Inhibitory effects of sodium valproate on oxidative phosphorylation

Richard Haas, B. Chir, David A. Stumpf*, Janice K. Parks, Luis Eguren

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

83 Scopus citations

Abstract

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 α-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.

Original languageEnglish (US)
Pages (from-to)1473-1476
Number of pages4
JournalNeurology
Volume31
Issue number11
DOIs
StatePublished - Nov 1981

ASJC Scopus subject areas

  • Clinical Neurology

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