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Inhibitory effects of sodium valproate on oxidative phosphorylation

Departments of Pediatrics and Neurology, School of Medicine, University of Colorado Health Sciences Center, Denver, CO.

Address correspondence and reprint requests to Dr. Stumpf, Director of pediatric Neurology, Box C229, University of Colorada Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262.

Sodium valproate (VP) inhibited oxidative phosphorylation in isolated rat liver mitochondria. State 3 rates of oxygen consumption with glutamate as substrate were 80% of control values at a low VP concentration (24 µM). At 240 µM, there was more than 50% inhibition of glutamate and -ketoglutarate state 3 rates. Succinate state p rates were 80% of control values, and uncoupling was noted at 2400 µM VP. These VP effects were similar to those of propionate and isovalerate, suggesting a common mechanism of toxicity. Inhibition of mitochondrial oxidative phosphorylation may explain why VP intoxication causes a hepatocerebral disorder that resembles Reye syndrome.

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