Skip to main content
U.S. Department of Energy
Office of Scientific and Technical Information

Is there a role for leukotrienes as mediators of ethanol-induced gastric mucosal damage

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:7027145
; ;  [1]
  1. Queen's Univ., Kingston, Ontario (Canada)
The role of leukotriene (LT) C{sub 4} as a mediator of ethanol-induced gastric mucosal damage was investigated. Rats were pretreated with a number of compounds, including inhibitors of leukotriene biosynthesis and agents that have previously been shown to reduce ethanol-induced damage prior to oral administration of absolute ethanol. Ethanol administration resulted in a fourfold increase in LTC{sub 4} synthesis. LTC{sub 4} synthesis could be reduced significantly by pretreatment with L651,392 or dexamethosone without altering the susceptibility of the gastric mucosa to ethanol-induced damage. Furthermore, changes in LBT{sub 4} synthesis paralleled the changes in LTC{sub 4} synthesis observed after ethanol administration. The effects of ethanol on gastric eicosanoid synthesis were further examined using an ex vivo gastric chamber preparation that allowed for application of ethanol to only one side of the stomach. These studies confirm that ethanol can stimulate gastric leukotriene synthesis independent of the production of hemorrhagic damage. Inhibition of LTC{sub 4} synthesis does not confer protection to the mucosa, suggesting that LTC{sub 4} does not play an important role in the etiology of ethanol-induced gastric damage.
OSTI ID:
7027145
Journal Information:
American Journal of Physiology; (USA), Journal Name: American Journal of Physiology; (USA) Vol. 254:1; ISSN 0002-9513; ISSN AJPHA
Country of Publication:
United States
Language:
English