L-carnitine protects gastric mucosa by decreasing ischemia-reperfusion induced lipid peroxidation.

Studies have shown that reactive oxygen metabolites and lipid peroxidation play important roles in ischemia-reperfusion injury in many organs such as heart, brain and stomach. The aim of this study is to evaluate the antioxidant effect of L-carnitine on gastric mucosal barrier, lipid peroxidation and the activities of antioxidant enzymes in rat gastric mucosa subjected to ischemia-reperfusion injury. Rats were subjected to 30 min of ischemia followed by 60 min of reperfusion. L-carnitine (100 mg/kg), was given to rats intravenously five minutes before the ischemia. In our experiment, lesion index, thiobarbituric acid reactive substances, prostaglandin E2 and mucus content in gastric tissue were measured. The results indicated that the lesion index and the formation of thiobarbituric acid reactive substances increased significantly with the ischemia-reperfusion injury in the gastric mucosa. L-carnitine treatment reduced these parameters to the values of sham operated rats. The tissue catalase and superoxide dismutase activities and prostaglandin E2 production decreased significantly in the gastric mucosa of rats exposed to ischemia-reperfusion. L-carnitine pretreatment increased the tissue catalase activity and prostaglandin E2 to the levels of sham-operated rats but did not change superoxide dismutase activity. There were no significant difference in glutathione peroxidase activity and mucus content between the groups in the gastric mucosa. In summary, L-carnitine pretreatment protected gastric mucosa from ischemia-reperfusion injury by its decreasing effect on lipid peroxidation and by preventing the decrease in prostaglandin E2 content of gastric mucosa.

Protective effect of L-carnitine on gastric mucosal barrier in rats exposed to cold-restraint stress.

AIM: The protective effect of L-carnitine on stress-induced gastric mucosal injury was investigated in rats exposed to cold-restraint stress (CRS). METHODS: The animals were divided into four groups. Groups 1 and 3 received saline by intragastric gavage for 10 days. Groups 2 and 4 received L-carnitine (50 mg/Kg/day) in the same manner. Groups 3 and 4 were exposed to CRS in the form of immobilization at 4 degrees C for 4 h on day 10. Ulcer index, gastric acid secretion and hemoglobin leakage, and gastric mucosal mucin and PGE2 content were measured. RESULTS: In rats exposed to CRS, as compared to control rats (group 1), ulcer index was higher, gastric acid production was lower, hemoglobin leakage into the gastric lumen was increased, and gastric mucosal mucin and PGE content were reduced. L-carnitine treatment prior to CRS led to attenuation of changes in ulcer index, gastric acid secretion, amount of hemoglobin leakage into the gastric lumen and gastric PGE2 content. In rats receiving L-carnitine but not exposed to CRS, gastric acid secretion, mucin and PGE2 content of gastric mucosa were similar to those in control rats. CONCLUSION: L-carnitine decreases CRS-induced gastric mucosal injury.

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

PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Effect of cold-restraint stress on the distribution of trace elements in rat tissues.

The aim of this study was to assess the effects of cold-restraint stress on blood and the other tissue levels of trace elements. The experiment was performed on male Swiss albino rats. The animals were divided to two groups: control and stressed groups. In the stressed group, the rats were subjected to immobilization for 4 h at 4 degrees C. At the end of the experimental period, blood and tissue samples were collected from all of the animals. The levels of zinc, copper, magnesium, and manganese were measured using flame and graphite furnace atomic absorption spectrometry. In rats subjected to stress, the zinc levels of serum were increased, whereas in the duodenum and brain, zinc was found to decrease when compared to the control. The magnesium content of both the stomach and duodenum were reduced, but the manganese levels of the liver, kidneys, and brain significantly increased because of stress. In conclusion, cold-restraint stress may affect the metabolic process by changing the distributions of zinc, magnesium, and manganese in tissues.