- Email: [email protected]
Aspartic-Glutamic Transaminase Activity in Chick Liver
96
J. E. ALICATA
of the adult parasites was noted among chickens when the drug was fed in a small amount of wet mash at the rate of 200 to 300 mg./kg. bodyweight. The inclusion of 0.05 percent of piperazine citrate in the normal ration was only partially effective in preventing ascarid infection. A concentration of 0.1 percent was comparatively effective, but this level is considered too high for practical use.
Horton-Smith, C , and P. L. Long, 1956. The anthelmintic effect of three piperazine derivatives on Ascaridia galli (Schrank 1788). Poultry Sci. 35: 606-614. Roberts, F. H. S., 1937. Studies on the biology and control of the large roundworm of fowls Ascaridia galli (Schrank 1788) Freeborn 1923. Animal Health Sta. Yeerongpilly, Queensland, Bui. 2, 106 pp., pis.
Bradley, R. E., 1955. Observations on the anthelmintic effect of piperazine citrate in chickens. Vet. Med. 50: 444-447.
Shumard, R. F., and D. F. Eveleth, 1956. Further studies on the anthelmintic action of piperazine citrate. Vet. Med. 51: 515-517.
Aspartic-Glutamic Transaminase Activity in Chick Liver M . N . D . GOSWAMI AND A. R . ROBBLEE Department of Animal Science, University of Alberta, Edmonton, Alberta (Received for publication July 15. 1957)
T
HE importance of enzymatic transamination in the biological system and its implication in amino acid metabolism has become evident in recent years (Meister, 1955). Of the various transaminases, the classical aspartic-glutamic transaminase has been studied in most detail. As a result of their studies, Schlenk and Snell (1945) and later Schlenk and Fisher (1947) suggested that vitamin B 6 may function as a coenzyme for transaminase. Green et al. (1945) showed that pyridoxal phosphate acted as a coenzyme of aspartic-glutamic transaminase. In studies on the relationship of vitamin I$6 to aspartic-glutamic transaminase, Ames et al. (1947) showed that tissues of vitamin B6 deficient rats exhibited only 40 percent of the enzyme activity of those receiving adequate vitamin B e . Similar results have been reported by Schwartzman and Hift (1951) in the heart muscle of hamsters and by Caldwell and McHenry (1953) in the liver of rats. Working with
ducks, Brin and Olson (1951) reported that in a pyridoxine-deficiency the activity of aspartic-glutamic transaminase in the cardiac muscle was 30 percent below normal. While numerous reports are available concerning the relationship of vitamin B6 to aspartic-glutamic transaminase of mammalian tissues, there is no information on the levels of aspartic-glutamic transaminase in the chick. The present investigation was designed to study the aspartic-glutamic transaminase activity in the tissues of chicks fed purified rations varying in vitamin B6 content. METHODS
The chicks used in this study were dayold Single Comb White Leghorn chicks. The experimental groups were housed in electrically heated batteries with raised screen floors. Feed and water were supplied ad libitum. Four comparable groups of 30 chicks were fed the pyridoxine-
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
REFERENCES
Shumard, R. F., and D. F. Eveleth, 1955. A preliminary report of the anthelmintic action of piperazine citrate on Ascaridia galli and Heterakis gallinae in hens. Vet. Med. 50: 203-205.
97
TRANSAMINASE ACTIVITY
TABLE 1.—Composition of basal ration (gm. per 100 gm. of ration) Ingredients Sucrose Vitamin-test casein Gelatin Corn oil Fish oil (2,250A, 300D) Salt V DL-Methionine
60.7 18 10 4.75 0.25 6 0.3
Level of pyridoxine Lot no. (mcgm./lOO gm. • of ration) 0 0 150 300 600 0 150 300 600 0 150 300 600
Age in weeks 1 2
Heart (QT 10 ) 538 394 284 538 682 677 538 660 699 538 583 791 Liver ( Q T 1 0 ) 258 266 196 258 369 340 258 351 287 258 398 320 Blood (T.A.A. units) 540 460 2X0 540 400 353 540 425 375 540 500 440
3 221
4
5
*
563 — 560 709 640 637 620 674 677 138 291 336 282 259 293 287 284 318 293 270 —* —* 295 295 360 380 380 400 350 335 380
* No chicks alive after 3 weeks of age.
deficient purified basal ration shown in Table 1, supplemented with four levels of pyridoxine, namely, 0, 150, 300 and 600 micrograms per 100 gm. of ration. The aspartic-glutamic transaminase in the heart, liver and blood was measured at 0, 7, 14, 21, 28 and 35 days of age. For transaminase assay, the birds were killed b y severing the jugular vein and the pooled samples of blood from chicks of the same group were frozen at — 20°C. and held for future analysis. The heart and liver tissues were removed and weighed in a cold room at 4°C. Each sample of heart and liver tissues was then divided into weighed portions. One portion was dried a t 100°C. in a vacuum oven for 24 hours for determination of dry weight. Another portion was homogenized in a glass-homogenizer of the PotterElvehjem type with ten times its weight of ice-cold phosphate buffer of p H 7.4 and then diluted with the same buffer to yield a 1.0% homogenate. Transaminase activities of heart and liver were measured according to the colorimetric procedure outlined by Tonhazy et al. (1950) using a Bausch and L o m b photoelectric colorimeter a t 520 mju. The activity is expressed in Q T 1 0 units, defined b y Ames and Elvehjem (1946) as the ml. of C 0 2 (pyruvate) liberated per hour per mg. of dry weight
of the tissues (heart and liver) during a 10 min. incubation period. The whole blood was hemolyzed by freezing and thawing a number of times and then homogenized in the glass homogenizer. A volume of 0.1 or 0.2 ml. of the hemolyzed blood was used for the analyses. The enzyme activity is expressed in units of aspartic-glutamic transaminase activity (T.A.A.) as outlined by Marsh et al. (1955). The enzyme activities reported represent the average of two determinations, each made on individual samples RESULTS AND DISCUSSION Levels of aspartic-glutamic transaminase activity in the heart, liver and blood of chicks fed rations containing varying levels of pyridoxine are shown in Table 2. I n the group receiving the pyridoxinedeficient basal ration (Lot 1), there was a rapid decrease in transaminase activity with age. The levels of activity in heart, liver and blood at three weeks of age were approximately 40, 53 and 50 percent respectively of those observed in day-old chicks. No chicks survived in the pyridoxine-deficient group after three weeks of age. In groups receiving supplemental pyridoxine (Lots 2, 3 and 4), the levels of transaminase activity in heart and liver tissues to five weeks of age were slightly
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
Vitamins were added at the following levels in milligrams per 100 gm. of ration: thiamine hydrochloride 0.4, riboflavin 0.6, calcium pantothenate 2.0, niacin 5,0, biotin0.03, folic acid 0.5, 2 methyl 1-4 naphthoquinone 0.05, Bi2 0.003, vitamin E acetate 1.0, choline chloride 150.0.
TABLE 2.—Aspartic-glutamic transaminase activity in the tissues of chicks fed rations containing different levels of pyridoxine
98
M . N . D . GOSWAMI AND A. R . ROBBLEE
enzyme activity over those receiving the requirement level (Lot 3). SUMMARY
(1) Feeding chicks a pyridoxine-deficient ration resulted in a rapid decrease in aspartic-glutamic transaminase activity. The levels of activity in heart, liver and blood at three weeks of age were 40, 53 and 50 percent respectively of those found in newly-hatched chicks. (2) In the groups of chicks fed supplemental pyridoxine, the transaminase activity in the heart and liver remained relatively constant to five weeks of age. The enzyme concentration in the blood declined to a level approximately two-thirds of that found in day-old chicks. ACKNOWLEDGMENTS
The vitamins used were kindly supplied by Merck and Co. Ltd., Montreal, Quebec; Lederle Laboratories, Pearl River, New York and Hoffmann-La Roche, Inc., Nutley 10, New Jersey. Financial assistance from the National Research Council of Canada for the purchase of apparatus used in this study and for a Postdoctorate Fellowship to one of us(M.N.D.G.) is gratefully acknowledged. REFERENCES Ames, S. R., and C. A. Elvehjem, 1946. Determination of aspartic-glutamic transaminase in tissue homogenates. J. Biol. Chem. 166: 81-86. Ames, S. R., P. S. Sarma and C. A. Elvehjem, 1947. Transaminase and pyridoxine deficiency. J. Biol. Chem. 167:135-141. Brin, M., and B. E. Olson, 1951. Effect of pyridoxine deficiency upon respiration and transaminase activity of cardiac muscle in ducklings. Federation Proc. 10: 166-167. Caldwell, E. F., and E. W. McHenry, 1953. Studies on vitamin B 6 and transamination in rat liver. Arch. Biochem. Biophys. 45: 97-104. Green, D. E., L. F. Leloir and V. Nocito, 1945. Transaminases. J. Biol. Chem. 161: 559-582. Marsh, M. E., L. D. Greenberg and J. F. Rinehart,
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
higher than those observed in day-old chicks; however, the enzyme concentration in the blood declined gradually during the first four weeks to a level approximately two-thirds of that found in dayold chicks. Heart. The transaminase activity in heart tissue of pyridoxine-deficient chicks was approximately 65 percent lower at three weeks of age than the average level of the enzyme activity in the pyridoxinesupplemented groups. The depression in enzyme activity is more than twice that recorded by Brin and Olson (1951) in the case of ducks. The difference in response may be a result of types of rations used, duration of feeding or the different species of birds used as experimental subjects. Liver. The enzyme activity of the livers of chicks from the deficient group, after three weeks of feeding, is approximately 50 percent of that recorded for the pyridoxine-fed groups. Although data for liver transaminase in avian species are not available for comparison, this depression in the enzyme activity compares well with the range observed by Schlenk and Snell (1945) and Ames et al. (1947) in pyridoxine-deficient rats. Blood. The level of enzyme activity in the blood of pyridoxine-deficient chicks was found to be 21 percent lower than the average level in pyridoxine-supplemented groups at three weeks of age. This observation is in general agreement with that of Marsh et al. (1955) that the level of aspartic-glutamic transaminase activity was depressed in monkey and man when the intake of pyridoxine was lowered. While increasing the intake of pyridoxine has been reported to result in a significant rise in blood transaminase activity (Marsh et al., 1955), in the present experiment feeding pyridoxine at the level in excess of the chick's requirements (Lot 4) did not result in any increase in
99
TRANSAMINASE ACTIVITY 1955. The relationship between pyridoxine ingestion and transaminase activity. I. Blood hemolysates. J. Nutrition, 56: 115-127. Meister, A., 1955. Transamination in amino acid metabolism. Federation Proc. 14: 683-689. Schlenk, F., and E. E. Snell, 1945. Vitamin B 6 and transaminase. J. Biol. Chem. 157: 425-426. Schlenk, F., and A. Fisher, 1947. Studies on glutamic-aspartic transaminase. Arch. Biochem.
12: 69-78. Schwartzman, G., and H. Hift, 1951. Transamination reaction in normal and B$-deficient hamsters. J. Nutrition, 44: 575-584. Tonhazy, N. E., N. G. White and W. W. Umbreit, 1950. A rapid method for the estimation of the glutamic-aspartic transaminase in tissues and its application to radiation sickness. Arch. Biochem. 28: 36-42.
J. BIELY AND B. E. MARCH Poultry Nutrition Laboratory], The University of British Columbia, Vancouver, B. C. (Received for publication July 15, 1957)
H
to severe visceral gout in which the organs and serous membranes were coated with urate deposits. The results of the experiments described below show that susceptibility to renal dysfunction varies among strains.
ICKS (1953) reported differences in susceptibility to nephritis among breeds of chickens and among sire groups within breeds. The present report summarizes data obtained in three experiments with regard to the incidence of renal disorders in different strains of Single Comb White Leghorns. Mortality was classified as renal disorder only when this condition was considered to be the primary cause of death. Under the heading of renal -disorder the post mortem findings ranged from kidney enlargement with the tubules and ureters engorged with urates
EXPERIMENTAL AND RESULTS Experiment 1. Birds from 12 strains of Single Comb White Leghorns were put on experiment as day-old chicks. The same starting, growing and laying rations were fed to each of the different strains. Birds from all strains were distributed into each pen so that management conditions and exposure to disease were similar for all strains. The data on mortality from dayold to 78 weeks are summarized in Table 1.
* Supported in part by the National Cancer Institute of Canada, Ottawa, Canada, t Contribution No. 99.
TABLE 1.—Experiment 1 Strain 1 0-5 weeks No. of day-old chicks Mortality from renal disorders Percent 5-24 weeks No. of 5 week-old chicks Mortality from renal disorders Percent 24-78 weeks N o . 24 week-old birds Mortality from renal disorders Percent 0-7S weeks Mortality from renal disorders Percent
2
3
4
5
6
7
8
9
10
11
12
122 0 0
124 1 0.8
130 2 1.5
130 0 0
127 6 4.7
127 0 0
159 1 0.6
123 1 0.8
228 0 0
165 1 0.6
156 0 0
184 3 1.6
113 0 0
118 2 1.7
120 0 0
112 0 0
112 1 0.9
105 0 0
142 0 0
110 0 0
177 0 0
143 0 0
122 0 0
128 1 0.8
105 3 2.9
114 4 3.5
115 4 3.5
102 3 2.9
109 6 5.5
100 0 0
138 3 2.2
105 0 0
167 5 3.0
132 2 1.5
113 2 1.8
121 1 0.8
3 2.S
7 5.6
6 4.6
3 2.3
13 10.2
0 0
4 2.5
5 2.2
3 1.8
2 1.3
5 2.7
1 0.8
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
Strain Differences in Susceptibility of Chickens to Renal Disorders*
J. E. ALICATA
of the adult parasites was noted among chickens when the drug was fed in a small amount of wet mash at the rate of 200 to 300 mg./kg. bodyweight. The inclusion of 0.05 percent of piperazine citrate in the normal ration was only partially effective in preventing ascarid infection. A concentration of 0.1 percent was comparatively effective, but this level is considered too high for practical use.
Horton-Smith, C , and P. L. Long, 1956. The anthelmintic effect of three piperazine derivatives on Ascaridia galli (Schrank 1788). Poultry Sci. 35: 606-614. Roberts, F. H. S., 1937. Studies on the biology and control of the large roundworm of fowls Ascaridia galli (Schrank 1788) Freeborn 1923. Animal Health Sta. Yeerongpilly, Queensland, Bui. 2, 106 pp., pis.
Bradley, R. E., 1955. Observations on the anthelmintic effect of piperazine citrate in chickens. Vet. Med. 50: 444-447.
Shumard, R. F., and D. F. Eveleth, 1956. Further studies on the anthelmintic action of piperazine citrate. Vet. Med. 51: 515-517.
Aspartic-Glutamic Transaminase Activity in Chick Liver M . N . D . GOSWAMI AND A. R . ROBBLEE Department of Animal Science, University of Alberta, Edmonton, Alberta (Received for publication July 15. 1957)
T
HE importance of enzymatic transamination in the biological system and its implication in amino acid metabolism has become evident in recent years (Meister, 1955). Of the various transaminases, the classical aspartic-glutamic transaminase has been studied in most detail. As a result of their studies, Schlenk and Snell (1945) and later Schlenk and Fisher (1947) suggested that vitamin B 6 may function as a coenzyme for transaminase. Green et al. (1945) showed that pyridoxal phosphate acted as a coenzyme of aspartic-glutamic transaminase. In studies on the relationship of vitamin I$6 to aspartic-glutamic transaminase, Ames et al. (1947) showed that tissues of vitamin B6 deficient rats exhibited only 40 percent of the enzyme activity of those receiving adequate vitamin B e . Similar results have been reported by Schwartzman and Hift (1951) in the heart muscle of hamsters and by Caldwell and McHenry (1953) in the liver of rats. Working with
ducks, Brin and Olson (1951) reported that in a pyridoxine-deficiency the activity of aspartic-glutamic transaminase in the cardiac muscle was 30 percent below normal. While numerous reports are available concerning the relationship of vitamin B6 to aspartic-glutamic transaminase of mammalian tissues, there is no information on the levels of aspartic-glutamic transaminase in the chick. The present investigation was designed to study the aspartic-glutamic transaminase activity in the tissues of chicks fed purified rations varying in vitamin B6 content. METHODS
The chicks used in this study were dayold Single Comb White Leghorn chicks. The experimental groups were housed in electrically heated batteries with raised screen floors. Feed and water were supplied ad libitum. Four comparable groups of 30 chicks were fed the pyridoxine-
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
REFERENCES
Shumard, R. F., and D. F. Eveleth, 1955. A preliminary report of the anthelmintic action of piperazine citrate on Ascaridia galli and Heterakis gallinae in hens. Vet. Med. 50: 203-205.
97
TRANSAMINASE ACTIVITY
TABLE 1.—Composition of basal ration (gm. per 100 gm. of ration) Ingredients Sucrose Vitamin-test casein Gelatin Corn oil Fish oil (2,250A, 300D) Salt V DL-Methionine
60.7 18 10 4.75 0.25 6 0.3
Level of pyridoxine Lot no. (mcgm./lOO gm. • of ration) 0 0 150 300 600 0 150 300 600 0 150 300 600
Age in weeks 1 2
Heart (QT 10 ) 538 394 284 538 682 677 538 660 699 538 583 791 Liver ( Q T 1 0 ) 258 266 196 258 369 340 258 351 287 258 398 320 Blood (T.A.A. units) 540 460 2X0 540 400 353 540 425 375 540 500 440
3 221
4
5
*
563 — 560 709 640 637 620 674 677 138 291 336 282 259 293 287 284 318 293 270 —* —* 295 295 360 380 380 400 350 335 380
* No chicks alive after 3 weeks of age.
deficient purified basal ration shown in Table 1, supplemented with four levels of pyridoxine, namely, 0, 150, 300 and 600 micrograms per 100 gm. of ration. The aspartic-glutamic transaminase in the heart, liver and blood was measured at 0, 7, 14, 21, 28 and 35 days of age. For transaminase assay, the birds were killed b y severing the jugular vein and the pooled samples of blood from chicks of the same group were frozen at — 20°C. and held for future analysis. The heart and liver tissues were removed and weighed in a cold room at 4°C. Each sample of heart and liver tissues was then divided into weighed portions. One portion was dried a t 100°C. in a vacuum oven for 24 hours for determination of dry weight. Another portion was homogenized in a glass-homogenizer of the PotterElvehjem type with ten times its weight of ice-cold phosphate buffer of p H 7.4 and then diluted with the same buffer to yield a 1.0% homogenate. Transaminase activities of heart and liver were measured according to the colorimetric procedure outlined by Tonhazy et al. (1950) using a Bausch and L o m b photoelectric colorimeter a t 520 mju. The activity is expressed in Q T 1 0 units, defined b y Ames and Elvehjem (1946) as the ml. of C 0 2 (pyruvate) liberated per hour per mg. of dry weight
of the tissues (heart and liver) during a 10 min. incubation period. The whole blood was hemolyzed by freezing and thawing a number of times and then homogenized in the glass homogenizer. A volume of 0.1 or 0.2 ml. of the hemolyzed blood was used for the analyses. The enzyme activity is expressed in units of aspartic-glutamic transaminase activity (T.A.A.) as outlined by Marsh et al. (1955). The enzyme activities reported represent the average of two determinations, each made on individual samples RESULTS AND DISCUSSION Levels of aspartic-glutamic transaminase activity in the heart, liver and blood of chicks fed rations containing varying levels of pyridoxine are shown in Table 2. I n the group receiving the pyridoxinedeficient basal ration (Lot 1), there was a rapid decrease in transaminase activity with age. The levels of activity in heart, liver and blood at three weeks of age were approximately 40, 53 and 50 percent respectively of those observed in day-old chicks. No chicks survived in the pyridoxine-deficient group after three weeks of age. In groups receiving supplemental pyridoxine (Lots 2, 3 and 4), the levels of transaminase activity in heart and liver tissues to five weeks of age were slightly
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
Vitamins were added at the following levels in milligrams per 100 gm. of ration: thiamine hydrochloride 0.4, riboflavin 0.6, calcium pantothenate 2.0, niacin 5,0, biotin0.03, folic acid 0.5, 2 methyl 1-4 naphthoquinone 0.05, Bi2 0.003, vitamin E acetate 1.0, choline chloride 150.0.
TABLE 2.—Aspartic-glutamic transaminase activity in the tissues of chicks fed rations containing different levels of pyridoxine
98
M . N . D . GOSWAMI AND A. R . ROBBLEE
enzyme activity over those receiving the requirement level (Lot 3). SUMMARY
(1) Feeding chicks a pyridoxine-deficient ration resulted in a rapid decrease in aspartic-glutamic transaminase activity. The levels of activity in heart, liver and blood at three weeks of age were 40, 53 and 50 percent respectively of those found in newly-hatched chicks. (2) In the groups of chicks fed supplemental pyridoxine, the transaminase activity in the heart and liver remained relatively constant to five weeks of age. The enzyme concentration in the blood declined to a level approximately two-thirds of that found in day-old chicks. ACKNOWLEDGMENTS
The vitamins used were kindly supplied by Merck and Co. Ltd., Montreal, Quebec; Lederle Laboratories, Pearl River, New York and Hoffmann-La Roche, Inc., Nutley 10, New Jersey. Financial assistance from the National Research Council of Canada for the purchase of apparatus used in this study and for a Postdoctorate Fellowship to one of us(M.N.D.G.) is gratefully acknowledged. REFERENCES Ames, S. R., and C. A. Elvehjem, 1946. Determination of aspartic-glutamic transaminase in tissue homogenates. J. Biol. Chem. 166: 81-86. Ames, S. R., P. S. Sarma and C. A. Elvehjem, 1947. Transaminase and pyridoxine deficiency. J. Biol. Chem. 167:135-141. Brin, M., and B. E. Olson, 1951. Effect of pyridoxine deficiency upon respiration and transaminase activity of cardiac muscle in ducklings. Federation Proc. 10: 166-167. Caldwell, E. F., and E. W. McHenry, 1953. Studies on vitamin B 6 and transamination in rat liver. Arch. Biochem. Biophys. 45: 97-104. Green, D. E., L. F. Leloir and V. Nocito, 1945. Transaminases. J. Biol. Chem. 161: 559-582. Marsh, M. E., L. D. Greenberg and J. F. Rinehart,
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
higher than those observed in day-old chicks; however, the enzyme concentration in the blood declined gradually during the first four weeks to a level approximately two-thirds of that found in dayold chicks. Heart. The transaminase activity in heart tissue of pyridoxine-deficient chicks was approximately 65 percent lower at three weeks of age than the average level of the enzyme activity in the pyridoxinesupplemented groups. The depression in enzyme activity is more than twice that recorded by Brin and Olson (1951) in the case of ducks. The difference in response may be a result of types of rations used, duration of feeding or the different species of birds used as experimental subjects. Liver. The enzyme activity of the livers of chicks from the deficient group, after three weeks of feeding, is approximately 50 percent of that recorded for the pyridoxine-fed groups. Although data for liver transaminase in avian species are not available for comparison, this depression in the enzyme activity compares well with the range observed by Schlenk and Snell (1945) and Ames et al. (1947) in pyridoxine-deficient rats. Blood. The level of enzyme activity in the blood of pyridoxine-deficient chicks was found to be 21 percent lower than the average level in pyridoxine-supplemented groups at three weeks of age. This observation is in general agreement with that of Marsh et al. (1955) that the level of aspartic-glutamic transaminase activity was depressed in monkey and man when the intake of pyridoxine was lowered. While increasing the intake of pyridoxine has been reported to result in a significant rise in blood transaminase activity (Marsh et al., 1955), in the present experiment feeding pyridoxine at the level in excess of the chick's requirements (Lot 4) did not result in any increase in
99
TRANSAMINASE ACTIVITY 1955. The relationship between pyridoxine ingestion and transaminase activity. I. Blood hemolysates. J. Nutrition, 56: 115-127. Meister, A., 1955. Transamination in amino acid metabolism. Federation Proc. 14: 683-689. Schlenk, F., and E. E. Snell, 1945. Vitamin B 6 and transaminase. J. Biol. Chem. 157: 425-426. Schlenk, F., and A. Fisher, 1947. Studies on glutamic-aspartic transaminase. Arch. Biochem.
12: 69-78. Schwartzman, G., and H. Hift, 1951. Transamination reaction in normal and B$-deficient hamsters. J. Nutrition, 44: 575-584. Tonhazy, N. E., N. G. White and W. W. Umbreit, 1950. A rapid method for the estimation of the glutamic-aspartic transaminase in tissues and its application to radiation sickness. Arch. Biochem. 28: 36-42.
J. BIELY AND B. E. MARCH Poultry Nutrition Laboratory], The University of British Columbia, Vancouver, B. C. (Received for publication July 15, 1957)
H
to severe visceral gout in which the organs and serous membranes were coated with urate deposits. The results of the experiments described below show that susceptibility to renal dysfunction varies among strains.
ICKS (1953) reported differences in susceptibility to nephritis among breeds of chickens and among sire groups within breeds. The present report summarizes data obtained in three experiments with regard to the incidence of renal disorders in different strains of Single Comb White Leghorns. Mortality was classified as renal disorder only when this condition was considered to be the primary cause of death. Under the heading of renal -disorder the post mortem findings ranged from kidney enlargement with the tubules and ureters engorged with urates
EXPERIMENTAL AND RESULTS Experiment 1. Birds from 12 strains of Single Comb White Leghorns were put on experiment as day-old chicks. The same starting, growing and laying rations were fed to each of the different strains. Birds from all strains were distributed into each pen so that management conditions and exposure to disease were similar for all strains. The data on mortality from dayold to 78 weeks are summarized in Table 1.
* Supported in part by the National Cancer Institute of Canada, Ottawa, Canada, t Contribution No. 99.
TABLE 1.—Experiment 1 Strain 1 0-5 weeks No. of day-old chicks Mortality from renal disorders Percent 5-24 weeks No. of 5 week-old chicks Mortality from renal disorders Percent 24-78 weeks N o . 24 week-old birds Mortality from renal disorders Percent 0-7S weeks Mortality from renal disorders Percent
2
3
4
5
6
7
8
9
10
11
12
122 0 0
124 1 0.8
130 2 1.5
130 0 0
127 6 4.7
127 0 0
159 1 0.6
123 1 0.8
228 0 0
165 1 0.6
156 0 0
184 3 1.6
113 0 0
118 2 1.7
120 0 0
112 0 0
112 1 0.9
105 0 0
142 0 0
110 0 0
177 0 0
143 0 0
122 0 0
128 1 0.8
105 3 2.9
114 4 3.5
115 4 3.5
102 3 2.9
109 6 5.5
100 0 0
138 3 2.2
105 0 0
167 5 3.0
132 2 1.5
113 2 1.8
121 1 0.8
3 2.S
7 5.6
6 4.6
3 2.3
13 10.2
0 0
4 2.5
5 2.2
3 1.8
2 1.3
5 2.7
1 0.8
Downloaded from http://ps.oxfordjournals.org/ at New York University on May 9, 2015
Strain Differences in Susceptibility of Chickens to Renal Disorders*