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J.Health Sci., 50(3), 277-285, 2004
Effect of Long-Term Excessive L-Methionine Consumption on
Transferrin Receptor
Abundance and Mitochondrial
H2O2
Generation in Rat Liver
Nobuko Mori* and Kimiko Hirayama
School of Health Sciences, Kumamoto University, 4-24-1
Kuhonji, Kumamoto 862-0976, Japan
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.
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