title: Burn-induced oxidative injury of the gut is ameliorated by the leukotriene receptor blocker montelukast.
abstract: There is increasing evidence that oxidative stress has an important role in the development of multiorgan failure after major burn injury. In the present study, we investigated whether the leukotriene receptor blocker montelukast is protective against burn-induced injury of the gut. Under brief ether anaesthesia, shaved dorsum of the rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10 s. Montelukast (10 mg/kg) or saline was administered intraperitoneally immediately after and at the 12th hour of the burn injury. Rats were decapitated 24 h after burn injury and the skin samples, as well as tissue samples from stomach, ileum and colon, were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Tissues were also examined microscopically. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) were assayed in serum samples. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, serum TNF-alpha and LDH were elevated in the burn group as compared to control group. On the other hand, montelukast treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by thermal trauma. Findings of the present study suggest that montelukast possesses an anti-inflammatory effect on burn-induced gastrointestinal damage and protects against oxidative injury by a neutrophil-dependent mechanism.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Marmara University, 34668 Haydarpaşa, Istanbul, Turkey.
authors.forename: Levent
authors.initials: L
authors.lastname: Kabasakal
authors.forename: Göksel
authors.initials: G
authors.lastname: Sener
authors.forename: Sule
authors.initials: S
authors.lastname: Cetinel
authors.forename: Gazi
authors.initials: G
authors.lastname: Contuk
authors.forename: Nursal
authors.initials: N
authors.lastname: Gedik
authors.forename: Berrak C
authors.initials: BC
authors.lastname: Yeğen
mesh_terms: D000085:Acetates / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D002056:Burns / Q000188:drug therapy / Q000378:metabolism*; D003521:Cyclopropanes; D005978:Glutathione / Q000032:analysis; D007422:Intestines / Q000473:pathology*; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D020024:Leukotriene Antagonists / Q000494:pharmacology*; D008315:Malondialdehyde / Q000032:analysis; D009504:Neutrophils / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects*; D011804:Quinolines / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000473:pathology; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000085:Acetates; D015415:Biomarkers; D003521:Cyclopropanes; D020024:Leukotriene Antagonists; D011804:Quinolines; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D005978:Glutathione; C093875:montelukast