ABSTRACT
Valproic acid (VPA) is a very effective anticonvulsant agent that is widely used in the management of various forms of epilepsy. This chapter shows that VPA enhances lipid peroxidation rate when administered to rats in vivo. Lipid peroxidation in the liver is a function of dose and time. Promotion in the liver of lipid peroxidation might be explained by a reduced antioxidant activity of the tissue at low doses, which further impairs at high doses with the shift in the redox potential of liver tissue to less reducing conditions. However, the relative importance of lipid peroxidation in the subsequent development of clinically significant pathologic changes in liver during VPA therapy remains to be substantiated by further research. The major cellular targets at risk following drug-induced depletion of liver glutathione are membrane lipids. The molecular damage is expressed as the autocatalytic process of lipid peroxidation, resulting in impairment of membrane functioning.
