Mechanisms of Action of Diallyl Disulfide Against Trichloromethane-Induced Renal Toxicity is Via Inhibitions of Oxidative Stress, NFkB Activation, and Apoptosis in Rats

The renal-protective effect of diallyl disulfide (DADS) on tricholoromethane (CHCl3)-induced renal toxicity was investigated. Twenty five rats, divided into five groups of five animals each were used. CHCl3 at the dose of 200 mg/kg was orally administered, and concomitantly treated with DADS (50 mg/kg), 5 days/week for a period of 3 weeks. Compared with control, there was no significant increase in kidney malondialdehyde (MDA), but a significant increase in levels of nuclear factor kappa B (NFkB) expressions, TUNEL positive cells (apoptosis), as well as hydrogen peroxide (H2O2), nitric oxide (NO) and reduced glutathione (GSH) concentrations. In addition, a significant decrease in expressions of kidney p53 and catalase (CAT) activity, and a non-significant decrease in glutathione peroxidase (GPx) activity were recorded following CHCl3 administration. Conversely, following DADS treatment, there was a significant increase in the expressions of p53, and a significant and non-significant decrease in apoptotic positive cells and NFkB expressions respectively. Administration of DADS significantly reduced the levels of H2O2 and NO, but did not have effect on the level of GSH, while CAT and GPx activities were significant improved. Protection by DADS against TCM-induced renal-toxicity may therefore be via suppressions of NFkB activation, oxidative stress and apoptosis in rats. Keywords: Apoptosis, Diallyl disulfide, NFkB, Oxidative stress, p53, Trichloromethan