Influence of acute ethanol administration on hepatic glutathione peroxidase and glutathione transferase activities in the rat

̧ak-Toker, Necla Ko; Uysal, M.; ̧, Gu ̈l ̧in Ayka; Sıvas, Ahmet; ̧in, Su ̈ha Yal; ̈z, Hikmet O

doi:10.1016/0031-6989(85)90098-0

Cited by 38 publications

(5 citation statements)

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“…34 It has been reported that acute ethanol administration decreases hepatic GSH content. 4,35,36 Multiple mechanisms play an important role in the depletion of GSH in liver by ethanol intake. Since ethanol administration is associated with oxidative stress, it has been suggested that increased lipid peroxidation or binding to acetaldehyde would be responsible for the depletion of hepatic GSH.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] The oxidative stress induced by ethanol is a result of the production of free radical species during several stages of ethanol metabolism. [1][2][3] Several experimental [4][5][6][7][8][9][10][11][12] and clinical [13][14][15] studies have shown that ethanol ingestion alters the pro-oxidant-antioxidant balance in the organism. Therefore, the potential role of several substances such as antioxidants and thiol compounds has been investigated in ethanol-induced liver injury.…”

Section: Introductionmentioning

confidence: 99%

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The effect of carnosine pretreatment on oxidative stress and hepatotoxicity in binge ethanol administered rats

et al. 2010

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Carnosine is a dipeptide having strong antioxidant effects. Oxidative stress plays an important role in pathogenesis of alcohol-induced liver injury. In this study, we investigated the effect of carnosine pretreatment on ethanol-induced oxidative stress and hepatotoxicity. Rats were given carnosine (2 g/L in drinking water) for 4 weeks and then ethanol was administered orally to rats at a dose of 5 g/kg every 12 hours for 3 doses totally (binge model). All rats were killed 6 hours after last ethanol injection. Plasma alanine (ALT) and aspartate (AST) transaminase activities and liver triglyceride, malondialdehyde (MDA), diene conjugate (DC), glutathione (GSH), vitamin E and vitamin C levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities were determined. Binge ethanol administration resulted in significant increases in plasma transaminase activities, hepatic triglyceride and lipid peroxide levels. However, GSH, vitamin E, vitamin C levels and GSH-Px and GST activities were found to be decreased following ethanol administration. Macromicrovesicular steatosis was also seen. Carnosine pretreatment appeared to prevent the increase of plasma ALT and AST activities and hepatic MDA and DC levels following ethanol treatment. In addition, hepatic GSH levels increased, but there were no changes in triglyceride, vitamin E, vitamin C levels and SOD, GSH-Px and GST activities, following ethanol treatment in carnosine-pretreated rats. There was also no change in liver histopathological appearance. In conclusion, carnosine prevented the increases in serum transaminase activities and lipid peroxides in liver of ethanol-treated rats, without any change on steatosis in liver.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effect of carnosine pretreatment on oxidative stress and hepatotoxicity in binge ethanol administered rats

et al. 2010

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“…In the liver, different studies in adult animals have shown that when alcohol is administered acutely, via drinking water or a forced method, the cytochrome P450 2E1 (CYP2E1) isoform of the enzyme MEOS, which produces the highest amount of ROS, increases its activity and delivers greater amounts of toxic radicals. − Other studies in the liver of adult animals have shown a depletion in the mitochondrial antioxidant glutathione (GSH), an increase in lipid and protein oxidation, and an increase in SOD activity, compromising oxidative stress. − In this context, binge drinking in adult animals has been related to high plasma transaminase activity, macro-microvesicular steatosis, and hepatic apoptosis via Fas and cytochrome c. ,, However, little is known about adolescent binge drinking and its relation to hepatic oxidation during this developmental period.…”

Section: Introductionmentioning

confidence: 99%

Oral or Intraperitoneal Binge Drinking and Oxidative Balance in Adolescent Rats

Nogales

Rua

Ojeda

et al. 2014

Chem. Res. Toxicol.

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Oxidative imbalance is one of the most important mechanisms of alcohol-induced injury. Acute alcohol exposure induces a significant amount of reactive oxygen species during its hepatic metabolism via the microsomal ethanol oxidizing system. During adolescence, the physiological development is still taking place; therefore, ethanol's effects differ in adolescents compared to that in adults. Because binge drinking is the most important model of ethanol intake used by adolescents and because little is known about its effects on the liver, we have used two routes of acute ethanol administration (oral and intraperitoneal) in adolescent rats in order to analyze the oxidative damage caused in the periphery and liver. Here, it has been demonstrated for the first time that binge drinking in adolescents causes peripheral oxidation of lipid and DNA as well as lipid and protein hepatic oxidation, which are related to lower glutathione peroxidise (GPx) activity, higher catalase (CAT) activity, and higher expression of NADPHoxidase, contributing to hepatic damage. In addition, it is shown that the intraperitoneal administration route results in increased oxidative damage, which is probably related to the resulting general stress response that causes higher DNA and protein oxidation due to higher NADPHoxidase expression and higher CAT and superoxide dismutase (SOD) activities. According to these results, it is concluded that binge drinking induces hepatic damage during adolescence, at least in part, as consequence of oxidative stress because the antioxidant response was insufficient to avoid liver oxidation. Alcohol administered intraperitoneally provoked more DNA oxidation than that from the oral alcohol exposure model.

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“…6 On the basis of the hypothesis that a decrease in antioxidant defense may contribute to the detrimental effects of pro-oxidants in alcoholic liver disease (ALD), many investigators have evaluated the role of antioxidant enzymes after administration of ethanol. [7][8][9][10][11] Many of these studies have used animal models that do not show evidence of pathological liver injury. Furthermore, the inconsistent results obtained in these studies may also reflect variations in experimental design, diet, and duration of ethanol administration.…”

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confidence: 99%

Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil

et al. 1998

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Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro-oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats. Male Wistar rats (5 per group) were fed ethanol with either medium-chain triglycerides (MCTE), palm oil (PE), corn oil (CE), or fish oil (FE). Control animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets. The following were evaluated in each group: liver pathology, lipid peroxidation, manganese superoxide dismutase (MnSOD) levels, copper-zinc SOD (CuZnSOD) levels, glutathione peroxidase (GPX) levels, and catalase (CAT) levels. All enzymes were evaluated using activity assays and immunoblots. Rats fed FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed moderate changes, those fed PE showed fatty liver only, and those fed MCTE were normal. Parameters indicative of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also greater in rat livers from animals fed the diets high in polyunsaturated fatty acids (CE and FE). CuZnSOD, GPX, and CAT activities showed an inverse correlation (r ‫؍‬ ؊.92, P F .01) with severity of pathological injury, with the lowest levels for both enzymes found in FE-fed rats. Decreased enzyme activity in CE-and FE-fed rats was accompanied by similar decreases in immunoreactive protein. Ethanol administration did not cause significant decreases in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE). MnSOD activity showed no significant change in any ethanol-fed group. Our results show that decreases in CuZnSOD, GPX, and CAT occur in rats showing pathological liver injury and also having the highest levels of lipid peroxidation. These results suggest that feeding dietary substrates that enhance lipid peroxidation can exacerbate both ethanol-induced oxidative damage as well as necroinflammatory changes. The decrease in activity of antioxidant enzymes observed in animals fed diets high in polyunsaturated fatty acids and ethanol could possibly increase the susceptibility to oxidative damage and further contribute to ethanol-induced liver injury. (HEPATOLOGY 1998;27:1317-1323.)

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Influence of acute ethanol administration on hepatic glutathione peroxidase and glutathione transferase activities in the rat

Cited by 38 publications

References 16 publications

The effect of carnosine pretreatment on oxidative stress and hepatotoxicity in binge ethanol administered rats

The effect of carnosine pretreatment on oxidative stress and hepatotoxicity in binge ethanol administered rats

Oral or Intraperitoneal Binge Drinking and Oxidative Balance in Adolescent Rats

Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil

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