Glycogenolysis in the rat isolated perfused liver as a measure of chemically induced liver toxicity.
The relationship between chemically induced glycogenolysis and decreased thiol content in the rat isolated, perfused liver has been examined. Chemicals such as 2,4-dinitrophenol (DNP), diethyl maleate, alcohols and anti-inflammatory agents (except for sodium salicylate) accelerated glycogenolysis. Protein thiol loss correlated well with a marked increased rate of glucose release. Non-protein thiol loss, without significant loss of protein thiol, caused by a slight increase in the rate of glycogenolysis compared with controls. Since it has been reported that protein thiol loss rather than non-protein thiol loss is correlated to liver cell injury, a marked glucose release from the perfused liver may be a convenient measure of hepatic toxicity for a variety of chemicals.
D000818:Animals; D004140:Dinitrophenols / Q000633:toxicity; D005947:Glucose / Q000378:metabolism; D066298:In Vitro Techniques; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism*; D008297:Male; D008298:Maleates / Q000633:toxicity; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D012459:Salicylates / Q000633:toxicity; D013438:Sulfhydryl Compounds / Q000378:metabolism*
D004140:Dinitrophenols; D008112:Liver Glycogen; D008298:Maleates; D012459:Salicylates; D013438:Sulfhydryl Compounds; C014476:diethyl maleate; D005947:Glucose