In vivo effect of dietary factors on the molecular action of aflatoxin B1: role of vitamin A on the catalytic activity of liver fractions.
Weanling rats were kept on a synthetic vitamin A free diet for 9 weeks, and subsequently on the same diet but with oral supplementation of vitamin A palmitate at different doses for 2-3 weeks. The ability of liver microsomes to catalyze reactions of aflatoxin B1 (AFB1) leading to its activation and DNA adduct formation was measured after each period of experimental feeding. An increased molecular reactivity of AFB1 was evident during vitamin A deficiency such that the degree of its conversion to its reactive metabolite and subsequent DNA adduct formation was higher with microsomes from vitamin A-deficient rats as compared to rats maintained on normal supply of vitamin A. These activities of microsomes returned to normal after the rats had adequate supplements of vitamin A. The vitamin A status was also found to play a role in regulating glutathione S-transferase activity of the liver cytosol fraction, the activity being low in deficiency but increased progressively with increasing supplementation of vitamin A. Results suggest that vitamin A can afford protection against adverse effects of the potent hepatocarcinogen AFB.
Bhattacharya
R K
RK
Biochemistry Division, Bhabha Atomic Research Centre, Bombay, India.
Prabhu
A L
AL
Aboobaker
V S
VS
D016604:Aflatoxin B1; D000348:Aflatoxins / Q000494:pharmacology*; D000818:Animals; D004247:DNA / Q000378:metabolism; D004032:Diet; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D014801:Vitamin A / Q000502:physiology*; D014802:Vitamin A Deficiency / Q000378:metabolism
D000348:Aflatoxins; D014801:Vitamin A; D004247:DNA; D016604:Aflatoxin B1; D005982:Glutathione Transferase; D005978:Glutathione