Gentamicin induced lipid peroxidation and its control with ascorbic acid.

Lipid peroxidation is the oxidative deterioration of polyunsaturated fatty acids (PUFAs), which is a free radical related process. Studies showed that reactive oxygen species (ROS) are involved in a diversity of biological phenomena including atherosclerosis, neurodegenerative diseases, carcinogenesis etc. ROS and other pro-oxidant agents have the capacity to exhibit oxidative decomposition of PUFAs of membrane phospholipids leading to the formation of toxic end products, including malonyldialdehyde (MDA), 4-hydroxy-2-nonenal (HNE) etc. Drug-induced lipid peroxidation contributes to significant toxicity. Antioxidants have the ability to reduce generation of free radicals in the body by inhibiting lipid peroxidation process. In view of this concept, the present in vivo study is carried out to evaluate the inhibitory effect of ascorbic acid on lipid peroxidation induced by gentamicin, an aminoglycoside antibiotic. Levels of MDA, HNE, reduced glutathione (GSH) and nitric oxide (NO) are used as markers of lipid peroxidation. Rabbits divided into different experimental groups are treated with drug and co-administered with ascorbic acid. The levels of MDA, HNE, GSH and NO in the blood are estimated and compared with the control. The results revealed that gentamicin significantly increases MDA and HNE contents, but decreases GSH and NO levels; and ascorbic acid on co-administration has capability to inhibit drug-induced lipid peroxidation.