ORIGINAL ARTICLE Influence of N-acetylcysteine on renal toxicity of cadmium in rats Mustafa Kaplan & İrfan H. Atakan & Nurettin Aydoğdu & Tevfik Aktoz & Fulya Özpuyan & Gülay Şeren & Burcu Tokuç & Osman İnci Received: 19 July 2007 / Revised: 11 October 2007 / Accepted: 29 October 2007 / Published online: 7 December 2007 # IPNA 2007 Abstract The aim of this study was to investigate the ability of N-acetylcysteine (NAC) to prevent cadmium (Cd)- induced renal damage and whether NAC would reverse cadmium damage to the kidney. Fifty adult male rats were divided into five experimental groups: group 1 received tap water for 3 months and 7 days, group 2 received cadmium chloride (CdCl 2 ) for 3 months, group 3 (NAC cotreatment group) received CdCl 2 and 0.5% NAC in tap water for 3 months, group 4 received CdCl 2 in tap water for 3 months and 3 months later received only tap water for 7 days, and group 5 (NAC posttreatment group) received CdCl 2 in tap water for 3 months and 3 months later received 2% NAC in tap water for 7 days. NAC significantly decreased the elevated kidney malondialdehyde levels, as a marker of lipid peroxidation, in both cotreatment and posttreatment modalities. Cotreatment and posttreatment with NAC sig- nificantly increased kidney superoxide dismutase enzyme activity and glutathione level but did not change kidney catalase enzyme activity. NAC decreased fractional excre- tion of sodium in posttreatment group. Neither Cd nor NAC affected the glomerular filtration rate (GFR). Cotreatment and posttreatment with NAC reduced the effects of Cd on proximal tubules. It was found that NAC showed these ef- fects without changing kidney accumulation of cadmium. Exogenously administrated NAC might reduce toxic effects of Cd on the kidney without any reduction in tissue Cd level. Keywords Antioxidant enzyme . Cadmium . N-acetylcysteine . Nephrotoxicity . Oxidative stress Introduction Cadmium (Cd) is very harmful to the environment and subsequently humans because of in vivo accumulation in the kidney and liver. It is widely used in occupational settings such as smelting, zinc refining, electroplating, galvanizing, nickel-Cd battery production, and welding and is also present in tobacco [1]. Cd induces oxidative stress in the kidney by increasing lipid peroxidation and altering the antioxidant status [2]. The kidney is known to be the main target organ of Cd, and chronic and acute exposure induces proximal tubular dysfunction and results in kidney damage [3]. In an attempt to prevent and/or treat Cd-induced nephrotoxicity, various substances, such as vitamin E, selenium, melatonin, and taurine, have been used in experimental studies [2, 4–6]. Pediatr Nephrol (2008) 23:233–241 DOI 10.1007/s00467-007-0696-7 M. Kaplan (*) : İ. H. Atakan : T. Aktoz : O. İnci Department of Urology, Faculty of Medicine, Trakya University, Edirne, Turkey e-mail: mustafakaplan99@yahoo.com N. Aydoğdu Department of Physiology, Faculty of Medicine, Trakya University, Edirne, Turkey F. Özpuyan Department of Pathology, Faculty of Medicine, Trakya University, Edirne, Turkey G. Şeren Department of Chemistry, Faculty of Art and Science, Trakya University, Edirne, Turkey B. Tokuç Department of Public Health, Faculty of Medicine, Trakya University, Edirne, Turkey