FURTHER STUDIES ON THE REDUCTION OF VITAMIN A CONTENT IN THE LIVERS OF RATS GIVEN POLYCHLORINATED BIPHENYLS
Further investigations on the, reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vita...
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| Published in | Journal of Nutritional Science and Vitaminology Vol. 22; no. 6; pp. 409 - 418 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Japan
Center for Academic Publications Japan
1976
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0301-4800 1881-7742 1881-7742 |
| DOI | 10.3177/jnsv.22.409 |
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| Abstract | Further investigations on the, reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduc tion was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A oc curred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed. |
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| AbstractList | Further investigations on the, reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduc tion was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A oc curred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed. Further investigations on the reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduction was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A occurred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed. Further investigations on the reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduction was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A occurred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed.Further investigations on the reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduction was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A occurred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed. |
| Author | MIYAZAKI, Motoyoshi INNAMI, Satoshi NISHIDE, Eiichi NAKAMURA, Atsuko NAGAYAMA, Sumiko |
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| References | 2) INNAMI, S., TOJO, H., UTSUGI, S., NAKAMURA, A., and NAGAYAMA, S., Jap. J. Nutr., 32, 58 (1974). 22) FUJITA, S., TSUJI, H., KATO, K., SAEKI, S., and TSUKAMOTO, H., Fukuoka Acta Med., 62, 30 (1971). 7) FUJITA, A, and KIMURA, K., J.. Vitaminol., 6, 6 (1960). 20) DAs, M. L., ORRENIUS, S., and ERNSTER, L., European J. Biochem., 4, 519 (1968). 1) VILLENEUVE, D. C., GRANT, D. L., PHILLIPS, W. E. J., CLARK, M. L., and CLEGG, D. J., Bull. Environ. Contam. Toxicol., 6,120 (1971). 10) MUTO, Y. and GOODMAN, DEW. S., J. Biol. Chem., 247, 2533 (1972). 8) MANCINI, G., CARBONARA, A. D., and HEREMANS J. F., Immunochemistry, 2, 235 (1965). 23) TURNER, J. C. and GREEN, R. S., Bull. Environ. Contam. Toxicol., 12, 669 (1974). 13) PHILLIPS, W. E. J., Can. J. Biochem. Physiol., 41,1793 (1963). 27) BEAUCHAMP, C. and FRIDOVICH, I., J. Biol. Chem., 245, 4611 (1970). 6) FISKE, C. H. and SUBBAROW, Y., J. Biol. Chem., 66, 375 (1925). 3) INNAMI, S., NAKAMURA, A., and NAGAYAMA, S., J. Nutr. Sci. Vitaminol., 20, 363 (1974). 15) LITTERST, C. L., FARBER, T. M., BAKER, A. M., and VAN LOON, E. J., Toxicol. Appl!. Pharma col., 23,112 (1972). 26) GUNSALUS, I. C., PEDERSON, T. C., and SLIGAR, S. G., Ann. Rev. Bioch., 44, 377 (1975). 9) KANAI, M., RAZ, A., and GOODMAN, DEW. S., J. Clin. Invest., 47, 2025 (1968). 17) TALALAY, P., Ann. Rev. Bioch., 34, 347 (1965). 12) MUTO, Y., SMITH, J. E., MILCH, P. 0., and GOODMAN, DEW. S., J. Biol. Chem., 247, 2542 (1972). 28) KELLOGG, E. W., III and FRIDOVICH,'I., J. Biol. Chem., 250, 8812 (1975). 19) PREISS, B. and BLOCK, K. J., J. Biol, Chem., 239, 85 (1964). 29) HABER, F. and WEiss, J., Proc. R. Soc., Lond., A147, 332 (1934). 14) LEE, M., HARRIS, K., and TROWBRIDGE, H., J. Nutr., 84, 136 (1964). 4) TANAKA, K., FUJITA, S., KOMATSU, F., and TAMURA, N., Fukuoka Acta Med., 60, 544 (1969). 25) STROBEL, H. W. and CooN, M. J., J. Biol. Chem., 246, 7826 (1971). 11) SMITH, F. R, and GOODMAN, DEW. S., J. Clin. Invest., 50, 2426 (1971). 16) BRODIE, B. B., GILLETTE, J. R., and LA DU B. N., Ann. Rev. Bioch., 27, 427 (1958). 5) INNAMI, S., NAKAMURA, A., NAGAYAMA, S., KATO, T., MIYAZAKI, M., and NISHIDE, E., Fukuoka Acta Med., 66, 579 (1975). 21) OMURA, T. and SATO, R., J. Biol. Chem., 239, 2370, 2379 (1964). 18) WAKABAYASHI, K. and SHIMAZONO, N., Biochim. Biophys. Acta, 70,132 (1963). 24) CONNBY, A. H., Pharm. Rev., 19, 317 (1967). |
| References_xml | – reference: 13) PHILLIPS, W. E. J., Can. J. Biochem. Physiol., 41,1793 (1963). – reference: 8) MANCINI, G., CARBONARA, A. D., and HEREMANS J. F., Immunochemistry, 2, 235 (1965). – reference: 11) SMITH, F. R, and GOODMAN, DEW. S., J. Clin. Invest., 50, 2426 (1971). – reference: 2) INNAMI, S., TOJO, H., UTSUGI, S., NAKAMURA, A., and NAGAYAMA, S., Jap. J. Nutr., 32, 58 (1974). – reference: 14) LEE, M., HARRIS, K., and TROWBRIDGE, H., J. Nutr., 84, 136 (1964). – reference: 21) OMURA, T. and SATO, R., J. Biol. Chem., 239, 2370, 2379 (1964). – reference: 9) KANAI, M., RAZ, A., and GOODMAN, DEW. S., J. Clin. Invest., 47, 2025 (1968). – reference: 12) MUTO, Y., SMITH, J. E., MILCH, P. 0., and GOODMAN, DEW. S., J. Biol. Chem., 247, 2542 (1972). – reference: 20) DAs, M. L., ORRENIUS, S., and ERNSTER, L., European J. Biochem., 4, 519 (1968). – reference: 4) TANAKA, K., FUJITA, S., KOMATSU, F., and TAMURA, N., Fukuoka Acta Med., 60, 544 (1969). – reference: 26) GUNSALUS, I. C., PEDERSON, T. C., and SLIGAR, S. G., Ann. Rev. Bioch., 44, 377 (1975). – reference: 7) FUJITA, A, and KIMURA, K., J.. Vitaminol., 6, 6 (1960). – reference: 17) TALALAY, P., Ann. Rev. Bioch., 34, 347 (1965). – reference: 5) INNAMI, S., NAKAMURA, A., NAGAYAMA, S., KATO, T., MIYAZAKI, M., and NISHIDE, E., Fukuoka Acta Med., 66, 579 (1975). – reference: 22) FUJITA, S., TSUJI, H., KATO, K., SAEKI, S., and TSUKAMOTO, H., Fukuoka Acta Med., 62, 30 (1971). – reference: 3) INNAMI, S., NAKAMURA, A., and NAGAYAMA, S., J. Nutr. Sci. Vitaminol., 20, 363 (1974). – reference: 6) FISKE, C. H. and SUBBAROW, Y., J. Biol. Chem., 66, 375 (1925). – reference: 10) MUTO, Y. and GOODMAN, DEW. S., J. Biol. Chem., 247, 2533 (1972). – reference: 1) VILLENEUVE, D. C., GRANT, D. L., PHILLIPS, W. E. J., CLARK, M. L., and CLEGG, D. J., Bull. Environ. Contam. Toxicol., 6,120 (1971). – reference: 29) HABER, F. and WEiss, J., Proc. R. Soc., Lond., A147, 332 (1934). – reference: 15) LITTERST, C. L., FARBER, T. M., BAKER, A. M., and VAN LOON, E. J., Toxicol. Appl!. Pharma col., 23,112 (1972). – reference: 27) BEAUCHAMP, C. and FRIDOVICH, I., J. Biol. Chem., 245, 4611 (1970). – reference: 23) TURNER, J. C. and GREEN, R. S., Bull. Environ. Contam. Toxicol., 12, 669 (1974). – reference: 16) BRODIE, B. B., GILLETTE, J. R., and LA DU B. N., Ann. Rev. Bioch., 27, 427 (1958). – reference: 25) STROBEL, H. W. and CooN, M. J., J. Biol. Chem., 246, 7826 (1971). – reference: 19) PREISS, B. and BLOCK, K. J., J. Biol, Chem., 239, 85 (1964). – reference: 18) WAKABAYASHI, K. and SHIMAZONO, N., Biochim. Biophys. Acta, 70,132 (1963). – reference: 24) CONNBY, A. H., Pharm. Rev., 19, 317 (1967). – reference: 28) KELLOGG, E. W., III and FRIDOVICH,'I., J. Biol. Chem., 250, 8812 (1975). |
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| SubjectTerms | Animals Chemical Phenomena Chemistry Dose-Response Relationship, Drug Drug Stability Frozen Foods Liver - anatomy & histology Liver - drug effects Liver - metabolism Male Organ Size Polychlorinated Biphenyls - pharmacology Rats Retinol-Binding Proteins - metabolism Time Factors Vitamin A - metabolism |
| Title | FURTHER STUDIES ON THE REDUCTION OF VITAMIN A CONTENT IN THE LIVERS OF RATS GIVEN POLYCHLORINATED BIPHENYLS |
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