enalapril and diethyl-maleate

enalapril has been researched along with diethyl-maleate* in 1 studies

Other Studies

1 other study(ies) available for enalapril and diethyl-maleate

Article	Year
Enalapril cytotoxicity in primary cultures of rat hepatocytes. II. Role of glutathione. Toxicology letters, 1991, Volume: 58, Issue:3 The cytotoxicity of enalapril maleate (EN) in primary cultures of rat hepatocytes, at concentrations of 0.5 mM or greater, was measured by the release of lactate dehydrogenase (LDH) into the culture medium. Pretreatment of the hepatocytes with L-buthionine-(S,R)-sulfoximine (BSO) and diethyl maleate (DEM) potentiated the toxicity whereas N-acetyl-L-cysteine (NAC) provided protection. EN produced a dose-dependent reduction in intracellular glutathione (GSH) concentration. This was an early effect, apparent after only 1 h of exposure to the drug, whereas loss of cell viability occurred after 6-18 h. These results suggest that the mechanism of EN cytotoxicity involves a GSH-dependent detoxification pathway. Topics: Acetylcysteine; Animals; Antimetabolites; Buthionine Sulfoximine; Cell Survival; Cells, Cultured; Drug Synergism; Enalapril; Glutathione; Glutathione Reductase; Glutathione Transferase; L-Lactate Dehydrogenase; Liver; Male; Maleates; Methionine Sulfoximine; Rats; Rats, Inbred F344	1991

Article

Year

Enalapril cytotoxicity in primary cultures of rat hepatocytes. II. Role of glutathione.

Toxicology letters, 1991, Volume: 58, Issue:3

The cytotoxicity of enalapril maleate (EN) in primary cultures of rat hepatocytes, at concentrations of 0.5 mM or greater, was measured by the release of lactate dehydrogenase (LDH) into the culture medium. Pretreatment of the hepatocytes with L-buthionine-(S,R)-sulfoximine (BSO) and diethyl maleate (DEM) potentiated the toxicity whereas N-acetyl-L-cysteine (NAC) provided protection. EN produced a dose-dependent reduction in intracellular glutathione (GSH) concentration. This was an early effect, apparent after only 1 h of exposure to the drug, whereas loss of cell viability occurred after 6-18 h. These results suggest that the mechanism of EN cytotoxicity involves a GSH-dependent detoxification pathway.

Topics: Acetylcysteine; Animals; Antimetabolites; Buthionine Sulfoximine; Cell Survival; Cells, Cultured; Drug Synergism; Enalapril; Glutathione; Glutathione Reductase; Glutathione Transferase; L-Lactate Dehydrogenase; Liver; Male; Maleates; Methionine Sulfoximine; Rats; Rats, Inbred F344

1991