Rise of hepatic glutathione concentration induced in rats by chronic lead nitrate treatment. Its role in aflatoxin B1 intoxication.
Liver concentration of the reduced form of glutathione is increased by chronic lead nitrate administration. Hepatic glutathione content is lowered by acute aflatoxin B1 intoxication while in lead-pretreated rats this decrement is not evident. The administration of lead nitrate which increases liver glutathione also decreases acute aflatoxin B1 toxicity. This provides additional evidence that, in the liver, glutathione concentration plays a role in controlling acute aflatoxin B1 toxicity.
D016604:Aflatoxin B1; D000348:Aflatoxins / Q000633:toxicity*; D000818:Animals; D005978:Glutathione / Q000378:metabolism*; D006591:Hexobarbital / Q000494:pharmacology; D007854:Lead / Q000633:toxicity*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D006899:Mixed Function Oxygenases / Q000378:metabolism; D009566:Nitrates / Q000633:toxicity*; D051381:Rats; D012890:Sleep / Q000187:drug effects
D000348:Aflatoxins; D009566:Nitrates; D007854:Lead; C017461:lead nitrate; D016604:Aflatoxin B1; D006591:Hexobarbital; D006899:Mixed Function Oxygenases; D005978:Glutathione