Kaplan, MustafaAtakan, Irfan H.Aydogdu, NurettinAktoz, TevfikOzpuyan, FulyaSeren, GuelayTokuc, Burcu2024-06-122024-06-1220080931-041X1432-198Xhttps://doi.org/10.1007/s00467-007-0696-7https://hdl.handle.net/20.500.14551/18584The 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 (CdCl2) for 3 months, group 3 (NAC cotreatment group) received CdCl2 and 0.5% NAC in tap water for 3 months, group 4 received CdCl2 in tap water for 3 months and 3 months later received only tap water for 7 days, and group 5 (NAC posttreatment group) received CdCl2 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 significantly increased kidney superoxide dismutase enzyme activity and glutathione level but did not change kidney catalase enzyme activity. NAC decreased fractional excretion 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 effects 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.en10.1007/s00467-007-0696-7info:eu-repo/semantics/closedAccessAntioxidant EnzymeCadmiumN-AcetylcysteineNephrotoxicityOxidative StressLipid-PeroxidationGlutathioneKidneyLiverSuperoxideMechanismsSeleniumNephrotoxicityAccumulationProtectionArticle232233241Q2WOS:0002522986000082-s2.0-3834901849118064495Q1