No abstract

The online version of this article (doi:10.1007/s12291-011-0121-7) contains supplementary material, which is available to authorized users.

Alcohol induced oxidative stress is linked to the metabolism of ethanol. In this study it has been observed that administration of ethanol in lower concentration caused gain in body and liver weight. while higher concentration of ethanol caused lesser gain in body and liver weight. Ethanol treatment enhanced lipid peroxidation significantly, depletion in levels of hepatic glutathione and ascorbate, accompanied by a decline in the activities of glutathione peroxidase and glutathione reductase, and increased in hepatic glutathione s-transferase activity. Interestingly catalase activity increases in lower concentration of ethanol exposure, and decreased in higher concentration. Superoxide dismutase activity was also increased on ethanol exposure. But, ethanol feeding did not show any effect on glucose-6-phosphate dehydrogenase activity. Ethanol ingestion perturbs the antioxidant system in a dose and time dependent manner.

A variety of laboratory tests are available to assist in the diagnosis of alcohol consumption and related disorders. The levels of intake at which laboratory results become abnormal vary from person to person. Laboratory tests are particularly useful in settings where cooperativeness is suspected orwhen a history is not available. Several biochemical and hematological tests, such as T-glutamyltransferase (GGT) activity, aspartate aminotransferase (AST) activity, highdensity lipoprotein cholesterol (HDL-C) content of serum, and erythrocyte mean corpuscular volume (MCV) are established markers of alcohol intake. Their validity as markers is based largely on correlations with recent intake at a single time point and on decreases in elevated values when heavy drinkers abstain from alcohol. These readily available laboratory tests provide important prognostic information and should be integral part of the assessment of persons with hazardous alcohol consumption. There are several other markers with considerable potential for more accurate reflection of recent alcohol intake. These include carbohydrate deficient transferrin, ~-hexosaminidase, acetaldehyde adducts and the urinary ratio of serotonin metabolites, 5-hydroxytryptophol and 5-hydroxyindoleacetic acid. These markers provide hope for more sensitive and s.pecific aids to diagnosis and improved monitoring for intake.

Oxidative stress is implicated in the pathogenesis of liver disease. We investigated oxidative stress-related parameters and correlated with clinical findings in 35 non-alcoholic fatty liver disease (NAFLD) patients, 38 alcoholic liver disease (ALD) patients and 38 normal subjects. NAFLD patients showed significantly higher body mass index, cholesterol, LDL-cholesterol, VLDL-cholesterol levels and transaminase activities compared to the other two groups. Haematological parameters were significantly altered in ALD patients and were reported only in male subjects. Glutathione content, catalase activity, glutathione reductase activity and glutathione peroxidase activity in NAFLD patients were reduced by 10.7 %, 18.5 %, 8.1 % and 16.8 %, respectively, and in ALD patients by 21.8 %, 29.6 %, 24.3 % and 45.3 %, respectively, compared to the normal group. However, thiobarbituric acid reactive substance content, superoxide dismutase activity and glutathione s-transferase activity were increased by 35.2 %, 31.6 % and 5.4 %, respectively, in NAFLD patients, and in ALD patients by 75.2 %, 72.7 % and 32.4 %, respectively, compared to the normal group. Oxidative stress is associated with collagen production and leads to fibrosis. Type IV collagen level in NAFLD patients (190.6 +/- 83 ng/mL) was significantly higher than in the normal group (124.5 +/- 14.5 ng/mL) and lower than in ALD patients (373.4 +/- 170 ng/mL). While type IV collagen level of >124 ng/mL was a predictor of NAFLD patients from normal subjects, elevated ALT (>40 IU/L) activity could discriminate either of the liver disease patients from normal subjects.

Medically diagnosed alcoholics can be differentiated reliably from non-alcoholics using clinically laboratory tests. In the present study, patients with liver diseases either due to alcohol or without alcohol compared with a group of normal healthy persons. Heavy drinkers showed significantly lower body weight and percent body fat, and low BMI compared with other groups. The percentage of hemoglobin and total number of RBC were found to be significantly decreased, whereas mean corpuscular volume (MCV) significantly increased in alcoholic liver disease (ALD). Hyperbilirubinemia, hyperuricemia and hypoalbuminemia correlate with alcohol intake. Albumin/globulin ratio significantly decreased in ALD. In acute liver injury AST/ALT ratio is ≤1.0, whereas in alcoholic hepatitis it is always >1.0. Moderately elevated level of ALP and high GGT values are good discriminator of alcoholic patients. Alcohol-induced liver injury is linked to oxidative stress as observed by decreased level of reduced glutathione and ascorbic acid, and increased level of thiobarbituric acid reactive substances.

Current status of carbohydrate defi cient transferrin,total serum sialic acid, sialic acid index of apolipoprotein J and serum b-hexosaminidase as markers for alcohol consumption. Addiction, 2003:98;(Suppl. 2), 45 -50

Ethanol-induced liver injury may be linked, at least partly, to an oxidative stress resulting from increased free radical production and/or decreased antioxidant defence. Distinguishing alcoholic and non-alcoholic liver disease has important implications. This study looked at the possible changes between alcoholic and non-alcoholic liver diseases by examining the presence of oxidative damage, as monitored by several parameters relating to oxidative stress. Lipid peroxides concentration, superoxide dismutase activity and glutathione S-transferase activity increased, where as glutathione content, glutathione peroxidase activity and glutathione reductase activity decreased among the tested subjects in comparison to normal healthy group. Determination of these parameters may be valuable in the evaluation of liver disease. However, oxidative stress related enzymes and non-enzymes can not be utilized as a marker for alcoholic liver diseases, as these parameters responded in the same way after liver is damaged irrespective of their cause. Their level may help in determining the degree of liver damage. Degree of oxidative injury was similar in patients with non-alcoholic liver disease and in moderate drinkers; while significantly higher in heavy drinkers. The differences between the groups might be based on the type of liver pathological condition rather than its etiology (i.e. alcohol and non alcohol related causes).