973. Toxicity of mercury to young chickens. 1. Effect on growth and mortality. Poultry Science 52: 266-272. Rissanen, K., and J. K. Mietlinen, 1968. Thinlayer chromatography of alkyl and alkoxy mercury derivatives and location of mercury in the yolks of the hen egg. Ann. Agr. Fenn., Suppl. 7.: 22-23.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 12, 2015

and Korstad (1971). The increased heart weight suggests that mercury is exerting a direct effect on cardiac muscle tissue. Femreite and Korstad (1971) noted degenerative changes in the myocardium of the redtailed hawk which consisted of nuclear pyknosis and granular swelling of sarcoplasm. Possibly, the increased heart weight that was observed in this study was a compensatory response to ameliorate the degenerative changes occurring in the myocardium. The increase in total adrenal weight concomitant with a decrease in the relative weights of the spleen and bursa of Fabricius suggests that mercury caused a classic physiological stress response. Siegel (1971) has reviewed the relationship of the adrenals of avian species to the physiological responses which are collectively termed stress. The high levels of HgCl2 (250 and 500 p.p.m.) prevented the normal development of the testes which occurred in the controls and the birds which received the non-toxic levels (5, 25, and 125 p.p.m.) between 14 and 16 weeks. These data offer indirect evidence that the male bird which is experiencing chronic mercury toxicity does not develop its normal reproduction potential. The loss of reproductive performance in birds exhibiting mercury toxicity has been attributed to the female. The specific effect of mercury in female birds is a decreased number of fertile eggs which possess thinned shells (Stoewsand et al., 1971; Tejning, 1967). An equally attractive alternative is that the reproductive potential of the male is diminished by mercury toxicity. Clarification of the role of mercury in the development of the reproductive potential of male chickens is necessary to determine the relationship of mercury to reproductive performance in birds. The question of how and why mercury is toxic to birds, and chickens in particular,

281

MERCURY TOXICITY Siegel, H. S., 1971. Adrenals, stress and the environment. World's Poultry Sci. J. 27: 329349. Stoewsand, G. S., J. L. Anderson, W. H. Gutewmann, G. A. Bache and D. J. Lish, 1971. Eggshell thinning in Japanese Quail fed mercuric chloride. Science, 173: 1030-1031. Tejning, S., 1967. Biological effects of methyl

mercury dicyandiamide treated grain in the domestic fowl Gallus gallus L. I. Studies on food consumption, egg production and general health. Oikos, Suppl. 8: 7-17. Westoo, G., 1967. Determination of methylmercury compounds in foodstuffs. II. Determination of methylmercury in fish, egg, meat and liver. Acta Chem. Sand. 2 1 : 1790-1800.

Factors Influencing the Liver Fat Content of Laying Hens

(Received for publication May 4, 1972)

ABSTRACT An incidence of mortality from hemorrhage in fatty livers of Cornell experimental flocks is described. Hens fed diets varying in energy or protein content showed a wide range in liver fat content when sampled at various times during the laying year. The ability of individual hens to adjust to changes in energy concentration of the diet was not correlated with liver fat content. In hens fed specific diets, liver fat was not correlated with energy intake or rate of egg production. Feeding a low energy diet for 21 days caused a reduction in liver fat, compared to that in hens fed a control diet. However, when the hens were returned to the control diet, liver fat quickly returned to the level found in hens fed the control diet continuously. When hens were force fed 10% more feed than ad libitum controls consumed, marked increases in liver size and fat content occurred, but no mortality was observed from liver hemorrhages. Fatty livers had a higher content of neutral lipid, mainly triglyceride, than livers lower in fat. The content of oleic acid increased and linoleic acid decreased as liver fat increased. This suggests that fatty acid biosynthesis is the major source of the lipid in fatty livers. These studies showed that liver fat content of hens is variable and that high levels of liver fat are not necessarily detrimental to laying performance. Hemorrhages from fatty livers may be related to other factors than liver fat content per se. POULTRY SCIENCE 52:

E

XCESSIVELY fatty livers have been cited by several investigators as being related to field observations of mortality in laying hens, and in some cases, poor laying performance (Couch, 1956; Ringer and Sheppard, 1963; Wolford et al., 1971). A "fatty liver syndrome" has been described which has been associated with lowered egg production, excess abdominal fat, fatty livers and liver hemorrhages (Couch, 1956). The condition as described in field observations has not been reproduced in the laboratory, although Barton (1967) and Duke 1 Present address: Procter and Gamble Ivorydale Research Center, Cincinnati, Ohio.

281-291,

1973

et al. (1968) found that hens fed diets very high in energy and relatively low in protein developed high levels of liver fat. Several reports have dealt with factors affecting liver fat content. Hartfiel et al. (1970b) observed that hens kept in cages had a higher average liver fat content than hens housed in floor pens. In a further study, Hartfiel et al. (1970a) showed that forced exercise and consumption of feces caused a reduction of liver fat in hens housed in cages. Barton (1967) observed that feeding low energy diets reduced liver score measurement, a measure associated with liver fat content. Other workers have

Downloaded from http://ps.oxfordjournals.org/ by guest on May 12, 2015

C. A. IVY 1 AND M. C. NESHEIM Department of Poultry Science, Cornell University, Ithaca, New York 14850