Biochemical studies on polychlorinated biphenyl toxicity in rats: manipulation by vitamin C.
The effects of chronic polychlorinated biphenyl (PCB) compound toxicity on L-ascorbic acid metabolism in rats have been studied. PCB treatment brought about a depression in the activities of the enzymes L-gluonolactone oxidase and dehydroascorbatase along with an increased tissue levels and urinary excretion of L-ascorbic acid. PCB toxicity drastically disturbed the normal histological pattern of the liver cells and also significantly changed the hepatic lipid composition. L-ascorbic acid supplementation to the toxicated group of animals, although could not prevent the growth retardative effect of PCB, could afford a definite protection against the enzyme activity alterations and histological changes as caused by PCB toxicity.
D000429:Alcohol Oxidoreductases / Q000378:metabolism; D000818:Animals; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000378:metabolism* / Q000652:urine; D003682:Dehydroascorbatase / Q000378:metabolism; D005965:Glucuronates / Q000378:metabolism; D006454:Hemoglobins / Q000032:analysis; D007668:Kidney / Q000473:pathology; D007783:Lactones; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008297:Male; D011078:Polychlorinated Biphenyls / Q000633:toxicity*; D051381:Rats; D013400:Sugar Acids
D005965:Glucuronates; D006454:Hemoglobins; D007783:Lactones; D013400:Sugar Acids; D011078:Polychlorinated Biphenyls; D000429:Alcohol Oxidoreductases; D003682:Dehydroascorbatase; D001205:Ascorbic Acid