ARSENIC INDUCED OXIDATIVE HEMATOTOXICITY IN RATS AND ITS PROTECTION BY DIALLYL TRISULFIDE
As being a potent environmental toxicant, leads to the development of various hazardous effects on both human and animal health. It has been reported that diallyl trisulfide (DATS) is one of the most persuasive organo sulfur compounds which can boost up antioxidant enzymes through Nrf2 activation. Heme biosynthesis pathway is influenced by as exposure in animal and humans through the induction of oxidative stress. Since, blood is among the most vulnerable biological system during oxidative stress. Hence, the present study was aim to investigate the effects of DATS on lipid peroxidation, antioxidant activity, clinical hematological variables and ROS level of As treated rat blood. Oral administration of arsenic (5mg/kg/b.w/day) for 4 weeks significantly increased the lipid peroxidation markers that is thiobarbituric acid reactive substances (TBARS) and malondialdehyde (MDA) in As treated rat blood. The activities of non-enzymic antioxidants glutathione (GSH) and enzymic antioxidants such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) were also decreased in As treated rats blood. As intoxication significantly decreased the counts of white blood cell (WBC), red blood cell (RBC) and platelets and significantly reduced the levels of HGB, MCH and MCHC and significantly increased levels of MCV and HCT. Blood ROS level was also increased significantly in rat blood due to As induced oxidative stress. Administrations of DATS (80mg/kg body weight) for 4 weeks in As intoxicated rats significantly reduced the levels TBARS and MDA, and also significantly increased the activities of non-enzymic and enzymic antioxidants. Further, DATS administration significantly reduced the ROS level with an increased WBC, RBC and PLT counts, increased concentration of HGB, MCH and MCHC and decreased levels of MCV and HCT. The results of the present study clearly interpret that DATS shows a significant protective effect against As induced oxidative stress in rat blood.