Gastroprotective and anti-oxidative properties of ascorbic acid on indomethacin-induced gastric injuries in rats.
Reactive oxygen species (ROS) have been implicated in the etiology of indomethacin-induced gastric mucosal damage. This study investigated ascorbic acid (vitamin C)'s protective effects against oxidative gastric mucosal damage induced by indomethacin. Ascorbic acid is a powerful antioxidant because it can donate a hydrogen atom and form a relatively stable ascorbyl free radical. We have investigated alterations in the levels of myeloperoxidase, antioxidant system enzymes (glutathione S-transferase, superoxide dismutase, glutathione reductase, catalase, glutathione peroxidase), lipid peroxidation and glutathione, as markers for ulceration process following oral administration of ascorbic acid, famotidine, lansoprazole, and ranitidine in rats with indomethacin-induced ulcers. In the present study, we found that (1) ascorbic acid, famotidine, lansoprazole and ranitidine reduced the development of indomethacin-induced gastric damages; (2) the administration of indomethacin caused a significant decrease in the levels of superoxide dismutase, glutathione peroxidase, glutathione S-transferase and glutathione, and an increase in the lipid peroxidation level; (3) the administration of ascorbic acid reversed the trend, inducing a significant increase of these enzymes' levels and a reduction in lipid peroxidation level in tissues; and (4) catalase, glutathione reductase and myeloperoxidase activities, increased by indomethacin, were found to be lower in the ascorbic acid, famotidine, lansoprazole and ranitidine-treated groups. The results indicate that the gastroprotective properties of ascorbic acid could be related to its positive effects on the antioxidant system and myeloperoxidase activity in indomethacin-induced gastric ulcers in rats.
Koc
Murat
M
Faculty of Art and Sciences, Department of Biology, Bozok University, Yozgat, Turkey.
Imik
Halit
H
Odabasoglu
Fehmi
F
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007213:Indomethacin / Q000009:adverse effects*; D008297:Male; D020556:Neutrophil Infiltration / Q000187:drug effects; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000188:drug therapy* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D002374:Catalase; D009195:Peroxidase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D001205:Ascorbic Acid; D007213:Indomethacin