MONITORING OXIDATIVE DAMAGE IN PATIENTS WITH LIVER-CIRRHOSIS AND DIFFERENT DAILY ALCOHOL INTAKE

Citation
P. Clot et al., MONITORING OXIDATIVE DAMAGE IN PATIENTS WITH LIVER-CIRRHOSIS AND DIFFERENT DAILY ALCOHOL INTAKE, Gut, 35(11), 1994, pp. 1637-1643
Citations number
43
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
GutACNP
ISSN journal
0017-5749
Volume
35
Issue
11
Year of publication
1994
Pages
1637 - 1643
Database
ISI
SICI code
0017-5749(1994)35:11<1637:MODIPW>2.0.ZU;2-V
Abstract
This study looked at the possible association between alcohol abuse an d free radical mediated oxidative injury by examining the presence of oxidative damage, as monitored by erythrocyte malonildialdehyde and pl asma lipid hydroperoxides, in patients with liver cirrhosis and differ ent lifetime daily alcohol intake. Ah patients with an alcohol intake above 100 g/day (ALC) showed concentrations of malonildialdehyde and l ipid hydroperoxide on average four to fivefold higher than cirrhotic p atients with alcohol intake below 100 g/day (NAC) or healthy controls. Further subgrouping of ALC patients showed that those with alcohol in take ranging between 100 and 200 g/day (ALC1) had malonildialdehyde an d Lipid hydroperoxide concentrations significantly lower than those wi th an intake higher than 200 g/day (ALC2). These differences were not related to the extent of liver injury or to the Liver derangement as a ssessed by Child's classification. The increase in lipid peroxidation markers in ALC cirrhotic patients was associated with a decrease in, r espectively, plasma alpha-tocopherol and erythrocyte glutathione conce ntrations. Significant differences were also seen between ALC1 and ALC 2 groups in plasma alpha-tocopherol, but not in erythrocyte glutathion e concentrations. The concentrations of alpha-tocopherol and glutathio ne in the blood of NAC patients were in contrast not substantially dif ferent from those of healthy controls. The close association between o xidative damage and alcohol abuse suggested that free radical intermed iates produced during ethanol metabolism might be responsible for caus ing oxidative damage.