L-carnitine is a quaternary
amine that is essential for the normal oxidation of long-chain
fatty acids by mitochondria. It is known that
L-carnitine and its derivatives prevent the formation of
reactive oxygen species, scavenge
free radicals and protect cells from peroxidative stress.
Oxygen-derived
free radicals and lipid peroxidation products play a critical role in the pathogenesis of
ethanol-induced gastric mucosal injury. The aim of the present study was to determine the effect of
L-carnitine on lipid peroxidation induced by
ethanol in the rat stomach. In our study, gastric mucosal injury was induced by the intragastric administration of 1 ml of absolute
ethanol. Test compounds were given to rats by gavage 30 min before the
ethanol administration. The animals were killed 60 min after the administration of
ethanol. The stomach of each animal was removed. Mucosal damage was evaluated by macroscopic examination, histological analysis and by measurement of lipid peroxidation and
glutathione activity. The intragastric administration of
ethanol induced
hyperemia and hemorrhagic erosions in the rat stomachs.
L-carnitine significantly prevented gastric ulcerogenesis induced by
ethanol and decreased the
ulcer index. Plasma and gastric lipid peroxidation that was increased significantly by
ethanol was decreased
after treatment with
L-carnitine.
Ethanol treatment decreased significantly the gastric
glutathione levels, and pretreatment with
L-carnitine increased them significantly. Based on these data, the beneficial effects of
L-carnitine on
ethanol-induced gastric mucosal injury may be attributed to its antiperoxidative effects.