Absence of potentiation of bromoform hepatotoxicity and lethality by chlordecone.
Our previous studies indicated that the toxicity of chloro- or bromo-methanes is potentiated by chlordecone (CD). The present work was conducted to study the effect of prior dietary exposure to CD on toxicity of bromoform. Male S-D rats (175-200 g) were fed 0 or 10 ppm CD in the powdered ration for 15 days. Bromoform (25 to 300 microliters/kg) was given i.p. on day 15. 24 h later, hepatotoxicity was assessed by functional, biochemical and histopathological parameters. Excretion of phenolphthalein glucuronide in bile and the rate of bile flow were unaltered by either bromoform or CD-bromoform combination. Serum enzymes (GPT, GOT and isocitric dehydrogenase (ICD) were also not significantly elevated by any treatment. The results suggest that, unlike chloroform, CHBr3 does not act as a potent hepatotoxin and that its effects are not potentiated by CD to any significant extent.
D000818:Animals; D001711:Biotransformation; D002273:Carcinogens; D007631:Chlordecone / Q000633:toxicity*; D004357:Drug Synergism; D006842:Hydrocarbons, Brominated / Q000378:metabolism / Q000633:toxicity*; D007306:Insecticides / Q000633:toxicity*; D007928:Lethal Dose 50; D008099:Liver / Q000187:drug effects*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D022882:Trihalomethanes
D002273:Carcinogens; D006842:Hydrocarbons, Brominated; D007306:Insecticides; D022882:Trihalomethanes; D007631:Chlordecone; C015044:bromoform