Pregnancy outcome following high doses of Vitamin E supplementation.

 (>or=400 IU/day) have been shown to attenuate or even prevent the damaging effect of 

 and diabetes on the fetus in experimental animal models.

Absorption, transport and metabolism of vitamin E.

Clinical evidence from heavy drinkers and from experimental work in rats suggests that

, causing reduced tissue concentrations of alpha-tocopherol.

Absorption, transport and distribution of vitamin E.

New clinical evidence from heavy drinkers and from experimental work in rats suggests that

Studies on the stability of vitamin A in the stomach and small intestine

 improved the absorption curve of vitamin A 

 in man by protecting it in gastric and duodenal juice.

CYP4F2 repression and a modified alpha-tocopherol (vitamin E) metabolism are two independent consequences of ethanol toxicity in human hepatocytes.

 antagonized the cytotoxicity and CYP4F2 gene repression effect of 

Vitamin and carotenoid intake and risk of head-neck cancer subtypes in the Netherlands Cohort Study.

 (P-interaction = 0.003) with lower risks in alcohol abstainers.

Selected micronutrients and oral and pharyngeal cancer

The association with vitamin C and carotene was independent of smoking and drinking habits, while that with

 was less evident in those heavily exposed to 

Effect of heavy alcohol consumption on serum concentrations of fat-soluble vitamins and selenium.

Effects of vitamin E therapy on ethanol‐induced changes in platelet aggregation, thromboxane formation, factor VIII levels and serum lipids

The results demonstrate that a high dose of

 men slightly (P < 0·05) decreases aggregation‐associated platelet thromboxane formation during ethanol oxidation.

Alpha-Tocopherol Counteracts the Effect of Ethanol on Cortical Spreading Depression in Rats of Various Ages, With and Without Ethanol Abstinence.

 on CSD, returning CSD velocities to levels in control groups (p < 0.05).

The protective effect of vitamin E against prenatal and early postnatal ethanol treatment-induced heart abnormality in rats: a 3-month follow-up study.

Additive effect of alpha-tocopherol and ascorbic acid in combating ethanol-induced hepatic fibrosis

The activities of antioxidant enzymes which were reduced by

 administration were enhanced on combined administration of 

Effects of α-Tocopherol Supplementation on Liver of Rats Chronically Exposed to Ethanol

 intake induces free radical synthesis, resulting in the depletion of antioxidants, especially 

, which has an important role in lipid peroxidation.

Results: Alcohol exposure for 6 weeks did not decrease hepatic α-tocopherol levels; however, both groups exposed to

Vasoprotective effect of vitamin E: rescue of ethanol-induced atherosclerosis and inflammatory stress in rat vascular wall.

In addition, it intends to find out whether

Influence of vitamin E on alcohol-induced changes in antioxidant defenses in mice liver

 and can be suitably used as a potential therapeutic agent for alcohol-induced oxidative damage in liver.

The effect of carnosine pretreatment on oxidative stress and hepatotoxicity in binge ethanol administered rats

, vitamin C levels and GSH-Px and GST activities were found to be decreased following 

Effect of grape (Vitis vinifera L.) leaf extract on alcohol induced oxidative stress in rats.

 (7.9 g/kg bw/day) for 45 days resulted an activity of liver marker enzymes (AST, ALT, ALP …, lipid hydroperoxides) in liver and kidney with significantly lower activity of SOD, CAT, GPx, GST and non-enzymatic antioxidants (

, vitamin C and GSH) … compared with control rats.

Effect of mixed organic substrate on α-tocopherol production by Euglena gracilis in photoheterotrophic culture

 production per dry cell weight was enhanced by adding 

Effect of vitamin E on alcohol-induced changes in oxidative stress and expression of transcription factors NFkappaB and AP-1 in mice brain cerebral hemispheres.

 and thus can be suitable as a potential therapeutic agent for alcohol-induced oxidative damage in brain.

Hepatic and renal concentrations of vitamins E and C in lead- and ethanol-exposed rats. An assessment of their involvement in the mechanisms of peroxidative damage.

 alone and in combination led to a decrease in 

 concentration in the liver compared to the control group (by 30%, 26% and 50%, respectively).

The treatment with Pb alone and in combination with

 concentration in the kidney (by 13% and 21%, respectively).

The influence of ethanol intake and its withdrawal on the anticonvulsant effect of alpha-tocopherol in the penicillin-induced epileptiform activity in rats.

 influence on the neuroprotective actions of 

 are still a crucial issue associated with epilepsy.

Vitamin E prevents ethanol-induced inflammatory, hormonal, and cytotoxic changes in reproductive tissues

Ethanol significantly increased hypothalamic, pituitary and testicular TNF-α and IL-6, all changes prevented by the higher dose … LHRH, LH, testosterone, and testicular germ cell apoptosis were similarly prevented by vitamin E. These data strikingly show that

 and suggests that the … anti-inflammatory and antioxidant.

The effects of ethanol intake and withdrawal on penicillin-induced epileptiform activity in rats

significantly decreased the mean frequency of epileptiform activity in the 60, 70, and 120 min after

 in penicillin pretreated, ethanol-treated, 

Amelioration of ethanol-induced growth retardation by all-trans-retinoic acid and alpha-tocopherol in shell-less culture of the chick embryo.

All-trans-retinoic acid, the active form of Vitamin A, and/or

 significantly diminished both the EtOH-induced mortality and growth retardation.

Effect of an acute dose of ethanol on lipid peroxidation in rats: action of vitamin E.

Dietary vitamin E caused a dose-dependent increase in liver and plasma concentration of the vitamin, but

Effect of ethanol and the catalase inhibitor aminotriazole on lipid peroxidation in the rat myocardium

, reduced glutathione) or artificial (dibunol) antioxidants into the incubation media.

Pycnogenol and vitamin E inhibit ethanol-induced apoptosis in rat cerebellar granule cells.

 have the potential to act as therapeutic agents, antagonizing the induction of neuronal cell death by 

Vitamin E amelioration of ethanol neurotoxicity involves modulation of apoptotis-related protein levels in neonatal rat cerebellar granule cells.

It was found that ethanol significantly impaired neuronal survival in these preparations, and that survival in the presence of

THE EFFECTS OF ETHANOL CONSUMPTION ON THE LIPID PEROXIDATION AND GLUTATHIONE LEVELS IN THE RIGHT AND LEFT BRAINS OF RATS

The results suggested that the cerebral hemispheres of adult rats are susceptible to the oxidative neurotoxic effects of

Antioxidants prevent depletion of [Mg2+]i induced by alcohol in cultured canine cerebral vascular smooth muscle cells: Possible relationship to alcohol-induced stroke

However, preincubation of the cells with either

 or PDTC for 24 h completely inhibited the depletion of [Mg(2+)](i) induced by exposure to 10-100 mM 

 and PDTC prevent decreases in [Mg(2+)](i) produced by 

Content of liver and brain ubiquinol-9 and ubiquinol-10 after chronic ethanol intake in rats subjected to two levels of dietary α-tocopherol

, involves a compensatory enhancement in hepatic tGSH availability, and is not observed in the brain tissue, probably due to its limited capacity for ethanol biotransformation and glutathione synthesis.

Effect of palm vitamin E on the healing of ethanol-induced gastric injury in rats.

In the second phase of the study, the mean ulcer index of palm

 supplemented group killed after 1 week of 

 exposure was significantly lower compared to the respective control.

In vivo rates of skeletal muscle protein synthesis in rats are decreased by acute ethanol treatment but are not ameliorated by supplemental alpha-tocopherol.

Hepatic k(s) was not altered by ethanol, although

 concentrations in this tissue increased due to 

Regulation of manganese superoxide dismutase (MnSOD) in chronic experimental alcoholism: effects of vitamin E-supplemented and -deficient diets.

Since low vitamin E liver content seems to potentiate EtOH-linked oxidative stress, … from rats fed a diet deficient or supplemented with vitamin E. Chronic

 in both groups of EtOH-treated animals, irrespectively of the vitamin … effect was observed in both the microsomal and mitochondrial fractions.

Impact of massive ascorbic acid supplementation on alcohol induced oxidative stress in guinea pigs.

 level, which was reduced by alcohol intake, was raised by the co-administration of AA and 

The antioxidants vitamin E and beta-carotene protect against ethanol-induced neurotoxicity in embryonic rat hippocampal cultures.

 increased survival to 95%, 79%, 66%, and 75% during 1600, 1800, and 2000 and 2400 mg/dl 

Alpha-tocopherol prevents ethanol-induced elevation of [Ca2+]i in cultured canine cerebral vascular smooth muscle cells.

 (10-400 mM), the rises of [Ca2+]i induced by ethanol were attenuated markedly.

Changes in some pro- and antioxidants in rat cerebellum after chronic alcohol intake.

Effect of chronic ethanol feeding on lipid peroxidation and protein oxidation in relation to liver pathology

 and glutathione concentrations were significantly decreased in 

Independent antioxidant action of vitamins E and C in cultured rat hepatocytes intoxicated with allyl alcohol.

In cells supplemented with alpha-TP, allyl

 produced a concentration-dependent decline in the cellular content of 

, and these cells were more resistant to cell killing than hepatocytes not supplemented with alpha-TP.

Prevention of ethanol-induced changes in reactive oxygen parameters by alpha-tocopherol.

Other putative indices of hepatic pro-oxidant events, namely levels of mixed function oxidase and proteolytic activity, were elevated by

α-Tocopherol attenuates alcohol-induced cerebral vascular damage in rats: possible role of oxidants in alcohol brain pathology and stroke

 pretreatment either prevented or ameliorated greatly the cerebrovasospasm and vascular damage induced by 

Dietary vitamin E modulation of cytokine production by splenocytes and thymocytes from alcohol-fed mice.

 enhances immune responses, it may reduce dietary 

 (EtOH)-induced immune suppression, thereby favorably affecting host disease resistance.

Effects of ethanol, lovastatin and coenzyme Q10 treatment on antioxidants and TBA reactive material in liver of rats.

 from 28 to 12 micrograms/g wet weight and lovastatin diminished it to 12 micrograms; no additive effect was evident.

The effect of alcohol consumption on nutritional status during murine AIDS.

Intestinal levels of vitamin A and Cu were not affected by ETOH, whereas

 and Zn were significantly reduced in both normal mice and those with AIDS fed 

Ethanol-mediated promotion of oral carcinogenesis in hamsters: association with lipid peroxidation.

 consumption at 22 weeks, which increased further when combined with DMBA treatment, but at 35 weeks these values were intermediate.

Loss of alpha-tocopherol upon exposure to nitric oxide or the sydnonimine SIN-1.

 resulted in loss of the vitamin and quinone formation.

Effect of chronic consumption of ethanol and vitamin E on fatty acid composition and lipid peroxidation in rat heart tissue.

 in heart tissue by 30% irrespective of the vitamin E content in the diet.

NADH-dependent reductive stress and ferritin-bound iron in allyl alcohol-induced lipid peroxidation in vivo: the protective effect of vitamin E.

 dose-dependently against allyl alcohol-induced lipid peroxidation and liver injury in vivo.

Vitamin E inhibition of lipid peroxidation and ethanol-mediated promotion of esophageal tumorigenesis.

The results suggest that promotion of NMBzA-induced esophageal tumors by ethanol may in part result from increased lipid peroxidation and that

 promoter effects by inhibiting lipid peroxidation.

Vitamin E Inhibits the Carcinogenicity of N‐Nitrosomethylbenzylamine a

 reduced the number of mice with tumors and the number and size of tumors compared to similarly treated mice without dietary vitamin E supplementation.

In this study, we investigated a contributory mechanism whereby

 inhibits growth of esophageal tumors and inhibits the tumor-promoter effects of 

 reduced the cumulative products of free radical activity,' as well as elevated hepatic levels of vitamin E , thus reducing the potential … radical damage to the liver.4 Experimental studies in animals have demonstrated that vitamin E inhibits growth of chemically induced tumors.

Effect of chronic ethanol feeding on hepatic and extrahepatic distribution of vitamin E in rats.

 expressed per milligram of total lipids was significantly (p less than or equal to 0.01) decreased in the liver with 

The concentration of gamma-tocopherol (but not

) per milligram of lung tissue and per total lung was significantly (p less than or equal to 0.05) increased with 

 ingestion significantly alters the distribution of 

 and gamma-tocopherol in hepatic and extrahepatic tissues of the rat.

Fetal alcohol effects: Decreased synaptic formations in the field CA3 of fetal hippocampus

The administration of 0.01% zinc with ethanol or 0.02%

 during pregnancy resulted in an increased cerebral weight, but did not result in an increased synaptic formation compared to ethanol alone.

The effect of vitamin E (alpha-tocopherol) supplementation on hepatic levels of vitamin A and E in ethanol and cod liver oil fed rats.

 consumption decreased the levels of hepatic 

 (p less than 0.05), vitamin A (p less than 0.05) and the ratio of vitamin A/E (p less than 0.05).

 were less than that of control rats but were 4.3 times greater than that of rats on ethanol … with vitamin E. However, the vitamin A and E ratio was equal to normal in this group of rats.

Vitamin E reduction of lipid peroxidation products in rats fed cod liver oil and ethanol.

Levels of hepatic conjugated fatty acid dienes from rats fed

 were reduced 91% compared to rats fed ethanol diets.

Antioxidant protection systems of rat lung after chronic ethanol inhalation.

 inhalation lowered hepatic glutathione (19%) and hepatic 

 (33%), there was no increase in malondialdehyde content in either liver or lung of ethanol-exposed rats.

Effect of chronic ethanol consumption on the content of alpha-tocopherol in subcellular fractions of rat liver.

 promoted, however, a further enrichment of 

 (178% higher than controls) in the Golgi apparatus, possibly due to reduced secretion of very low density lipoprotein-associated alpha-tocopherol.

Lipid peroxidation and antioxidant defense systems in rat liver after chronic ethanol feeding

 metabolism in the liver and that the combination of ethanol with a low‐vitamin E intake results in a decrease of hepatic α‐tocopherol content which renders the liver more susceptible to free radical attack.

[Excretory function of the liver with an allyl alcohol lesion and the antioxidant correction of the disorders].

, sodium selenite, unithiol) reduced the toxic effect of allyl 

Oxidative stress from alcohol in the brain.

 load induces also a decrease in the cerebellar concentration of the three main endogenous anti-oxidant small molecules, i.e. 

Reduced hepatic alpha-tocopherol content after long-term administration of ethanol to rats.

 (35% of total energy) for 5-6 weeks concentration of 

 in whole liver was reduced by 25% as compared to the pair-fed controls (P less than 0.003).

Negative Correlation Between Vitamin A and Positive Correlation Between Vitamin E and Inflammation Among Healthy Adults in Korea: Based on the Korea National Health and Nutrition Examination Survey (KNHANES) 2016–2018 7th Edition

Development of chitosan based extended-release antioxidant films by control of fabrication variables.

Increasing the stirring speed of homogenization and the presence of

 considerably decreased the release rate of 

Our results indicated that the release rate of

 could be controlled by changing the stirring speed of homogenization and especially 

Singlet oxygen scavenging by α‐tocopherol and β‐carotene: Kinetic studies in phospholipid membranes and ethanol solution

 required for 50% inhibition of lipid peroxidation (IC50) were higher than those of β‐Car, being more than 6 times higher in 

 solution and less than 2 times higher in liposomes.

Effects of solvents and media on the antioxidant activity of alpha-tocopherol.

 in different solvents decreased in the order of acetonitrile = hexane > 

 = methanol, which indicates that the antioxidant activity of alpha-tocopherol is smaller in protic solvent than in aprotic solvent.

Solvent influence on model oxidations of alpha-tocopherol.

 concentration brought about a decrease in the oxidation of 

 and in the formation of 5-ethoxymethyl-7,8-dimethyltocol.

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Possible Interaction: Ethanol and Vitamin E

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Ethanol

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Research Papers that Mention the Interaction