International Journal of Pharmacology and Toxicology, 1 (2) (2013) 17-28 ©Science Publishing Corporation www.sciencepubco.com/index.php/IJPT Mentha piperita protects against Cadmium induced oxidative renal damage by restoring antioxidant enzyme activities and suppressing inflammation in rats S.Thangapandiyan, NC Sumedha and S.Miltonprabu* Faculty of Science, Department of Zoology, Annamalai University, Annamalai nagar, Chidambaram, Tamil Nadu, India *Corresponding author E-mail: smprabu73@gmail.com Abstract 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. Cd- induced 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 Cd- induced 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. Keywords: Mentha Piperita, Cadmium, Kidney, Renal Markers, Inflammatory Markers, Rat. 1 Introduction Cadmium is a ubiquitous environmental toxicant that affects biological systems in various ways. The molecular mechanisms of its toxicity are not yet well defined. Humans are exposed to cadmium from the sources of tobacco smoke, food, industrial, occupational and environmental pollution. Cadmium exposure has been shown to have adverse effects on a variety of tissues and is linked with various chronic diseases. It has long been recognized as one of the most toxic environmental and occupational heavy metal pollutant [1]. Cd stimulates the formation of reactive oxygen species, including oxygen free anion radical [2], hydrogen peroxide [3] and probably hydroxyl radical [4]. As a consequence, enhanced lipid peroxidation, DNA damage, altered calcium and sulfhydryl homeostasis, as well as marked disturbances of antioxidant defense system (ADS) occur [5]. Cd-related diseases including cardiovascular disease, hypertension, osteoporosis, nephrotoxicity, hepatotoxicity, diabetes, and cancers of many organs [6]. Mechanism of cadmium toxicity may be multifactorial. It has been suggested that cadmium acts as a catalyst in the oxidative reactions of biological