Background and Aim: L-Carnitine is an essential cofactor in the mitochondrial transfer of fatty acids, and it is also a scavenger of free radicals in mammalian tissues. The aim of the study was to determine the effect of L-carnitine on chronic restraint stress-induced gastric mucosal injury. Methods: Wistar rats were applied restraint stress (1 h/day) and L-carnitine (50 mg/kg) for 21 days. The lesion index, prostaglandin E 2 and mucus content, lipid peroxidation, superoxide dismutase, and catalase activity in gastric mucosa were evaluated. Results: Chronic restraint stress increased the lesion index, lipid peroxidation, and superoxide dismutase activity in gastric mucosa, and it decreased prostaglandin E 2 and mucus content. L-Carnitine treatment prevented the stress-induced increase in lesion index, lipid peroxidation and a stress-induced decline in prostaglandin E 2 , and mucus content in gastric mucosa, but it increased catalase activity. Conclusions: L-Carnitine prevents the occurrence of lesion by strengthening the gastric mucosal barrier and by reducing lipid peroxidation against the harmful effects of chronic restraint stress.
The aim of the present study was to investigate the effects of stress-induced lipid peroxidation on macrophages' functions. Animals were subjected to 4 h immobilization at 4 degrees C in restraining devices. The peritoneal macrophages obtained from rats exposed to cold and restraint stress exhibited an increase in lipid peroxidation and a decline of chemotaxis and phagocytosis compared with control rats. After supplementation with vitamin E, the increment in thiobarbituric acid reactive substances (TBARS) content as the oxidative stress marker and the decline of chemotaxis and phagocytosis in peritoneal macrophages observed during cold-restraint stress was significantly removed. No significant change in catalase activity of peritoneal macrophages was observed in groups exposed to cold-restraint stress and treated with vitamin E. These findings indicate that phagocytic and chemotactic capacities of peritoneal macrophages are decreased by cold-restraint stress and this effect of stress may be related to lipid peroxidation.
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