PMID- 15890506
OWN - NLM
STAT- MEDLINE
DCOM- 20051018
LR  - 20211203
IS  - 0952-3278 (Print)
IS  - 0952-3278 (Linking)
VI  - 72
IP  - 6
DP  - 2005 Jun
TI  - Burn-induced oxidative injury of the gut is ameliorated by the leukotriene 
      receptor blocker montelukast.
PG  - 431-40
AB  - 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.
FAU - Kabasakal, Levent
AU  - Kabasakal L
AD  - Department of Pharmacology, School of Pharmacy, Marmara University, 34668 
      Haydarpasa, Istanbul, Turkey.
FAU - Sener, Goksel
AU  - Sener G
FAU - Cetinel, Sule
AU  - Cetinel S
FAU - Contuk, Gazi
AU  - Contuk G
FAU - Gedik, Nursal
AU  - Gedik N
FAU - Yegen, Berrak C
AU  - Yegen BC
LA  - eng
PT  - Journal Article
PL  - Scotland
TA  - Prostaglandins Leukot Essent Fatty Acids
JT  - Prostaglandins, leukotrienes, and essential fatty acids
JID - 8802730
RN  - 0 (Acetates)
RN  - 0 (Biomarkers)
RN  - 0 (Cyclopropanes)
RN  - 0 (Leukotriene Antagonists)
RN  - 0 (Quinolines)
RN  - 0 (Sulfides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - GAN16C9B8O (Glutathione)
RN  - MHM278SD3E (montelukast)
SB  - IM
MH  - Acetates/administration & dosage/pharmacology
MH  - Animals
MH  - Biomarkers/analysis
MH  - Burns/drug therapy/*metabolism
MH  - Cyclopropanes
MH  - Glutathione/analysis
MH  - Intestines/*pathology
MH  - L-Lactate Dehydrogenase/analysis
MH  - Leukotriene Antagonists/*pharmacology
MH  - Malondialdehyde/analysis
MH  - Neutrophils/physiology
MH  - Oxidative Stress/*drug effects
MH  - Quinolines/administration & dosage/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Skin/pathology
MH  - Sulfides
MH  - Tumor Necrosis Factor-alpha/analysis
EDAT- 2005/05/14 09:00
MHDA- 2005/10/19 09:00
CRDT- 2005/05/14 09:00
PHST- 2004/11/22 00:00 [received]
PHST- 2005/02/10 00:00 [revised]
PHST- 2005/02/27 00:00 [accepted]
PHST- 2005/05/14 09:00 [pubmed]
PHST- 2005/10/19 09:00 [medline]
PHST- 2005/05/14 09:00 [entrez]
AID - S0952-3278(05)00035-9 [pii]
AID - 10.1016/j.plefa.2005.02.008 [doi]
PST - ppublish
SO  - Prostaglandins Leukot Essent Fatty Acids. 2005 Jun;72(6):431-40. doi: 
      10.1016/j.plefa.2005.02.008.