Biochemical basis of valproic acid toxicity: role of oxidative stress and effects of L-carnitine

Bykov I.L.1 , Maltsev A.N.2, Gurinovich V.A.2, Nefyodov L.I.2

1. Institute of Biochemistry of National Academy of Science of Belarus, Medical University; BLK
2. Medical University; BLK
Section: Experimental/Clinical Study
PubMed Id: 15518185
Year: 2004  Volume: 50  Issue: 4  Pages: 384-389
Reduced hepatic mitochondrial β-oxidation and changes in L-carnitine metabolism are important biochemical manifestations of valproate (VA)-induced hepatic toxicity. Lipid peroxidation activation as a possible mechanism implicated in VA - induced damage as well as the possibility of L-carnitine (LC) attenuation of lipid peroxidation activity were studied. The level of malondialdehyde (MDA), lipid peroxide concentration and antioxidant activity (AOA), catalase activity, free S-S groups content in plasma and liver homogenates from male albino rats supplemented with VA (200 mg/kg, 8 days) and VA plus LC (100 mg/kg, 8 days) were measured. There were insignificant differences in MDA formation and catalase activity in the plasma and liver of control and VA - treated groups, however decreases in the plasma AOA activity and S-S groups level were observed in VA-treated rats. The LC administration significantly decreased liver lipid peroxide concentration and increased plasma AOA activity and S-S groups. Our results suggest that lipid peroxidation may be involved as an additional mechanism for VA - induced liver damage in rats. The potential antioxidant activity of LC may be particularly relevant in understanding the pharmacological and biochemical properties of LC in VA - induced pathologic conditions.
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Bykov, I. L., Maltsev, A. N., Gurinovich, V. A., Nefyodov, L. I. (2004). Biochemical basis of valproic acid toxicity: role of oxidative stress and effects of L-carnitine. Biomeditsinskaya Khimiya, 50(4), 384-389.
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