Effect of carnitine on stress-induced lipid peroxidation in rat gastric mucosa

Abstract

Carnitine is an essential cofactor in the mitochondrial transfer of fatty acids, but is also a scavenger of oxygen free radicals in mammalian tissues. It has been shown that cold-restraint stress (CRS) produces gastric mucosal injury due to oxygen free radicals. The aim of this study was to determine the effect of L-carnitine on lipid peroxidation induced by CRS in rat stomachs. Rats pretreated with L-carnitine (50 mg/kg per day for 10 days) were restrained in a wire cage for 4 h at 4 degrees C. At the end of the experimental period, the lesion index in gastric mucosa was determined. In blood and gastric mucosa samples, the content of mucin, prostaglandin (PG)E2, the products of lipid peroxidation, and catalase activity were measured. CRS caused a significant decrease in gastric mucin and PGE2 content, while in the gastric mucosa of rats pretreated with L-carnitine, the changes in gastric mucin and PGE2 content, as well as gastric lesion development and enhanced lipid peroxide formation due to stress, were prevented. On the other hand, catalase activity in blood increased in the CRS group, while its value in gastric mucosa was not different from that in the control rats. L-Carnitine treatment increased catalase activity in both blood and gastric mucosa in control animals. Following stress, increased catalase activity of blood was associated with decreased mucosal catalase activity in rats that received L-carnitine. L-Carnitine prevents the occurrence of mucosal lesions by strengthening the gastric mucosal barrier and by reducing the products of lipid peroxidation against noxious factors that cause elevation of lipid peroxidation, such as CRS.