Influence of N-acetylcysteine on renal toxicity of cadmium in rats.
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 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.
Kaplan
Mustafa
M
Department of Urology, Faculty of Medicine, Trakya University, Edirne, Turkey. mustafakaplan99@yahoo.com
Atakan
Irfan H
IH
Aydoğdu
Nurettin
N
Aktoz
Tevfik
T
Ozpuyan
Fulya
F
Seren
Gülay
G
Tokuç
Burcu
B
Inci
Osman
O
D000111:Acetylcysteine / Q000627:therapeutic use*; D000818:Animals; D019256:Cadmium Chloride / Q000378:metabolism / Q000633:toxicity*; D002374:Catalase / Q000378:metabolism; D018890:Chemoprevention; D003401:Creatine / Q000097:blood / Q000652:urine; D004195:Disease Models, Animal; D004336:Drug Antagonism; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D005919:Glomerular Filtration Rate / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D014508:Urea / Q000097:blood / Q000652:urine
D016166:Free Radical Scavengers; D014508:Urea; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione; D019256:Cadmium Chloride; D003401:Creatine; D000111:Acetylcysteine