Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036474 (scurvy)
 685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the requirement of ascorbic acid for the induction by polychlorinated biphenyls (PCB) of hepatic drug-metabolizing enzymes in ODS-od/od rat (OD rat) which is a rat mutant unable to synthesize ascorbic acid. ODS- +/+ rats (+/+ rat), which can synthesize ascorbic acid, were used as controls. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and prevent any signs of scurvy is about 300 mg of ascorbic acid per kilogram diet. In this study, dietary levels of ascorbic acid tested were 0, 50, 300, 1000 and 3000 mg ascorbic acid per kilogram diet with or without 200 mg of PCB per kilogram diet. Feeding PCB did not affect growth in rats of either genotype. When statistical analysis was done within groups fed diets without PCB, ascorbic acid deficiency caused significant decreases in body weight gain, hepatic activities of drug-metabolizing enzymes and level of hepatic cytochrome P-450. When OD rats were fed a diet without PCB, the supplementation of about 300 mg ascorbic per kilogram diet was sufficient to maintain normal activities of hepatic aminopyrine N-demethylase, aniline hydroxylase, cytochrome c reductase and reduction of cytochrome P-450 and a normal level of hepatic cytochrome P-450. However, when OD rats were fed a diet supplemented with 200 mg PCB per kilogram of diet, significantly higher activities of hepatic aminopyrine N-demethylase and aniline hydroxylase and significantly higher level of hepatic cytochrome P-450 were observed in OD rats fed a diet supplemented with 1000 mg or 3000 mg ascorbic acid per kilogram of diet than in rats fed a diet supplemented with 300 mg of ascorbic acid. It is concluded that the dietary requirement of ascorbic acid is increased severalfold by the administration of xenobiotics, such as PCB, for the maximum induction of hepatic drug metabolism.
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PMID:Ascorbic acid requirement for the induction of microsomal drug-metabolizing enzymes in a rat mutant unable to synthesize ascorbic acid. 309 36

1. Male guinea-pigs were administered 8, 180 and 360 mg ascorbic acid/day via drinking water for 1 and 2 months. The two high levels of ascorbic acid were not able to produce saturation in either blood or any of the three tissues (liver, lung and kidney) while the lowest ascorbic acid level was sufficient to prevent scurvy. 2. There was no significant differences among the groups receiving three distinct ascorbic acid levels in body weights, tissue weights or protein contents. 3. No significant alterations were observed in microsomal ethylmorphine N-demethylase activity of any of the three tissues among the groups after experimental periods. 4. The two high ascorbic acid levels produced significant increases in liver microsomal aniline 4-hydroxylase activity as compared to the lowest supplementation of ascorbic acid after 2 months. However, no significant enzyme activity changes were found among the groups after 1 month. 5. In lung, after 1 month significant increase was observed in microsomal aniline 4-hydroxylase activity with the two high ascorbic acid levels as compared to the lowest supplementation of ascorbic acid whereas after 2 months no significant changes were observed. 6. Kidney microsomal aniline 4-hydroxylase activity was unaffected by changes in ascorbate status.
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PMID:Effects of ascorbic acid supplementation on liver, lung and kidney microsomal drug metabolizing enzymes of the guinea-pig. 362 14