The plasma or serum levels of various enzymes and components are known to increase in rats with water-immersion restraint stress (WIRS). We examined whether oxidative stress is involved in increases in the serum levels of various enzymes and components in rats with WIRS. Rats were exposed to WIRS for 6 h after oral administration of vitamin E (VE) (50 or 250 mg/kg). Rats with WIRS had increased serum alanine aminotransferase, aspartate aminotranseferase, lactate dehydrogenase, creatine kinase, urea nitrogen, creatinine, glucose, corticosterone, adrenocorticotropic hormone and lipid peroxide (LPO) levels, increased kidney and heart VE levels, decreased skeletal muscle VE level, and increased LPO levels in all tissues studied. Pre-administered VE (50 or 250 mg/kg) attenuated the increased serum alanine aminotransferase, aspartate aminotranseferase, lactate dehydrogenase, creatine kinase, urea nitrogen, creatinine, and LPO levels, the decreased skeletal muscle VE level, and the increased LPO levels in all tissues studied more effectively at its higher dose than at its lower dose. However, either dose of the pre-administered VE did not affect the increased serum glucose, corticosterone, and adrenocorticotropic hormone levels. These results suggest that oxidative stress is involved in increases in the serum levels of various enzymes and components in rats with WIRS.

We examined how oxidative stress and cell damage develop in the liver of rats subjected to water-immersion stress (WIRS). In rats subjected to WIRS for 1.5, 3 or 6 h, serum alanine aminotransferase and aspartate aminotransferase activities increased time-dependently. In the liver tissue, vacuolization and apoptosis occurred at 1.5 h of WIRS and vacuolization further developed without further appearance of apoptosis at 3 h or 6 h. Serum lipid peroxide (LPO) and NOx (nitrite/nitrate) concentrations increased at 3 h of WIRS and these increases were enhanced at 6 h. In liver tissue, increases in LPO and NOx concentrations and myeloperoxidase activity and decreases in ascorbic acid and reduced glutathione concentrations and superoxide dismutase activity occurred at 3 h of WIRS and these changes were enhanced at 6 h, although vitamin E concentration and xanthine oxidase activity were unchanged. These results indicate that oxidative stress in the liver of rats with WIRS develops after the appearance of cell damage in the tissue, and suggests that oxidative stress is caused through disruption of the antioxidant defense system and increases in NO generation and neutrophil infiltration in the liver, which may contribute to the progression of cell damage in the tissue.

Gastric mucosal AA plays a critical role in the progression of C48/80-induced acute gastric mucosal lesions in rats.

No abstract

We examined whether L-ascorbic acid (AA) (or reduced ascorbic acid) protects against oxidative damage in the liver of rats subjected to water-immersion stress (WIRS). AA (100, 250 or 500 mg/kg) was orally administered at 0.5 h before the onset of WIRS. Rats with 6 h of WIRS had increased serum corticosterone, glucose, total ascorbic acid (T-AA), AA, lipid peroxide (LPO), and NOx concentrations and alanine aminotransferase and aspartate aminotrasferase activities. The stressed rats had increased hepatic LPO, NOx, and dehydroascorbic acid concentrations and myeloperoxidase activity, decreased hepatic T-AA, AA, reduced glutathione concentrations and superoxide dismutase activity, and unchanged hepatic vitamin E concentration. Pre-administered AA attenuated the stress-induced changes in serum LPO and NOx concentrations and alanine aminotransferase and aspartate aminotrasferase activities and hepatic LPO, NOx, and T-AA, AA, dehydroascorbic acid, and reduced glutathione concentrations and myeloperoxidase and superoxide dismutase activities dose-dependently. Pre-administered AA did not affect the stress-induced changes in serum corticosterone and glucose concentrations. These results indicate that pre-administered AA protects against oxidative damage in the liver of rats with WIRS possibly by attenuating disruption of the antioxidant defense system and increases in NO generation and neutrophil infiltration in the tissue.