Journal
DRUG AND CHEMICAL TOXICOLOGY
Volume 45, Issue 3, Pages 1150-1157Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/01480545.2020.1810259
Keywords
Selenium; valproic acid; neurodegenerative disorders; oxidative stress; mitochondria
Funding
- Shahid Beheshti University of Medical Sciences
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This study demonstrates the protective effects of sodium selenite and L-carnitine against valproic acid-induced oxidative stress and mitochondrial dysfunction.
Oxidative stress and mitochondrial dysfunction have been associated with valproic acid (VPA) induced neurotoxicity. Mitochondria are vulnerable to oxidative damage and are also a major source of superoxide free radicals. Therefore, the need for mitochondrial protective and antioxidant agents for reducing valporic acid toxicity in central nerve system (CNS) is essential. In the present study, we investigated the potential beneficial effects of sodium selenite (SS) and L-carnitine (LC) against valproic acid -induced oxidative stress and mitochondrial dysfunction in isolated rat cortical neurons. Valproic acid (50, 100 and 200 mu M) treatment caused a significant decrease in cellular viability, which was accompanied by increases in reactive oxygen species (ROS) generation, GSSG and GSH content, lipid peroxidation and lysosomal and mitochondrial damages. Sodium selenite (1 mu M) and L-carnitine (1 mM) pretreatment attenuated valproic acid-induced decrease in cell viability. In addition, sodium selenite (1 mu M) and L-carnitine (1 mM) pretreatment significantly protected against valproic acid-induced raise in oxidative stress, mitochondrial and lysosomal dysfunction, lipid peroxidation levels and depletion of GSH content. Our results in the current study provided insights into the protective mechanism by L-carnitine and sodium selenite, which is liked, to neuronal ROS generation and mitochondrial and lysosomal damages.
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