This study is based on the hypothesis that antiepileptic drugs (other than Valproic acid) have an effect on the mitochondrial oxidative phosphorylation. The objective of this study is to evaluate this effect in an accessible tissue-human peripheral white blood cells.
Antiepileptic drugs adverse reactions, including hepatotoxicity, are rare but potentially fatal, especially among children. Although the mechanism of the liver toxicity remains elusive, mitochondrial oxidative stress, has been hypothesized to play a role. Most of the studies addressing antiepileptic drug effects on the mitochondria discuss the effect of valproic acid. The exact mechanisms involved in the drug-induced effects on oxidative phosphorylation are still far from being resolved. Most of the studies investigated the effect of valproic acid by using animal models or different in vitro methods.Mitochondrial diseases should be considered as a risk factor for valproic acid-induced hepatotoxicity, and there is a consensus for avoiding the administration of the drug for these patientsIs it possible that other antiepileptic drugs have similar effects? The knowledge regarding the effects of other antiepileptic drugs on the mitochondria is relatively scarce.
Study Type
OBSERVATIONAL
Enrollment
60
White blood cells from peripheral blood samples
Hadassah-Hebrew University Medical Center
Jerusalem, Israel
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