Methylmercury (MeHg)-induced neurotoxicity includes skeletal muscle sy
mptoms (extremity weakness and wasting, muscle cramp) in addition to a
taxia and disturbances of sensory and visual function. The underlying
mechanisms responsible for the skeletal muscle symptoms are still poor
ly understood. In this study the effects of MeHg exposure on skeletal
muscle were investigated in rats receiving orally administered MeHgCl
at 5 mg/kg/day for 12 days. MeHg-treated rats gradually lost body weig
ht and showed muscle weakness and wasting. Seven days after the last M
eHg dose, MeHg levels in the skeletal muscle were as high as those in
liver, kidney, or cerebrum. The obvious histopathological finding in s
keletal muscle was a decrease in mitochondrial enzyme activity. These
changes were more prominent in mitochondria-rich soleus muscle than in
extensor digitorum longus muscle. Our findings confirm that MeHg expo
sure disturbs mitochondrial energy metabolism in skeletal muscle. (C)
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