Drug Biochemistry Evaluation of Ascorbic Acid, Probucol, and Α-tocopherol as Suppressors of Dexamethasone Induced Lipid Peroxidation

Lipid peroxidation is a highly destructive process, which induces a plethora of alterations in structure and function of cellular membranes. It is involved in number of diseases and poisoning by several toxins. Lipid peroxidation occurs in response to oxidative stress, and a great diversity of aldehydes are formed when lipid hydroperoxides break down in biological systems. Among the aldehydic endproducts, most intensively studied is 4-hydroxy-nonenal (4-HNE), the major toxic mediator of consequences of lipid peroxidation. The present study deals with the lipid peroxidation induction potential of dexamethasone (DEX), a commonly used anti-inflammatory drug, and the scavenging capacity of some conventional antioxidants like ascorbic acid (AA), probucol (PR) and α-tocopherol (TOC) on drug induced lipid peroxidation. The drug (dexamethasone) induced lipid peroxidation studies have been performed using goat liver homogenate. Liver being the major site for detoxification is the primary target for environmental or occupational toxic exposure in biological system. The results of the present study indicate that DEX increased the 4-HNE content vis-·-vis decreased the nitric oxide (NO) level of tissue. This suggests that DEX caused significant extent of lipid peroxidation, which may be related to the toxic potential of the drugs, and the above antioxidants have potential protective effects against DEX induced lipid peroxidation to the significant extent.