Redox control of hepatic cell death
H Hentze, M Latta, G Künstle, R Lucas, A Wendel - Toxicology letters, 2003 - Elsevier
In necrotic liver failure like upon acetaminophen overdose, loss of the major intracellular
thiol antioxidant glutathione was shown to be causal for hepatic dysfunction. In sharp
contrast, fulminant apoptotic liver destruction upon overstimulation of the death receptors
TNFR1 and CD95 was not associated with reduced hepatic glutathione levels. In view of the
importance of the role of reactive oxygen intermediates versus antioxidants for apoptosis, we
investigated the effect of phorone-induced enzymatic GSH depletion on the sensitivity of the …
thiol antioxidant glutathione was shown to be causal for hepatic dysfunction. In sharp
contrast, fulminant apoptotic liver destruction upon overstimulation of the death receptors
TNFR1 and CD95 was not associated with reduced hepatic glutathione levels. In view of the
importance of the role of reactive oxygen intermediates versus antioxidants for apoptosis, we
investigated the effect of phorone-induced enzymatic GSH depletion on the sensitivity of the …