Diminished Serum Concentration of Vitamin E in Alcoholics

Bjørneboe, Gunn‐Elin Aa.; Johnsen, Jon; Bjørneboe, Anders; Bache-Wiig, Jon-Erik; Mørland, Jörg; Drevon, Christian A.

doi:10.1159/000177408

Cited by 53 publications

(6 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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: Discussionmentioning

confidence: 80%

“…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]. Reduced serum levels of ·-tocopherol in alcoholics may be normalized by vitamin E supplementation [13].…”

Section: Discussionmentioning

confidence: 81%

See 1 more Smart Citation

Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

Zima

Fialová

Mestek

et al. 2001

Journal of Biomedical Science

View full text Add to dashboard Cite

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...

show abstract

Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 81%

Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

Zima

Fialová

Mestek

et al. 2001

Journal of Biomedical Science

View full text Add to dashboard Cite

show abstract

“…The fate of antioxidants in an environment of oxidative stress resulting from chronic ethanol consumption is well documented. The vast majority of previous studies found a reduction in vitamin E levels associated with ethanol consumption (Bjorneboe and Bjorneboe, 1993; Bjorneboe et al., 1987a,b, 1988a,b; Grattagliano et al., 1997; Hartman et al., 2005; Johansson et al., 1986; Lecomte et al., 1994; Odeleye et al., 1991; Valls‐Belles et al., 2008), concluding the reduction resulted from either increased oxidative stress, differences in ethanol consumption or diet, altered lipoprotein status, or enzymatic changes in the liver. However, no other study has measured multiple indicators of vitamin E status.…”

mentioning

confidence: 96%

Individual Differences in Hyperlipidemia and Vitamin E Status in Response to Chronic Alcohol Self-Administration in Cynomolgus Monkeys

Lebold

Grant

Freeman

et al. 2010

Alcoholism: Clinical and Experimental Research

View full text Add to dashboard Cite

Background Chronic ethanol self-administration induces oxidative stress and exacerbates lipid peroxidation. α-Tocopherol is a potent lipid antioxidant and vitamin that is dependent upon lipoprotein transport for tissue delivery. Methods To evaluate the extent to which vitamin E status is deranged by excessive alcohol consumption, monkeys voluntarily drinking ethanol (1.36 to 3.98 g/kg/day for 19 months, n=11) were compared with non-drinkers (n=5, control) Results Three alcohol drinking animals developed hyperlipidemia with plasma triglyceride levels (1.8 ± 0.9 mmol/L) double those of normolipidemic (NL) drinkers (0.6 ± 0.2) and controls (0.6 ± 0.3, p<0.05); elevated plasma cholesterol (3.6 ± 0.5 mmol/L) compared with NL drinkers (2.3 ± 0.2, p<0.05) and controls (2.9 ± 0.3); and lower plasma α-tocopherol per triglycerides (14 ± 6 mmol/mol) than controls (27 ± 8) and NL drinkers (23 ± 6 p<0.05). Hyperlipidemic monkey liver α-tocopherol (47 ± 15 nmol/g) was lower than NL drinkers (65 ± 13) and controls (70 ± 15, p=0.080), as was adipose α-tocopherol (84 ± 37nmol/g) compared with controls (224 ± 118) and NL drinkers (285 ± 234, p<0.05). Plasma apolipoprotein (apo) CIII increased compared to baseline at both 12 and 19 months in the normolipidemic (P=0.0016 and P=0.0028, respectively) and in the hyperlipidemic drinkers (P<0.05 and P<0.05, respectively). Plasma apo H concentrations at 19 months were elevated hyperlipidemics (P<0.05) relative to concentrations in control animals. C-reactive protein (CRP), a marker of inflammation, was increased compared to baseline at both the 12- and 19-month time points in the normolipidemic (P=0.005 and P=0.0153, respectively) and hyperlipidemic drinkers (P=0.016 and P=0.0201, respectively). Conclusion A subset of alcohol drinking monkeys showed a predisposition to alcohol-induced hyperlipidemia. The defect in lipid metabolism resulted in lower plasma α-tocopherol per triglycerides and depleted adipose tissue α-tocopherol, and thus, decreased vitamin E status.

show abstract

“…Additionally, chronic ethanol consumption leads to diminished plasma and liver concentrations of ATs (Meydani et al 1991), and an inverse correlation between hepatic lipid peroxidation and AT levels has been identified (Kawase et al, 1989;Sadrzadeh et al, 1994). Studies in alcoholics confirm the fact that alcohol reduces the concentrations of AT in serum and various tissues (Bjorneboe et al, 1988;Horvath et al, 1992).…”

Section: Discussionmentioning

confidence: 97%