title: The relationship between N-acetylcysteine, hyperbaric oxygen, and inflammation in a rat model of acetaminophen-induced nephrotoxicity.
abstract: An overdose of acetaminophen (APAP) produces acute tubular necrosis. The aim of this study was to observe the effects of hyperbaric oxygen (HBO) only and combined with N-acetylcysteine (NAC) on inflammatory cytokines in kidney. Thirty-two male Sprague-Dawley rats were divided into four groups: sham, control (APAP), NAC, and NAC + HBO. In the APAP, NAC, and NAC + HBO groups, renal injury was induced by oral administration of 1 g/kg APAP. The NAC group received NAC (100 mg/kg/day). NAC + HBO group received NAC (100 mg/kg/day) intraperitoneally and HBO underwent at 2.8 ATA pressure with 100 % oxygen inhalation for 90 min every 12 h for 5 days. Rats in the sham group received distilled water only by gastric tube. All animals were killed on 6 days after APAP or distilled water administration. Creatinine, urea, neopterin, tumor necrosis factor-α (TNF-α), and interleukin (IL)-6 levels were measured in sera. There was a significant increase in serum creatinine and urea levels in the control group compared to the sham group (in both, p = 0.001). NAC and NAC + HBO significantly decreased serum neopterin, TNF-α, and IL-6 levels compared to control group. APAP administration caused tubular necrosis in the renal. NAC and NAC + HBO treatments significantly reduced APAP-induced renal damage. The results of this study showed that renal dysfunction in APAP toxicity was attenuated by the use of HBO and NAC treatments. The combination of NAC and HBO treatments might be recommended as an effective treatment modality for APAP-induced nephrotoxicity.
authors.affiliation: Pathology Service, Etimesgut Military Hospital, 06790, Etimesgut, Ankara, Turkey, hcermk@yahoo.com.
authors.forename: Hakan
authors.initials: H
authors.lastname: Cermik
authors.forename: Mine Yavuz
authors.initials: MY
authors.lastname: Taslipinar
authors.forename: Ibrahim
authors.initials: I
authors.lastname: Aydin
authors.forename: Mehmet
authors.initials: M
authors.lastname: Agilli
authors.forename: Fevzi Nuri
authors.initials: FN
authors.lastname: Aydin
authors.forename: Fatma
authors.initials: F
authors.lastname: Ucar
authors.forename: Bilal Firat
authors.initials: BF
authors.lastname: Alp
authors.forename: Mehmet
authors.initials: M
authors.lastname: Toygar
authors.forename: Esin
authors.initials: E
authors.lastname: Ozkan
authors.forename: Ertan
authors.initials: E
authors.lastname: Altayli
authors.forename: Tuncer
authors.initials: T
authors.lastname: Cayci
mesh_terms: D000082:Acetaminophen / Q000633:toxicity*; D000111:Acetylcysteine / Q000627:therapeutic use*; D058186:Acute Kidney Injury / Q000139:chemically induced / Q000188:drug therapy* / Q000628:therapy*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D003404:Creatinine / Q000097:blood; D016166:Free Radical Scavengers / Q000627:therapeutic use; D006931:Hyperbaric Oxygenation; D007249:Inflammation / Q000188:drug therapy / Q000628:therapy; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D019798:Neopterin / Q000097:blood; D010100:Oxygen / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014508:Urea / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D016166:Free Radical Scavengers; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D000082:Acetaminophen; D019798:Neopterin; D014508:Urea; D003404:Creatinine; D010100:Oxygen; D000111:Acetylcysteine