Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the cellular mechanism of muscular weakness in the Intermediate Myasthenia Syndrome (IMS) following acute organophosphate poisoning, we studied the cytotoxicity of dimethoate and its effects on the activity of acetylcholine esterase (AChE), Na+-K+-ATPase, succinate dehydrogenase (SDH), and Ca2+-ATPase in primary cultured skeletal muscle cells. The results showed that the activity of AChE was significantly inhibited in a dose and time-dependent manner when cells were exposed to dimethoate for 2 h, but the expression of heat-shock protein (HSP70) in muscle cells was significantly increased in a time-dependent manner following dimethoate exposure. Dimethoate can significantly increase the activity of Na+-K+-ATPase in the mitochondrial and cytoplasm fraction of muscle cells, and inhibit the activity of Ca2+-ATPase. This study suggests that the disruption of intracellular homeostasis and energy metabolism of the muscle cells may play a role in the etiology of IMS.
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PMID:Biochemical changes in primary culture of skeletal muscle cells following dimethoate exposure. 1198 85