Abstract
Valproic acid (VPA) has toxic metabolites that can elevate oxidative stress markers, and the hepatotoxicity of VPA has been reported. Coenzyme Q10 (CoQ10) is one of the most widely used antioxidants. The effect of CoQ10 on epileptogenesis and VPA hepatotoxicity were examined. Rats were randomly divided into five groups: the control group received 0.5% methylcellulose by oral gavages daily and saline by intraperitoneal injection three times weekly. The PTZ group received 1% methylcellulose by gavages daily and 30 mg/kg PTZ by intraperitoneal injection three times weekly. The valproic acid group received 500 mg/kg valproic acid by gavage and 30 mg/kg PTZ, as above. The CoQ10 group received 200 mg/kg CoQ10 by gavages daily and 30 mg/kg PTZ, as above. The Valproic acid + CoQ10 group received valproic acid and CoQ10, as above. Results: CoQ10 exhibited anticonvulsant activity and potentiated the anticonvulsant effect of VPA. CoQ10 combined with VPA induced a more significant reduction in oxidative stress and improved the histopathological changes in the brain and liver compared to VPA treatment. In addition, CoQ10 reduced the level of toxic VPA metabolites. These findings suggest that the co-administration of CoQ10 with VPA in epilepsy might have therapeutic potential by increasing antiepileptic activity and reducing the hepatotoxicity of VPA.
Highlights
Publisher’s Note: MDPI stays neutralOxidative damage can affect neuron excitability with increased susceptibility to seizure attacks
Regardless of the variety of anti-epileptic drugs (AEDs), there still has not been a complete improvement of epilepsy
Some AEDs have toxic metabolites that can elevate oxidative stress and mitochondrial dysfunction markers in other organs, such as liver toxicity associated with chronic valproic acid (VPA) use; VPA metabolites cause oxidative stress as a consequence of elevated
Summary
Publisher’s Note: MDPI stays neutralOxidative damage can affect neuron excitability with increased susceptibility to seizure attacks. Oxidative damage and mitochondrial dysfunction with excessive free radical production in the organs, in addition to the imbalance between free radical concentrations and antioxidant defenses, may be associated with epileptogenesis pathology and has been linked to the pathogenesis of liver fibrosis, stroke, diabetes mellitus, and atherosclerosis [1]. More than 30% of patients have drug-resistant epilepsy, in addition to other limitations in some AED treatments [2,3]. Some AEDs have toxic metabolites that can elevate oxidative stress and mitochondrial dysfunction markers in other organs, such as liver toxicity associated with chronic valproic acid (VPA) use; VPA metabolites cause oxidative stress as a consequence of elevated. These limitations of conventional AEDs highlight the necessity of the with regard to jurisdictional claims in published maps and institutional affiliations
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