1. Loss of mitochondrial membrane potential is not essential to hepatocyte killing by allyl alcohol
- Author
-
Cai Dy, Hornbook Kr, and Lora E. Rikans
- Subjects
Male ,Propanols ,Mitochondria, Liver ,1-Propanol ,Mitochondrion ,Toxicology ,Rhodamine 123 ,Dithiothreitol ,Membrane Potentials ,chemistry.chemical_compound ,Cyclosporin a ,medicine ,Animals ,Allyl alcohol ,Membrane potential ,Cell Death ,L-Lactate Dehydrogenase ,Chemistry ,organic chemicals ,food and beverages ,General Medicine ,Rats, Inbred F344 ,Trifluoperazine ,Rats ,medicine.anatomical_structure ,Cell killing ,Liver ,Biochemistry ,Hepatocyte ,Cyclosporine ,Biophysics - Abstract
Allyl alcohol-induced LDH leakage from isolated rat hepatocytes was preceded by a decrease in rhodamine 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.
- Published
- 1995