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.

Background: It is known that L-carnitine is a cofactor in the transport of fatty acids across the inner mitochondrial membrane for β-oxidation. However, L-carnitine is an antioxidant compound widely used for the treatment of deficits in functions due to the aging process. Objective: The purpose of the study was to investigate the effect of L-carnitine on carrageenan-induced inflammation in aged rats. Methods:L-Carnitine (50 mg/kg/day) or control vehicle was given by gavage for 30 consecutive days to young (2-month-old) and aged (24-month old) rats. 6 ml of air was injected subcutaneously into the dorsum of each rat, followed 2 days later by 4 ml of 2% carrageenan. After 2 days, the exudate was collected from the inflamed site of each rat. The quantity of collected exudate and the number of cells which have migrated to the inflamed site were determined. Results: No differences were observed in quantity of exudate in all groups; a decrease in the number of exudate cells was established in aged rats. However, L-carnitine treatment significantly increased the number of exudate cells in both young and aged rats. The exudate cells from the aged rats exhibited a decline of both phagocytic and chemotactic activities as compared with those from the young rats, and the decreased functions were significantly enhanced by L-carnitine treatment. However, superoxide anion release was seen to be unchanged in exudate cells due to aging, and L-carnitine intake decreased the production of superoxide anion by these cells in young and aged rats. Conclusions: These findings demonstrate that L-carnitine is capable of restoring the age-related changes in the functions of inflammatory cells. Moreover, L-carnitine may play a protective role in the tissue destruction in inflammation by decreasing the superoxide anion production.

The aim of this study was to determine the cadmium-induced immunohistochemical and morphological changes in the renal cortex of adult male rats exposed to high doses of cadmium for 30 d. Animals used as controls received a standard diet and water ad libitum. The animals used for this study received 15 ppm CdCl2 in their drinking water for 1 mo. The mean arterial pressure (MAP), the mean blood Cd level, and the mean tissue Cd content were significantly higher when compared to controls (p < 0.01). Immunohistochemical studies demonstrated a weak labeling to type IV collagen and laminin, but a strong labeling to fibronectin in the renal cortex of the Cd-treated animals when compared to controls. The ultrastructural alterations found in Cd-treated rats were a diminution in the amount of filtration slits, increased fusion of foot processes in epithelial cells of the glomeruli, increase of lysosomal structures and pinocytic vesicles as well as large mitochondria in proximal tubule cells, and degenerated cells in distal tubules. Additionally, the glomerular basement membrane was slightly thickened. In conclusion, cadmium toxicity results in alterations in the renal extracellular matrix and tubular or glomerular cells, which could play an important role in renal dysfunction.

Reactive oxygen metabolites play an important role in ischemia-reperfusion related gastric injury. Primary sources of reactive oxygen metabolites seem to be the xanthine/xanthine oxidase system and neutrophils accumulating within the reperfused tissue. Tissue myeloperoxidase activity is an important index of neutrophil accumulation. The purpose of the present study was to clarify the effect of L-carnitine on the accumulation of neutrophils and neutrophil-induced gastric mucosal damage in rats exposed to ischemia-reperfusion. Rats were randomly divided into three groups: sham-operated, ischemia-reperfusion and ischemia-reperfusion plus L-carnitine groups. Ischemia was induced by clamping the celiac artery for 30 min and then reperfusion was established for 60 min. Gastric injury was assessed by measuring myeloperoxidase activity in gastric tissue. The neutrophil accumulation and hemorrhagic lesions due to ischemia-reperfusion in gastric mucosa were ascertained in a histological study. L-Carnitine (100 mg kg(-1)) administrated intravenously 5 min before ischemia significantly reduced both the gastric injury and myeloperoxidase activity compared with the ischemia-reperfusion group. The results suggest that L-carnitine provides marked protection against ischemia-reperfusion-related gastric injury which could be due to its ability to reduce neutrophil accumulation in ischemic tissue.

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