Ethanol-induced Oxidative Stress In Liver Research Articles

Antioxidant Effect of Ardeh and Honey Combination on Ethanol-induced Oxidative stress in Liver and Kidney of Rats

Background: The pathogenesis of ethanol in the liver and kidney is associated with an increase in free radicals and oxidative stress that leads to structural and functional abnormalities in these vital organs. Methods: Forty-eight male wistar rats were placed in eight groups and were treated as follows: control group (normal saline), group of ethanol (4 g/ kg), three doses of Ardeh and honey combination (1, 2 and 5 g/ kg body weight), and the three groups received three doses of Ardeh and honey combination with ethanol (the same three doses of combinations along with 4 g/ kg ethanol). All treatments were performed once daily for 60 consecutive days with method of stomach gavages. Serum, liver and kidney tissue samples were obtained in order to assess serum components, tissue antioxidant enzyme activities, and the level of thiobarbituric acid reactive substances (TBARS). Results: Hepatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymes in the ethanol group significantly decreased compared with the control group, while the Ardeh and honey combination (5 g) could only significantly increased glutathione peroxidase activity. Renal GPx activity in ethanol consumption significantly increased compared to controls. GPx activity in Ardeh and honey combination and alcohol (5 g, 4 g) were significantly reduced compared to ethanol group. In the present study, the amount of TBARS which represents the rate of lipid peroxidation, in liver of ethanol group compared with the control group showed a significant increase (P<0.05). Conclusion: Ardeh and honey combination as a pre-treatment, protect liver and kidney against oxidative damage induced by ethanol.

Influence of aging on ethanol-induced oxidative stress in digestive tract of rats

Aging and ethanol induce oxidative stress due to increased prooxidant production and decreased antioxidative capacity. The aim was to investigate the influence of aging on oxidative stress in liver, stomach and pancreas in acute ethanol intoxication. Adult (3 months) and old (18 months) male Wistar rats were divided into the following groups: control (control group rats aged 3 months (C3) and control group rats aged 18 months (C18)) and ethanol-treated groups (ethanol-treated 3-month-old rats (E3) and ethanol-treated 18-month-old rats (E18)). Ethanol was administered in five doses of 2 g/kg at 12-h intervals by orogastric tube. Tissue samples were collected for the determination of oxidative stress parameters. Malondialdehyde (MDA) concentration was increased in all the experimental groups and investigated organs versus C3 group ( p < 0.01). The highest MDA level was observed in the stomach in E18 group when compared with C18 and E3 groups ( p < 0.01). Activity of total superoxide dismutase (SOD) and its isoenzymes (copper-/zinc-SOD and manganese-SOD) in E18 group was significantly decreased when compared with E3 and C18 groups ( p < 0.01). Nitrates and nitrites (NO x ) concentration was increased in stomach and pancreas for all the groups when compared with C3 group ( p < 0.01). Hepatic, gastric and pancreatic NO x level was significantly increased in E18 group when compared with E3 group ( p < 0.01). Moreover, level of NO x in liver and pancreas in E18 group was significantly increased when compared with C18 group ( p < 0.01). Aging potentiates ethanol-induced oxidative stress in liver, stomach and pancreas due to increased lipid peroxidation and nitrosative stress and decreased antioxidative tissue capacity.

FERMENTED SEA TANGLE (LAMINARIA JAPONICA) ATTENUATES ETHANOL-INDUCED OXIDATIVE STRESS IN SPRAGUE-DAWLEY RATS

ABSTRACT In this study, we fermented sea tangle (FST) using Lactobacillus brevis BJ20, and its protective effect against the ethanol-induced hepatotoxicity in Sprague-Dawley rats was evaluated. Administration of ethanol to rats for 3 weeks induced liver damage with significant increase in hepatic malondialdehyde level and decrease in glutathione and antioxidant enzyme activities including catalase, superoxide dismutase and glutathione peroxidase. However, pretreatment of rats with FST inhibited the ethanol-induced oxidative stress in liver by suppressing the lipid peroxidation, and maintained the levels of antioxidant enzymes as well as glutathione. Further, FST markedly decreased the lipid peroxidation in many vital organs such as kidney, heart, microsome, mitochondria, testis and spleen of rats. The biochemical changes were consistent with histopathological observations indicating marked hepatoprotective effect of FST. Hence, these results suggested that the FST exhibit potent hepatoprotection against the ethanol-induced oxidative stress in rats. PRACTICAL APPLICATIONS In this study, hepatoprotective effects of fermented sea tangle (FST) against the ethanol-induced hepatic damage in rats were evaluated. The FST significantly attenuated oxidative stress by induced ethanol by increasing antioxidant enzyme activities including catalase, superoxide dismutase and glutathione peroxidase, and in addition inhibited the lipid peroxidation in many vital organs. These results suggested that the FST can be used as potential ingredient for functional food and/or beverage.

Hepatoprotective effects of chestnut (Castanea crenata) inner shell extract against chronic ethanol-induced oxidative stress in C57BL/6 mice

This study was carried out to evaluate the protective effects of chestnut inner shell extract (CISE) on chronic ethanol-induced oxidative stress in liver. Mice were fed a control liquid diet (Normal-control), liquid diet containing ethanol alone (EtOH+Vehicle), or were administered CISE and ethanol (EtOH+CISE) for 6weeks. Administration of ethanol induced liver damage with significant increase of plasma GOT, GPT, hepatic triglyceride (TG) and thiobarbituric acid reactive substance (TBARS) levels. By contrast, co-treatment of CISE with ethanol significantly decreased the activities of GOT and GPT in the plasma, and hepatic TG and TBARS levels. Histological observations were consistent with the result obtained from hepatic lipid quantification. Moreover, CISE treatment with ethanol decreased CYP2E1 expression and increased activities of catalase and superoxide dismutase, which were significantly inhibited by treatment with ethanol alone. To determine the active compound of CISE, fractionation of CISE was conducted and scoparone and scopoletin were identified as main compounds. These compounds were also shown to inhibit the ethanol-induced reduction in antioxidant enzyme activity in an in vitro model system. These results suggest that CISE has protective effects against ethanol-induced oxidative damage, possibly by inhibition of lipid accumulation, peroxidation and increase of antioxidant defense system in the liver.

Protective effects of thiazolo[3,2-b]-1,2,4-triazoles on ethanol-induced oxidative stress in mouse brain and liver

A series of 3-[1-(4-(2-methylpropyl) phenyl) ethyl]-1 ,2,4-triazole-5-thione (I) and its bicyclic condensed derivatives 6-benzylidenethiazolo[3,2-b]-1,2,4-triazole-5(6H)-ones (IIa-IIf) were investigated for the prevention of ethanol-induced oxidative stress in liver and brain of mice. Administration of ethanol (0.1 mL/mice, p.o.) resulted in a drop of total thiol groups (T-SH) and non-protein thiol groups (NP-SH), and an increase in thiobarbituric acid reactive substances (TBARS) in both liver and brain tissue of mice (p < 0.001). Among the compounds investigated (at a dose of 200 mg/kg, p.o.), I and IId ameliorated the peroxidative injury in these tissues effectively. Compounds IIa, IIc and IIe improved the peroxidative tissue injury only in brain. These findings suggest that certain condensed thiazolo-triazole compounds may contribute to the control of ethanol-induced oxidative stress in an organ selective manner.