Loss of mitochondrial membrane potential is not essential to hepatocyte killing by allyl alcohol.
Allyl alcohol-induced LDH leakage from isolated rat hepatocytes was preceded by a decrease in rhodmine 123 retention, signifying a loss of mitochondrial membrane potential. Addition of dithiothreitol (DTT) prevented the drop in membrane potential and completely prevented cell killing by allyl alcohol. In contrast, cyclosporin A and trifluoperazine delayed the loss of membrane potential without affecting cytolethality. The results indicate that a drop in mitochondrial membrane potential is not essential for allyl alcohol lethality. The mitochondrial dysfunction produced by allyl alcohol appears to be the consequence of an earlier event in the toxicity that is reversible by DTT.
Rikans
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LE
Department of Pharmacology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, USA.
Cai
D Y
DY
Hornbook
K R
KR
D000433:1-Propanol / Q000633:toxicity; D000818:Animals; D016923:Cell Death / Q000187:drug effects; D016572:Cyclosporine / Q000494:pharmacology; D004229:Dithiothreitol / Q000494:pharmacology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000166:cytology* / Q000187:drug effects*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000502:physiology; D020005:Propanols; D051381:Rats; D011916:Rats, Inbred F344; D014268:Trifluoperazine / Q000494:pharmacology
D020005:Propanols; D014268:Trifluoperazine; C006463:allyl alcohol; D016572:Cyclosporine; D000433:1-Propanol; D007770:L-Lactate Dehydrogenase; D004229:Dithiothreitol