Acetaminophen-induced hepatic necrosis V. Correlation of hepatic necrosis, covalent binding and glutathione depletion in hamsters
WZ Potter, SS Thorgeirsson, DJ Jollow, JR Mitchell - Pharmacology, 1974 - karger.com
WZ Potter, SS Thorgeirsson, DJ Jollow, JR Mitchell
Pharmacology, 1974•karger.comWe previously postulated that acetaminophen-induced hepatic necrosis in mice results from
the formation of a reactive metabolite that arylates vital cellular macro-molecules. While
studying species differences in susceptibility to acetaminophen-induced hepatic necrosis,
hamsters were found to be particularly vulnerable. We now report the relationships between
hepatic glutathione depletion, arylation of hepatic macromolecules in vivo and in vitro and
hepatic necrosis after administration of acetaminophen to hamsters.
the formation of a reactive metabolite that arylates vital cellular macro-molecules. While
studying species differences in susceptibility to acetaminophen-induced hepatic necrosis,
hamsters were found to be particularly vulnerable. We now report the relationships between
hepatic glutathione depletion, arylation of hepatic macromolecules in vivo and in vitro and
hepatic necrosis after administration of acetaminophen to hamsters.
Abstract
We previously postulated that acetaminophen-induced hepatic necrosis in mice results from the formation of a reactive metabolite that arylates vital cellular macro-molecules. While studying species differences in susceptibility to acetaminophen-induced hepatic necrosis, hamsters were found to be particularly vulnerable. We now report the relationships between hepatic glutathione depletion, arylation of hepatic macromolecules in vivo and in vitro and hepatic necrosis after administration of acetaminophen to hamsters.
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