Vitamin E depletion enhances liver oxidative damage in rats with water-immersion restraint stress.

We examined the effect of vitamin E depletion on liver oxidative damage in rats with water-immersion restraint stress (WIRS). Male Wistar rats were fed a normal diet (N) or vitamin E-depleted diet (VE-D) for 4 wk. N- and VE-D-fed rats were exposed to WIRS for 6 h.

Water-immersion restraint stress disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats.

We examined whether water-immersion restraint stress (WIRS) disrupts nonenzymatic antioxidant defense systems through ascorbic acid depletion in the adrenal gland of rats. Rats were exposed to WIRS for 0.5, 1.

Disruption of non-enzymatic antioxidant defense systems in the brain of rats with water-immersion restraint stress.

We examined whether non-enzymatic antioxidant defense systems are disrupted in the brain of rats with water-immersion restraint stress. When rats were exposed to water-immersion restraint stress for 1.5, 3 or 6 h, the brain had decreased ascorbic acid and reduced glutathione contents and increased lipid peroxide and nitric oxide metabolites contents at 3 h and showed further changes in these components with a reduction of vitamin E content at 6 h.

Protective effect of L-ascorbic acid against oxidative damage in the liver of rats with water-immersion restraint stress.

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.

Vitamin E protects against stress-induced gastric mucosal lesions in rats more effectively than vitamin C.

In this study, we examined the protective effects of vitamin E (VE) against gastric mucosal lesions induced by water immersion restraint stress (WIRS) in rats in comparison with that of vitamin C (VC). The gastric mucosa of rats with 6 h of WIRS showed lesions with bleeding, decrease in nonprotein SH, VC, VE, and adherent mucus concentrations and constitutive nitric oxide synthase activity, and increase in lipid peroxide and NOx (nitrite/nitrate) concentrations and myeloperoxidase, xanthine oxidase, and inducible nitric oxide synthase activities. Either VE (0.

Involvement of oxidative stress in increases in the serum levels of various enzymes and components in rats with water-immersion restraint stress.

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).

Compound 48/80 causes oxidative stress in the adrenal gland of rats through mast cell degranulation.

Rats were intraperitoneally treated once with compound 48/80 (C48/80), a mast cell degranulator, (0.75 mg/kg). Serum serotonin, histamine and corticosterone levels increased 0.

Development of oxidative stress and cell damage in the liver of rats with water-immersion restraint stress.

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.

Melatonin attenuates disruption of serum cholesterol status in rats with a single alpha-naphthylisothiocyanate treatment.

The present study was performed to examine whether melatonin attenuates disruption of serum cholesterol status in rats treated once with alpha-naphthylisothiocyanate (ANIT). In the serum of rats treated with ANIT (75 mg/kg, i.p.

alpha-Tocopherol protects against alpha-naphthylisothiocyanate-induced hepatotoxicity in rats less effectively than melatonin.

The protective effect of alpha-tocopherol (alpha-Toc), which exerts antioxidant and anti-inflammatory actions, against alpha-naphthylisothiocyanate (ANIT)-induced hepatotoxicity in rats was compared with that of melatonin because orally administered melatonin is known to protect against ANIT-induced hepatotoxicity in rats through its antioxidant and anti-inflammatory actions. Rats intoxicated once with ANIT (75 mg/kg, intraperitoneal (i.p.

Effect of oral vitamin E administration on acute gastric mucosal lesion progression in rats treated with compound 48/80, a mast cell degranulator.

The effect of oral vitamin E administration on acute gastric mucosal lesion progression was examined in rats treated once with compound 48/80 (C48/80) (0.75 mg/kg, i.p.

Preventive effect of neutropenia on carbon tetrachloride-induced hepatotoxicity in rats.

The preventive effect of neutropenia on carbon tetrachloride (CCl4)-induced hepatotoxicity was examined in rats. In rats treated once with CCl4 (1 ml kg(-1), i.p.

Role of gastric mucosal ascorbic acid in gastric mucosal lesion development in rats with water immersion restraint stress.

We examined the role of gastric mucosal ascorbic acid (AA) in gastric mucosal lesion development in rats with water immersion restraint stress (WIRS). When fasted rats were subjected to WIRS for 1, 3 or 6 h, gastric mucosal lesions developed at 3 and 6 h. Gastric mucosal AA concentration decreased at 3 and 6 h after the onset of WIRS, while gastric mucosal non-protein SH concentration decreased at 1, 3, and 6 h and gastric mucosal vitamin E concentration decreased at 6 h.

Successively postadministered melatonin prevents disruption of hepatic antioxidant status in rats with bile duct ligation.

We have reported that orally administered melatonin exerts a therapeutic effect on cholestatic liver injury in rats treated with bile duct ligation (BDL) possibly through its antioxidant and anti-inflammatory actions. Herein, we examined whether successively postadministered melatonin prevents the disruption of hepatic antioxidant status in BDL-treated rats. Wistar rats with BDL were killed 5 and 13 days after BDL.

Effect of gefarnate on acute gastric mucosal lesion progression in rats treated with compound 48/80, a mast cell degranulator, in comparison with that of teprenone.

We have reported that teprenone (geranylgeranylacetone), an anti-ulcer drug, prevents acute gastric mucosal lesion progression in rats treated once with compound 48/80 (C48/80), a mast cell degranulator, possibly by suppressing mucus depletion, neutrophil infiltration, and oxidative stress in the gastric mucosa. Herein, we examined the preventive effect of gefarnate (geranyl farnesylacetate), an anti-ulcer drug, on acute gastric mucosal lesion progression in rats treated once with C48/80 (0.75 mg/kg, i.

Plaunotol prevents the progression of acute gastric mucosal lesions induced by compound 48/80, a mast cell degranulator, in rats.

We examined the preventive effect of plaunotol, an antiulcer drug, on acute gastric mucosal lesion progression in rats treated once with compound 48/80 (C48/80). Rats treated with C48/80 (0.75 mg/kg BW, i.

A critical role of gastric mucosal ascorbic acid in the progression of acute gastric mucosal lesions induced by compound 48/80 in rats.

Aim: To study the role of gastric mucosal ascorbic acid (AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats.

Methods: C48/80 (0.75 mg/kg) was intraperitoneally injected to fasted Wistar rats.

A change in gastric mucosal ascorbic acid status with the formation, progression, and recovery of compound 48/80-induced acute gastric mucosal lesions in rats.

We examined whether gastric mucosal ascorbic acid status changes with the formation, progression, and recovery of acute gastric mucosal lesions in rats treated with compound 48/80, a mast cell degranulator. Fasted Wistar rats received a single intraperitoneal injection of compound 48/80 (0.75 mg/kg).