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J.Health Sci., 47(2), 162-167, 2001
Chronic Low-Dose Methylmercury Administration Decreases Mitochondrial Enzyme Activities and Induces Myopathic Changes in Rats
Fusako Usuki,*, a Akira Yasutake,b Miyuki Matsumoto,a and Itsuro Higuchic
aDepartment of Clinical Medicine and bBiochemistry Section, National Institute for Minamata Disease, 4058-18 Hama, Minamata 867-0008, Japan, and cThird Department of Internal Medicine, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-0075, Japan
Methylmercury (MeHg)-induced neurotoxicity includes skeletal muscle symptoms (muscle weakness and wasting, muscle cramp). In this study the effects of long-term low dose exposure to MeHg on skeletal muscle were investigated using rats which had received food containing MeHg (5 ppm Hg; the average intake: 200 mu g Hg/kg/day). From six months after the first MeHg administration, total mercury levels in the skeletal muscle remained almost stable at 3.5-5.5 mu g/g, about one tenth of the levels achieved in the acute MeHg-intoxicated model receiving 5 mg MeHgCl/kg/day for 12 days. However low-dose, long-term administration of MeHg induces histochemical changes similar to those in the acute model with decreases in mitochondrial electron transport system enzyme activities. The results indicate that even low dose MeHg administration causes disturbances in mitochondrial enzyme activities if the administration continues long term. In rats treated with MeHg for 21 months, mild myopathic changes appeared: variations in fiber size, increases in central nuclei and an increase of acid phosphatase activity. The declining function of the redox system in skeletal muscle during aging may accentuate the effects of chronic MeHg intoxication on skeletal muscle.
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