Search

The aim of our study was to examine the effect of calorie restriction (CR) on oxidative and nitrosative liver injury in rats, induced by acute ethanol intoxication. Male Wistar rats were divided into groups: (1) control; (2) calorie-restricted groups with intake of 60-70% (CR60-70) and 40-50% of daily energy needs (CR40-50); (3) ethanol-treated group (E); (4) calorie-restricted, ethanol-treated groups (E+CR60-70 and E+CR40-50). Ethanol was administered in 5 doses of 2g/kg every 12h, and duration of CR was 5 weeks before ethanol treatment. Malondialdehyde and nitrite and nitrate level were significantly lower in E+CR60-70 and higher in E+CR40-50 vs. E group. Liver reduced glutathione content and activity of both superoxide dismutase izoenzymes were significantly higher in E+CR60-70 and lower in E+CR40-50 vs. E group. Oxidative stress may be a potential mechanism of hormetic effects of CR on acute ethanol-induced liver injury., (Copyright © 2013 Elsevier B.V. All rights reserved.)

The aim of our study was to evaluate the effects of cold stress on hepatic oxidative damage during binge drinking in rats. Male Wistar rats were divided into the following groups: group 1: control; group 2: ethanol-treated; group 3: stress-exposed; group 4: stress-exposed and ethanol-treated group. Oxidative and nitrosative stress parameters in the liver were determined spectrophotometrically, 12 h after treatment. Liver malondialdehyde concentration was significantly higher in group 4 when compared with groups 2 and 3. The highest increase in nitric oxide concentration was demonstrated in group 4 in comparison with groups 2 and 3. Superoxide dismutase (SOD) activity was significantly lower in group 4 when compared with groups 2 and 3. Ethanol administration induced a larger decrease in the activity of copper-/zinc-SOD in group 4 in comparison with group 2. Activity of manganese-SOD (Mn-SOD) was significantly higher in groups 3 and 4, when compared with control values, but the greatest increase in the activity of Mn-SOD was demonstrated in group 2. We also evaluated statistically significant decrease in the level of reduced gluthatione in the liver of group 4 in comparison with group 3. Based on our study, it can be concluded that cold-exposed stress and binge ethanol drinking have additive effects in imbalance between pro-oxidant and antioxidant defense system in liver.

Chronic ethanol consumption is a major risk factor for epilepsy, and seizures frequently occur during the withdrawal period. The aim of our study was to investigate effects of ethanol on lindane-induced seizures in rats. Male Wistar rats were injected i.p. with one of the following 5 treatments: (i) saline, (ii) dimethylsulfoxide, (iii) lindane (8 mg/kg) (L), (iv) ethanol in doses of 0.5 g/kg (E(0.5)), 1 g/kg (E(1)), and 2 g/kg (E(2)), and (v) groups that received ethanol 30 min before lindane (LE(0.5), LE(1), and LE(2)). Behavioral changes were described by using a descriptive scale as follows: 0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus; 3, generalized tonic-clonic convulsions; 4, status epilepticus. The incidence of convulsions in the LE(2) group was significantly lower than the incidence in the L (p < 0.01) and LE(0.5) groups (p < 0.05). The median grade of convulsive behavior was significantly lower in the LE(2) (p < 0.01) and LE(1) groups (p < 0.05) compared with the L group. Latencies to the first seizure response were not significantly different among groups. ED50 of ethanol was 1.40 (1.19-1.65). Our findings suggest that ethanol decreased severity and incidence of lindane-induced seizures in a dose-dependent manner.

The aim of our study was to investigate the effects of binge drinking on paracetamol induced oxidative stress in mice liver. Male Swiss mice were divided into groups: control; ethanol-treated group (E) in five subsequent doses of 2 g/kg by orogastric tube; paracetamol-treated group (P) in a dose of 300 mg/kg intraperitoneally; group that received paracetamol 12 hrs after the last dose of ethanol (PE). Blood and liver samples were collected for determination of oxidative stress parameters 6, 24 and 48 hrs after treatment. Prior binge drinking potentiated paracetamol-induced rise in liver malondialdehyde level 48 hours after treatment in comparison with P and E groups (17.14 ± 1.98 vs 13.14 ± 0.82 and 12.99 ± 1.18 μmol/L, p

The aim of our study was to investigate the effects of binge drinking on prooxidant/antioxidant system in rat liver in acute cadmium (Cd) intoxication. In experiment male Wistar rats were used and divided into following groups: 1. control, 2. ethanol-treated group, in five subsequent doses of 2 g/kg administered by orogastric tube, 3. Cd-treated group in a single dose of 2.5 mg/kg intraperitoneally, 4. group that received Cd 12 hours after the last dose of ethanol. Blood and liver samples were collected for determination of oxidative stress parameters, 24 hours after treatment. When administered in combination, ethanol and Cd induced a more pronounced increase in serum and liver malondialdehyde level than either of these substances alone (p