Some Aspects of Antioxidant Status in Blood from Alcoholics

Bjørneboe, Gunn‐Elin Aa.; Johnsen, Jon; Bjørneboe, Anders; Marklund, Stefan L.; Skylv, Nina; Høiseth, Arne; Bache-Wiig, Jon-Erik; Mørland, Jörg; Drevon, Christian A.

doi:10.1111/j.1530-0277.1988.tb01350.x

Cited by 56 publications

(23 citation statements)

References 38 publications

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“…Heavy consumption of ethanol reduced the plasma level of ·-tocopherol as well [12]. The serum concentration of ·-tocopherol was 30% lower in the alcoholics [13]; in another study it was reduced by 37% as compared to controls [11]. Such results support a role of free-radical-mediated damage, which can develop diseases frequently observed in alcoholics [11,80].…”

Section: Discussionsupporting

confidence: 62%

“…Such results support a role of free-radical-mediated damage, which can develop diseases frequently observed in alcoholics [11,80]. Reduced serum levels of ·-tocopherol in alcoholics may be normalized by vitamin E supplementation [13]. With the only exception of supplemental vitamin E, and possibly vitamin C, being able to significantly lower lipid oxidative damage in both smokers and nonsmokers, the current evidence is insufficient to conclude that antioxidant vitamin supplementation materially reduces oxidative damage in humans [52].…”

Section: Discussionmentioning

confidence: 44%

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Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

Zima

Fialová

Mestek

et al. 2001

Journal of Biomedical Science

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Alcohol-induced oxidative stress is linked to the metabolism of ethanol. Three metabolic pathways of ethanol have been described in the human body so far. They involve the following enzymes: alcohol dehydrogenase, microsomal ethanol oxidation system (MEOS) and catalase. Each of these pathways could produce free radicals which affect the antioxidant system. Ethanol per se, hyperlactacidemia and elevated NADH increase xanthine oxidase activity, which results in the production of superoxide. Lipid peroxidation and superoxide production correlate with the amount of cytochrome P450 2E1. MEOS aggravates the oxidative stress directly as well as indirectly by impairing the defense systems. Hydroxyethyl radicals are probably involved in the alkylation of hepatic proteins. Nitric oxide (NO) is one of the key factors contributing to the vessel wall homeostasis, an important mediator of the vascular tone and neuronal transduction, and has cytotoxic effects. Stable metabolites – nitrites and nitrates – were increased in alcoholics (34.3 ± 2.6 vs. 22.7 ± 1.2 µmol/l, p < 0.001). High NO concentration could be discussed for its excitotoxicity and may be linked to cytotoxicity in neurons, glia and myelin. Formation of NO has been linked to an increased preference for and tolerance to alcohol in recent studies. Increased NO biosynthesis also via inducible NO synthase (NOS, chronic stimulation) may contribute to platelet and endothelial dysfunctions. Comparison of chronically ethanol-fed rats and controls demonstrates that exposure to ethanol causes a decrease in NADPH diaphorase activity (neuronal NOS) in neurons and fibers of the cerebellar cortex and superior colliculus (stratum griseum superficiale and intermedium) in rats. These changes in the highly organized structure contribute to the motor disturbances, which are associated with alcohol abuse. Antiphospholipid antibodies (APA) in alcoholic patients seem to reflect membrane lesions, impairment of immunological reactivity, liver disease progression, and they correlate significantly with the disease severity. The low-density lipoprotein (LDL) oxidation is supposed to be one of the most important pathogenic mechanisms of atherogenesis, and antibodies against oxidized LDL (oxLDL) are some kind of epiphenomenon of this process. We studied IgG oxLDL and four APA (anticardiolipin, antiphosphatidylserine, antiphosphatidylethanolamine and antiphosphatidylcholine antibodies). The IgG oxLDL (406.4 ± 52.5 vs. 499.9 ± 52.5 mU/ml) was not affected in alcoholic patients, but oxLDL was higher (71.6 ± 4.1 vs. 44.2 ± 2.7 µmol/l, p < 0.001). The prevalence of studied APA in alcoholics with mildly affected liver function was higher than in controls, but not significantly. On the contrary, changes of autoantibodies to IgG oxLDL revealed a wide range of IgG oxLDL titers in a healthy population. These parameters do not appear to be very promising for the evaluation of the risk of atherosclerosis. Free radicals increase the oxidative modification of LDL. This is one of the most important mechanism...

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 44%

Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

Zima

Fialová

Mestek

et al. 2001

Journal of Biomedical Science

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“…Reduced hepatic alpha-tocopherol content after long-term ethanol feeding in rats under adequate intake of vitamin E [27] and also in alcoholics [28] has been reported. Alpha-tocopherol level was found to be reduced in the blood of the alcoholics [29] . In addition to acetaldehyde and free radical generation by the ethanol-induced microsomes, these deficient defense systems were suggested to contribute to liver damage via lipid peroxidation [17] .…”

Section: Discussionmentioning

confidence: 99%

N-acetylcysteine attenuates alcohol-induced oxidative stress in the rat

Özaras

Tahan²,

Aydın³

et al. 2003

WJG

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AIM:There is increasing evidence that alcohol-induced liver damage may be associated with increased oxidative stress. We aimed to investigate free-radical scavenger effect of nacetylcysteine in rats intragastrically fed with ethanol. METHODS:Twenty-four rats divided into three groups were fed with ethanol (6 g/kg/day, Group 1), ethanol and nacetylcysteine (1 g/kg, Group 2), or isocaloric dextrose (control group, Group 3) for 4 weeks. Then animals were sacrificed under ether anesthesia, intracardiac blood and liver tissues were obtained. Measurements were performed both in serum and in homogenized liver tissues. Malondialdehyde (MDA) level was measured by TBARS method. Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) levels were studied by commercial kits. Kruskal-Wallis test was used for statistical analysis. RESULTS:ALT and AST in Group 1 (154 U/L and 302 U/L, respectively) were higher than those in Group 2 (94 U/L and 155 U/L) and Group 3 (99 U/L and 168 U/L) (P=0.001 for both). Serum and tissue levels of MDA in Group 1 (1.84 nmol/ mL and 96 nmol/100 mg-protein) were higher than Group 2 (0.91 nmol/mL and 64 nmol/100 mg-protein) and Group 3 (0.94 nmol/mL and 49 nmol/100 mg-protein) (P<0.001 for both). On the other hand, serum GSH-Px level in Group 1 (8.21 U/g-Hb) was lower than Group 2 (16 U/g-Hb) and Group 3 (16 U/g-Hb) (P<0.001). Serum and liver tissue levels of SOD in Group 1 (11 U/mL and 26 U/100 mg-protein) were lower than Group 2 (18 U/mL and 60 U/100 mg-protein) and Group 3 (20 U/mL and 60 U/100 mg-protein) (P<0.001 for both). CONCLUSION:This study demonstrated that ethanolinduced liver damage is associated with oxidative stress, and co-administration of n-acetylcysteine attenuates this damage effectively in rat model. Ozaras R, Tahan V, Aydin S, Uzun H, Kaya S, Senturk H. Nacetylcysteine attenuates alcohol-induced oxidative stress in the rat. World J Gastroenterol 2003; 9(1): 125-128

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“…decreased compared with controls (39,40). Vitamins A and E have important immunoregulatory functions involving both T and B lymphocytes, NK cells and macrophages (6)(7)41).…”

Section: Discussionmentioning

confidence: 99%

Carnitine and/or GABA Supplementation Increases Immune Function and Changes Lipid Profiles and Some Lipid Soluble Vitamins in Mice Chronically Administered Alcohol

Soh¹,

Namseok²,

et al. 2010

JFN

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This study evaluated the effects of carnitine and/or GABA supplementation on immune function, lipid profiles and some vitamins in mice chronically administered alcohol. BALB/c mice were fed with either AIN-76 diet (N), control diet plus alcohol (4 g/kg bw, E), E plus 0.5 g/kg bw carnitine (EC), E plus 0.5 g/kg bw GABA (EG), or E plus 0.5 g/kg bw carnitine plus 0.5 g/kg bw GABA (ECG) for 6 weeks. Administrations of the carnitine and/or GABA prevented alcohol-induced increases in triglyceride concentrations in serum and liver. However, there was no difference among the supplemented groups. Serum vitamin E concentration was higher in mice supplemented with EC and EG, but not in mice given ECG. Phagocytic activity of peritoneal macrophages was increased in EG group compared with E group. The subpopulations of murine splenocyte's T H cells were increased significantly in EC and ECG groups. These data suggest that immune function, lipid profiles and some immune-related lipid soluble vitamins were positively changed by supplementation of carnitine or GABA, but do not show any synergistic effect of mixed supplementation.

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Some Aspects of Antioxidant Status in Blood from Alcoholics

Cited by 56 publications

References 38 publications

Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

N-acetylcysteine attenuates alcohol-induced oxidative stress in the rat

Carnitine and/or GABA Supplementation Increases Immune Function and Changes Lipid Profiles and Some Lipid Soluble Vitamins in Mice Chronically Administered Alcohol

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