Sensitivity of liver mitochondrial functions to various levels of ethanol intake in the rat.
Mitochondrial function appears to be an early target for ethanol toxicity, however it is not clear to what extent the effects of ethanol, which occur at levels of intake lower than those already reported in the literature, can induce an alteration of it. To produce different levels of ethanol intake, the spontaneous consumption of ethanol by genetically low (UChA) and genetically high (UChB) rats, as well as the forced intake obtained by offering 10% v/v ethanol solution as the only source of drinking fluid, were employed. The O2 uptake by liver mitochondria of rats submitted to these conditions in the presence of glutamate + malate, succinate or ascorbate + TMPD, was measured polarographically with a Clark electrode at 25 degrees C. Results indicate that alterations of the hepatic mitochondrial function can be detected at levels of ethanol intake much lower than those previously reported. Whereas, a level of a daily ethanol intake of 2-3 g/kg body weight in UChA rats under free choice was insufficient to produce detectable changes in the mitochondrial function, the latter was decreased in the high ethanol consumers (UChB), which drank 4-5 g/kg per day under free choice conditions, and in both strains forced to drink 10% ethanol as only source of fluid, which produced intakes of about 7 g/kg per day. Therefore, mitochondrial dysfunction may contribute to effects observed even at low levels of ethanol intake.