Abstract
This study obtained in vitro dose‐response data on the combined exposures of acetaldehyde (Ach) and 1‐napthol and t‐butanol and 1‐napthol effects on methemoglobln and reduced glutathione (GSH) level of human and sheep erythrocytes to determine if Increased red blood cell oxidant stress is caused by ethanol itself (membrane solubility effects) or by Ach (reactive metabolite effects). The results indicate that Ach was 50‐fold more potent a red blood oxidant than t‐butanol and displayed a significantly greater capacity to enhance 1‐napthol Induced oxidant effects in both species than t‐butanol. The data suggest that ethanol induced red cell effects may be mediated at least in part via its metabolite Ach.