Lipid peroxidation and antioxidant enzyme activities in erythrocytes of type I and II alcoholics

Abstract

Reduced and oxidized glutathione (GSH and GSSG), protein-bound glutathione, lipid peroxidation and antioxidant enzyme activities were determined in the erythrocyte lysates and membranes of type I and II alcoholics in order to clarify the effect of age-of-onset and the duration of the alcohol consumption on erythrocyte oxidant and antioxidant status. The osmotic fragility and susceptibility of the erythrocytes to haemolysis were also determined. Erythrocyte lipid peroxidation was significantly increased but, GSH and protein-bound GSH, GSH/GSSG ratio and antioxidant enzyme activities were markedly decreased in the erythrocytes of the alcoholic subgroups. Erythrocyte count and haemoglobin content in the blood of alcoholics were found to be decreased in accordance with the finding that erythrocytes were more fragile and less resistant to haemolysis particularly in type II alcoholics. The present study showed that ethanol-induced oxidative stress in erythrocytes can lead to haemolysis and membrane-specific injuries in erythrocytes of the alcoholic subtypes.

Influence of green tea on erythrocytes antioxidant status of different age rats intoxicated with ethanol

“…Reports on the effect of alcohol intoxication on the activity of those enzymes and the sensitivity of erythrocytes to oxidative stress accompanied by those changes are controversial (Schlorff et al, 1999;Devipriya et al, 2007). Decreased erythrocytes glutathione peroxidase activity was reported in rats chronically intoxicated with ethanol (Uçar et al, 2005). However, the decrease in superoxide dismutase and catalase activity in different cells after chronic alcohol consumption, was observed by other authors (Palavarapu et al, 1998).…”

“…During ageing as well as in alcohol intoxication, effi cacy of glutathione peroxidase action is also decreased by diminished level of glutathione -co-substrate of this enzyme. The decrease in glutathione level and glutathione peroxidase activity during ageing (Piccinini et al, 1995) as well as during alcohol intoxication (Uçar et al, 2005) is well documented. Because GSH and glutathione peroxidase are involved in hydrogen peroxide and lipid peroxides metabolizing pathway in the cell, the decrease of their level/activity can lead to high-level peroxides accumulation.…”

Glutathione and Transsulfuration in Alcohol-Associated Tissue Injury and Carcinogenesis

“…The liver is a major organ subject to ethanol-induced toxicity. There is a wealth of data from studies in human and experimental animals documenting ethanol-induced changes in hepatic GSH homeostasis, including GSH/GSSG and GSH-related antioxidant enzymes [32–35]. Collectively, these studies suggest that depletion of hepatic GSH, particularly mitochondrial GSH, is one of the early changes associated with chronic ethanol consumption [36].…”

“…Collectively, these studies suggest that depletion of hepatic GSH, particularly mitochondrial GSH, is one of the early changes associated with chronic ethanol consumption [36]. Importantly, plasma GSH concentrations are inversely correlated with the degree of liver damage and hepatic lipid peroxidation [32–34]. Prolonged ethanol consumption has been reported to inhibit multiple steps in methionine metabolism and transsulfuration pathways in the liver, resulting in increased homocysteine and SAH levels, and a lowered heptaic SAM/SAH ratio [37, 38].…”

“…In the context of alcohol-related cancer, ethanol-induced depletion of the cellular GSH pool and inhibition of transsulfuration/transmethylation pathways are of particular importance for the development of alcoholic HCC. Clinically, low levels of hepatocellular GSH and SAM and a low SAM/SAH ratio are commonly observed in chronic alcoholics with advanced stage ALD and they correlate with the severity of liver damage [32, 37, 38]. The significance of reduced SAM production in the development of HCC is supported by several findings: SAM feeding blocked the transformation of pre-neoplastic lesions into HCCs [105], SAM administration inhibited the expressions of selected proto-oncogenes [106], SAM decreased the survival of liver tumor cells in vitro in a dose-dependent manner [107], and SAM treatment prevented liver tumor formation in a xenograft model [108].…”