Ethanol Consumption, Amino Acid and Glutathione Blood Levels in Patients With and Without Chronic Liver Disease

Loguercio, C.; Blanco, Francesca Del Vecchio; Girolamo, V. De; Disalvo, D.; Nardi, G.; Parente, A.; Blanco, C. Del Vecchio

doi:10.1097/00000374-199911000-00010

Cited by 6 publications

(7 citation statements)

References 14 publications

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“…GSH is a major cellular thiol antioxidant with many functions that protect cells against oxidative stress and its consequences. Excessive exposure to alcohol can lead to GSH depletion and decreased antioxidant activity ( 36 – 38 ). It has been noted that chronic depletion of cytosolic GSH can lead to decreased levels of mitochondrial GSH ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Effects of acute exercise on liver function and blood redox status in heavy drinkers

Georgakouli

Manthou

Fatouros

et al. 2015

Experimental and Therapeutic Medicine

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Excessive alcohol consumption can induce oxidative stress, resulting in the development of several diseases. Exercise has been reported to prevent and/or improve a number of health issues through several mechanisms, including an improvement in redox status. It has also been previously suggested that exercise can help individuals with alcohol use disorders reduce their alcohol intake; however, research in this field is limited. The aim of the present study was to investigage the effects of acute exercise of moderate intensity on the liver function and blood redox status in heavy drinkers. For this purpose, a total of 17 heavy drinkers [age, 31.6±3.2 years; body mass index (BMI), 27.4±0.8 kg/m2; experimental group (EG)] and 17 controls [age, 33.5±1.3 years; BMI, 26.1±1.4 kg/m2; control group (CG), who did not exceed moderate alcohol consumption], underwent one trial of acute exercise of moderate intensity (50–60% of the heart rate reserve) for 30 min on a cycle ergometer, following an overnight fast, and abstaining from smoking and alcohol consumption. Blood samples were obtained before and immediately after exercise for later determination of the indices of liver function and blood redox status. The subjects in the EG had significantly higher (p<0.05) baseline γ-glutamyl transferase (γ-GT) levels compared to the subjects in the CG. Exercise thus resulted in significantly higher γ-GT levels (p<0.005) only in the EG. No significant differences in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) baseline levels were observed between the 2 groups. Following exercise, the AST levels increased significantly (p<0.001) in both groups, whereas the ALT levels increased significantly (p<0.01) only in the EG. The baseline glutathione (GSH) levels were significantly lower (p<0.05) and remained low following exercise in the EG. In addition, we observed a trend for higher (p=0.07) baseline levels of thiobarbituric acid-reactive substances (TBARS), which remained elevated post-exercise in the EG compared to the CG. Significantly increased post-exercise total antioxidant capacity (TAC; p<0.01) and uric acid (UA; p<0.05) levels were noted in the CG, whereas the TAC (p=0.06) and UA (p=0.08) levels increased and approached significance post-exercise in the EG. No significant differences in the baseline levels of total bilirubin and protein carbonyl were observed between the 2 groups, even post-exercise. Thus, the findings of the present study indicate that even though heavy drinkers may be prone to oxidative stress, their exercise-induced antioxidant response is similar to that of individuals who do not drink heavily.

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Section: Discussionmentioning

confidence: 99%

Effects of acute exercise on liver function and blood redox status in heavy drinkers

Georgakouli

Manthou

Fatouros

et al. 2015

Experimental and Therapeutic Medicine

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“…Decreased glutathione homeostasis has been linked to increased hepatocellular damage in many models of ALD 2,54–56 . Carbonylation of cytoskeletal proteins has been linked with inhibition of microtubule polymerization 57 and defects in hepatocyte microtubules and cytoskeletal elements have been identified in human ALD 58,59 .…”

Section: Discussionmentioning

confidence: 99%

Increased hepatocellular protein carbonylation in human end-stage alcoholic cirrhosis

Shearn

Orlicky

Saba

et al. 2015

Free Radical Biology and Medicine

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Objective Oxidative stress is a significant contributing factor in the pathogenesis of alcoholic liver disease (ALD). In the murine models of chronic alcohol consumption, induction of oxidative stress results in increased peroxidation of polyunsaturated fatty acids to form highly reactive electrophilic α/β unsaturated aldehydes that post-translationally modify proteins altering activity. Data are presented here suggesting that oxidative stress and the resulting carbonylation of hepatic proteins is an ongoing process involved in alcohol-induced cirrhosis. Methods Using age-matched pooled hepatic tissue obtained from healthy humans and patients with end stage cirrhotic ALD, overall carbonylation was assessed by immunohistochemistry and LC-MS/MS of streptavidin purified hepatic whole cell extracts treated with biotin hydrazide. Identified carbonylated proteins were further evaluated using bioinformatics analyses. Results Using immunohistochemistry and Western blotting, protein carbonylation was increased in end stage ALD occurring primarily in hepatocytes. Mass spectrometric analysis revealed a total of 1224 carbonylated proteins in normal hepatic and end-stage alcoholic cirrhosis tissue. Of these, 411 were unique to cirrhotic ALD, 261 unique to normal hepatic tissue and 552 common to both groups. Bioinformatic pathway analysis of hepatic carbonylated proteins revealed a propensity of long term EtOH consumption to increase post-translational carbonylation of proteins involved in glutathione homeostatic, glycolytic and cytoskeletal pathways. Western analysis revealed increased expression of GSTA4 and GSTπ in human ALD. Using LC-MS/MS analysis, a nonenaldehyde post-translational modification was identified on Lysine 235 of the cytoskeletal protein vimentin in whole cell extracts prepared from human end stage ALD hepatic tissue. Conclusions: These studies are the first to use LC-MS/MS analysis of carbonylated proteins in human ALD and begin exploring possible mechanistic links with end-stage alcoholic cirrhosis and oxidative stress.

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“…GSH was lower than normal in both AC and NAC [23], whereas GSSG was not significantly altered in either. These findings are in accordance with previous reports [24], describing nonsignificant changes in hepatic GSSG in alcohol-fed rats.…”

Section: Discussionmentioning

confidence: 63%

Red blood cell antioxidant and iron status in alcoholic and nonalcoholic cirrhosis

Fiorelli

Feo

Duca

et al. 2002

Eur J Clin Investigation

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Ethanol Consumption, Amino Acid and Glutathione Blood Levels in Patients With and Without Chronic Liver Disease

Cited by 6 publications

References 14 publications

Effects of acute exercise on liver function and blood redox status in heavy drinkers

Effects of acute exercise on liver function and blood redox status in heavy drinkers

Increased hepatocellular protein carbonylation in human end-stage alcoholic cirrhosis

Red blood cell antioxidant and iron status in alcoholic and nonalcoholic cirrhosis

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