Arsenic (As) is an environmental toxic metalloid that is present in everywhere such as air, water and soil. Generally, inorganic arsenic has a tendency to be more toxic than organic arsenic. The present study was designed to determine whether oral administration of silibinin (SB), which has been shown to have substantial antioxidant properties, when pre-administered (75 mg/kg body weight) once daily for 4 weeks along with arsenic (5 mg/kg) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX),glutathione-S-transferase (GST),glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione (GSH), total sulfhydryl groups (TSH) and vitamin C in rat brain regions such as cortex, striatum, cerebellum, hippocampus and brain stem. Our study also examined the effect of SB over arsenic-induced reactive oxygen species (ROS) production and lipid peroxidation level (LPO) and protein carbonyl content (PC) in distinct brain regions of rats. Moreover, As also alters the lipid profiles such as total lipids, phospholipids, cholesterol, cerebrosides and gangliosides in various regions of the brain. Pre-administration of SB restores the altered enzymatic and non-enzymatic antioxidants, lipid profiles and also markedly reduced the ROS, LPO, PC and accumulation of As in various regions of the brain. These results suggested that arsenic-induced deficits in antioxidant enzyme activities and increase in ROS production and lipid peroxidation levels in brain regions can be remarkably prevented by pre-administration of SB.

Background:The aim of this study was to investigate the possible protective role of the Mentha piperita leaf extract (MPE) on cadmium (Cd)-induced nephrotoxicity using biochemical and histopathological approaches. Methods:The control group received the vehicles only. The Cd treated group received Cdcl 2 (5 mg/kg) orally in isotonic saline for 4weeks. Cd + MPE treated group received the MPE at a dose of (100mg/kg in 5% tween 80) along with Cd. MPE alone treated group received the MPE alone orally at a dose of 100mg/kg in 5% tween 80 for 4 weeks. Results:In experimental rats oral administration of CdCl 2 (5 mg/kg) for 4weeks significantly induced renal damage which was evident from the increased levels of serum urea, uric acid and creatinine with a significant (p<0.05) decrease in creatinine clearance. Cd also significantly (p<0.05) decreased the levels of urea, uric acid and creatinine in urine. Cdinduced oxidative stress in kidney tissue was indicated by the increased levels of renal lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydro peroxides) and protein carbonyl content with a significant (p<0.05) decrease in non-enzymatic (total sulfhydryl group, reduced glutathione, vitamin C and E) and enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR). Moreover the kidneys of Cd-treated rats also exhibit significantly (p<0.05) increased levels of tumor necrosis factor (TNF-α) and nitric oxide (NO). The histopathology of Cd treated rats showed tubular necrosis, degeneration, dilation, desquamation, thickening of basement membrane and luminal cast formation. MPE (100mg/kg/day) treatment markedly attenuated the Cd-induced biochemical alterations in serum, urine and renal tissue, and brings the TNF-α and NO in to normal levels. MPE also ameliorated the Cd-induced pathological changes when compared with Cd-alone-treated group. Conclusions:These results indicate that the natural dietary antioxidant MPE might have significant protective effect against Cdinduced oxidative stress mediated in rats. Due to its antioxidant and anti-inflammatory effects, it will provide an accessible and cheap traditional medicine source for treatment of Cd mediated environmental and occupational ailments.