The activity of free radical processes in liver mitochondria was investigated in rats kept on high-sucrose and low protein/high-sucrose diets. Excess of dietary sucrose caused intensification of free radical processes in liver mitochondria as evidenced by increased hydroxyl radical generation, accumulation of primary (conjugated dienes, ketodienes) and secondary products (TBA-reactive products) of lipid peroxidation, increased cholesterol/phospholipids ratio and also accumulation of oxidative modification products of proteins (carbonyl derivatives). Additional nutritional protein deficiency (low protein/high-sucrose diet) enhanced destructive changes in liver mitochondria. This suggests a critical role of nutrient protein supplementation for maintaining the functional activity of mitochondria. The established changes can be considered as one of possible mechanisms of functional liver activity violation in conditions of nutrient imbalance.
Keywords: liver, hydroxyl radical, lipid peroxidation, protein oxidation, high-sucrose ration, low protein ration