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Iron acquisition is a fundamental requirement for many aspects of life, but excess iron may result in the formation of free radicals that damage cellular constituents. Therefore, the amount of iron within the cell is carefully regulated by the iron metabolism (IRE/IRP system) in order to assure an adequate level. We previously reported that long-term excessive L-methionine consumption increases iron and lipid peroxide levels in rat liver. To determine whether such excess iron accumulation depends on the elevation of transferrin receptor via oxidative stress, we investigated the possible effects of long-term excessive L-methionine intake on the iron metabolism and the mitochondrial function in rat liver. Wistar male rats were fed either an L-methionine-supplemented (16.0 g/kg) diet or a control diet for 3 and 6 mo. The expression of transferrin receptor is significantly elevated by excess L-methionine intake, indicating that an accumulation of iron may be accompanied by such an elevation in the liver. Long-term excessive L-methionine consumption significantly decreases the H2O2 production of rat liver mitochondria without inducing changes in mitochondrial oxygen consumption. No significant differences in either glutathione peroxidase activity or superoxide dismutase activity were shown between the two groups. In contrast, the glutathione concentration significantly increased in L-methionine-treated rats compared to controls. These results indicate that long-term consumption of excess L-methionine by rats may affect mitochondrial function, resulting in a reduction in H2O2 generation. Moreover, an accumulation of iron by excess L-methionine intake may be responsible for a mechanism other than the IRE/IRP system via mitochondrial oxidative stress.

Effect of Long-Term Excessive L-Methionine Consumption on Transferrin Receptor Abundance and Mitochondrial H2O2 Generation in Rat Liver