ABSTRACT
OBJECTIVES: The present study was carried out to study the protective effects of quercetin and α-lipoic acid alone and in combination against aluminum chloride induced neurotoxicity in rats. MATERIALS AND METHODS: The study consisted of eight groups, namely, Group 1: control rats, Group 2: rats receiving aluminium chloride 7 mg/kg body weight intraperitoneal route (i.p) for two weeks, Group 3: rats receiving quercetin 50 mg/kg body weight i.p. for two weeks, Group 4: rats receiving quercetin 50 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks, Group 5: rats receiving α-lipoic acid 20 mg/kg body weight i.p. for two weeks, Group 6: rats receiving lipoic acid 20 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks, Group 7: rats receiving α-lipoic acid 20 mg/kg body weight and quercetin 50 mg/kg body weight i.p. for two weeks, and Group 8: rats receiving α-lipoic acid 20 mg/kg body weight and quercetin 50 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks. The animals were killed after 24 hours of the last dose by cervical dislocation. RESULTS: Aluminium chloride treatment of rats resulted in significant increases in lipid peroxidation, protein carbonyl levels, and acetylcholine esterase activity in the brain. This was accompanied with significant decreases in reduced glutathione, activities of the glutathione reductase, and superoxide dismutase. Pretreatment of AlCl3 exposed rats to either quercetin or α-lipoic acid also restored altered lipid peroxidation and superoxide dismutase to near normal levels. Quercetin or α-lipoic acid pretreatment of AlCl3 exposed rats improved the protein carbonyl and reduced glutathione, glutathione reductase, and acetylcholine esterase activities in rat brains towards normal levels. Combined pretreatment of AlCl3 exposed rats with quercetin and α-lipoic acid resulted in a tendency towards normalization of most of the parameters. CONCLUSIONS: Quercetin and α-lipoic acid complemented each other in protecting the rat brain against oxidative stress induced by aluminium chloride.
ABSTRACT
BACKGROUND: The present study was undertaken to study the effect of mercuric chloride (HgCl2) on the collagen metabolism in rats and the protective effect of 2, 3-dimercapto-1-propane sulfonic acid (DMPS) in HgCl2-treated rats. MATERIAL/METHODS: The experimental groups studied were (i) a control group (ii) rats injected with a single intraperitoneal (ip) dose of 2 mg of HgCl2/kg body weight (HgCl2-treated group, n=10 rats), (iii) Rats injected with a single dose (ip) of 100 mg of DMPS/kg body weight (DMPS group, n=10 rats), (iv) rats injected with a single dose (ip) of 100 mg of DMPS/kg body weight followed by a single dose (ip) of 2 mg of HgCl2/kg body weight 1 hour after a 100-mg DMPS injection (DMPS + HgCl2-treated group, n=10 rats). Half of the rats from each group were sacrificed after 24 hours and the other half after 48 hours of treatment. RESULTS: A dose of 2.0 mg HgCl2/kg body weight caused an impairment of glomerular function, which was reflected by significant increases in the levels of serum creatinine and serum urea nitrogen in HgCl2-treated rats compared with control rats. Administration of 2.0 mg of HgCl2/kg body weight significantly increased urinary excretion of free hydroxyproline in HgCI2-treated rats compared with the control rats, reflecting increased collagen breakdown. CONCLUSIONS: Administration of DMPS one hour before HgCl2 treatment caused the restoration of altered parameters to near normal levels.
