This study has been designed to investigate the effect of alpha lipoic acid (ALA) in nicotine-induced vascular endothelial dysfunction (VED) in rabbits. Nicotine (7.5 mg/kg/day, sc, 6 weeks) was administered to produce VED in rabbits. The development of VED was assessed by employing aortic histopathology and estimating serum concentration of nitrite/nitrate (NOx). Further, serum lipid profile was assessed. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) reduced glutathione (GSH) and superoxide dismutase (SOD) generation. The administration of nicotine produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum concentration of NOx. Further, nicotine produced oxidative stress, which was assessed in terms of increase in serum TBARS and decreased GSH and SOD levels. However, treatment with ALA (20 mg/kg/day, orally) markedly prevented nicotine-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum NOx, decreasing serum TBARS and normalizing SOD and GSH activities. Thus, it may be concluded that ALA reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine-induced experimental VED.
Alpha lipoic acid; Endothelial damage; Nicotine; Nitric oxide; Vascular damage