Résumé
We evaluated the effect of melatonin (Mel) in male albino mice which received aluminum acetate (Al) for 6 weeks (3.5 mg/kg body weight) (b.w.) i.p. five times per week. Moreover mice received Mel (7mg/kg b.w.i.p. 5 days/week) for 6 weeks. At the end of the treatment hippocampus was removed and processed to examine the oxidative stress markers. Following Al exposure oxidative stress increased significantly, estimated by increased thiobarbituric acid reactive substances (TBARS) and decrease in the activity of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), reduced glutathione (GSH),glutathione peroxidase (GPx) and glutathione-s-transferase (GST). Al+Mel treatment significantly prevented the aluminum induced decrease in antioxidant enzymes as well as decrease in TBARS. Histopathological evidence in the hippocampi revealed the protective effect of melatonin against Al induced damage in light and transmission electron microscopic (TEM) studies. These results supported that melatonin suppresses the oxidative stress. This may result from the higher efficacy of melatonin in scavenging various free radicals and also because of its ability in stimulating the anti oxidant enzymes.
Résumé
This study has revealed significant variation in total ATPase activity after administration of aluminium acetate in different tissues of albino mice. With sublethal dose (3.5 mg/kg body weight) of aluminium acetate, total ATPase activity was decreased in brain (-50.61), liver (-50.69), kidney (-30.74), heart (-64.07), muscle (-51.50) and testis (-65.53) of albino mice. The decrement was enhanced with the increase of aluminium acetate. ATPases play an important role in the maintenance of cell permeability and energy transformation in the biological system. The results suggest that ATPase has a particular sensitivity to aluminium acetate.