title: The effect of N-acetylcysteine on oxidative stress in intestine and bacterial translocation after thermal injury.
abstract: Ischemia due to transient splanchnic vasoconstriction following major burns causes oxidative and/or nitrosative damage in intestinal tissue followed by reperfusion injury. Thus, burn injury leads to breakdown in the intestinal mucosal barrier which can induce bacterial translocation (BT). As an antioxidant and anti-inflammatory agent the protective effects of N-acetylcysteine (NAC) are documented in several studies. This study was designed to determine the effect of NAC treatment on the oxidative stress in the intestine and BT after burn injury. To evaluate this, 32 Wistar rats were randomly divided into four groups as sham (n = 8), burn (n = 8), pre-burn, NAC injection (150 mgkg(-1), intraperitoneally) 15 min before thermal injury (n = 8), post-burn, NAC injection (150 mgkg(-1), intraperitoneally) 2h after thermal injury. Under anesthesia, the shaved dorsal skin of rats was exposed to boiling water for 12s to induce burn injury in a standardized manner. Twenty-four hours later, tissue samples from mesenteric lymph nodes (MLN), spleen, and liver were obtained under sterile conditions for microbiological analysis and ileum samples were harvested for biochemical analysis. In the burn group, the incidence of isolating bacteria in MLN, spleen, and liver specimens was significantly higher than other groups. NAC treatment prevented burn-induced BT in both pre- and post-burn groups. Thermal injury caused a significant decrease in glutathione (GSH) level, significant increases in malondialdehyde (MDA) and myeloperoxidase (MPO) activity at post-burn 24th hour. Treatment of rats with NAC significantly elevated the reduced GSH levels while decreasing MDA levels and MPO activity. These data suggested that NAC has a crucial cytoprotective role in intestinal mucosal barrier and preventive effects against burn injury-induced BT.
authors.affiliation: Department of General Surgery, Faculty of Medicine, Mersin University, Mersin 33010, Turkey. korayocal@hotmail.com
authors.forename: Koray
authors.initials: K
authors.lastname: Ocal
authors.forename: Dinçer
authors.initials: D
authors.lastname: Avlan
authors.forename: Ismail
authors.initials: I
authors.lastname: Cinel
authors.forename: Ali
authors.initials: A
authors.lastname: Unlu
authors.forename: Candan
authors.initials: C
authors.lastname: Ozturk
authors.forename: Faik
authors.initials: F
authors.lastname: Yaylak
authors.forename: Musa
authors.initials: M
authors.lastname: Dirlik
authors.forename: Handan
authors.initials: H
authors.lastname: Camdeviren
authors.forename: Süha
authors.initials: S
authors.lastname: Aydin
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D018988:Bacterial Translocation / Q000187:drug effects*; D002056:Burns / Q000382:microbiology / Q000503:physiopathology*; D015169:Colony Count, Microbial; D005978:Glutathione / Q000032:analysis; D007082:Ileum / Q000187:drug effects / Q000378:metabolism*; D008099:Liver / Q000382:microbiology; D008198:Lymph Nodes / Q000382:microbiology; D008315:Malondialdehyde / Q000032:analysis; D008643:Mesentery / Q000382:microbiology; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013154:Spleen / Q000382:microbiology
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D008315:Malondialdehyde; D009195:Peroxidase; D005978:Glutathione; D000111:Acetylcysteine