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

Jordão, Alceu Afonso; Chiarello, Paula Garcia; Arantes, Maurício Rodrigues de; Meirelles, Mônica S. S.; Vannucchi, Hélio

doi:10.1016/j.fct.2003.10.008

Cited by 55 publications

(47 citation statements)

References 20 publications

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“…On the other hand, in the present study GSH level of the third group is decreased and it is concordant with the literature [5][6]28]. This result might be related to either the increase in GSH oxidation, which is a direct result of increase in free radical generation or acetaldehyde promotes peroxidation reaction binding to cysteine and/or glutathione, which causes depletion of GSH [5,28]. Moreover, this result might be affected by interaction between EtOH and [B(a)P].…”

Section: Discussionsupporting

confidence: 82%

Effects of Benzo(a)pyrene and Ethanol on Morphology and Antioxidant Status and Transaminases in Rat Liver

Emre¹,

Aktay²,

Polat³

et al. 2014

Med-Science

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Ethanol and benzo (a) benzo(a)pyrene [B(a)P], third group treated with benzo(a)pyrene[B(a)P] plus ethanol (EtOH) and fourth group was given ethanol(EtOH). Superoxide dismutase (SOD), alanin aminotransferase (ALT), aspartat aminotransferase (AST), gamma-glutamyl transferase (GGT), glutathione (GSH), malondialdehyde (MDA) levels as well as histological examination were evaluated to demonstrate the liver response following administration of [B(a)P] and (EtOH

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Section: Discussionsupporting

confidence: 82%

Effects of Benzo(a)pyrene and Ethanol on Morphology and Antioxidant Status and Transaminases in Rat Liver

Emre¹,

Aktay²,

Polat³

et al. 2014

Med-Science

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“…Many studies 1,[28][29][30] have demonstrated that liver injuries induced by ethanol are associated with free radicals and oxidative stress. Ethanol is converted to ethyl and 1-droxyethylradical.…”

Section: Discussionmentioning

confidence: 99%

Glycoprotein Isolated from Acanthopanax senticosus Protects against Hepatotoxicity Induced by Acute and Chronic Alcohol Treatment

Choi

Yoon²,

Kang

et al. 2006

Biological & Pharmaceutical Bulletin

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Acanthopanax senticosus (A. senticosus) is a common Asian herb known as "Siberian Ginseng" or "Eleutherococcus senticosus" 1) and used for rheumatism and prophylaxis of various diseases including chronic bronchitis, hypertension, and ischemia. The herb has also been known to effectively relieve stress or fatigue, and symptoms associated with diabetes, neuralgia, and cancer. 2,3) Today this oriental herb is called "adatogen" in the U.S.4) The major active components of A. senticosus are acanthoside, eleutheroside, chiisanoside, senticoside, triterpenic saponin, syringin, flavone, vitamin, minerals, b-sitosterol, sesamine and savinine. 4,5) Each chemical compound is known to produce diverse biological activities. In Korea, the extract of the A. senticosus plant is used a component in traditional herbal Korean medicine, and is available as a functional beverage commercially marketed for reducing liver damage and accelerating alcohol detoxification. The efficacy of A. senticosus in animal modes and the mechanisms underlying the aforementioned physiological properties involved in alcohol metabolism is unclear, and is therefore the purpose of this investigation.As much as 80-90% of ingested alcohol is metabolized in the liver, where alcohol is oxidized to acetadehyde. [6][7][8] The process is catalyzed by 3 different enzymes: alcohol dehydrogenase (ADH), microsomal ethanol metabolizing system (MEOS), and acetaldehyde dehydrogenase (ALDH). Since acetaldehyde is much more toxic than alcohol, it is associated with a larger number of the metabolic abnormalities in liver disease induced by alcohol.9,10) Under normal conditions, acetaldehyde is rapidly converted to acetate by ADH, and therefore very low level of acetaldehyde should remain in the liver tissue or blood. ALDH also plays an important role in the elimination of acetaldehyde through oxidative reactions.11) Therefore, the severity of liver diseases can be proportional to reductions in ADH or ALDH activities. 2,12) Development of fatty liver and hyperlipidemia frequently occurs in chronic alcoholics; mainly because ethanol becomes a preferred fuel for the liver and displaces fat as a source of energy, which results in fat accumulation. Furthermore, the redox state secondary to ethanol oxidation is altered, promotings lipogenesis through increasing a-glycerophosphate and acylglycerols. The depressed oxidative capacity of mitochondria caused by chronic alcohol also contributes to fatty liver. Increasing fat accumulations in the liver can also stimulate secretion of lipoproteins into the bloodstream, facilitating the development of hyperlipidemia. Acetyl CoA carboxylase (ACC) is an enzyme that catalyzes the first step in fatty acids biosynthesis and is a rate-limiting enzyme in lipogenesis.5,13) Moreover, malic enzyme (ME), glucose-6-phosphate dehydrogenase (G6PDH), and 6-phosphoglucuronic acid dehydrogenase (6-PGDH) are also involved in lipogenesis by supplying NADPH, an essential cofactor for fatty acids and cholesterol biosynthesis. Alcohol has also been suggested ...

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“…Generation of free radicals during ethanol oxidation by cytochrome P4502E1 is an important step in the pathogenesis of ethanol-associated liver injury [30]. CYP2E1 is likely to play a critical role in promoting the generation of ROS, resulting in hepatocyte damage, which is primarily blocked by anti-oxidant enzymes, especially at the pericentral area [31]. Therefore, inhibition of the CYP2E1 pathway is critical for protection against ethanol-induced liver injury [32].…”

Section: Discussionmentioning

confidence: 99%

Ascorbic Acid Attenuates Acute Ethanol-Induced Liver Injury in SMP30 Knockout Mice

Cho¹,

Ullah²,

Elfadl³

et al. 2017

FNS

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Ascorbic acid (AA) is recognized as a free radical scavenger that protects cells from oxidative stress-induced damage. However, no studies have investigated the role of AA in acute alcoholic liver disease using senescence marker protein-30 (SMP30) knockout (KO) mice. SMP30 is a novel 34-kDa protein involved in AA biosynthesis. The present study aimed to elucidate the physiological functions of AA in acute ethanol-induced liver injury using SMP30 KO mice, which cannot synthesize AA in vivo. After a 4-week experimental period, mice were divided into six groups. The following three groups comprised the ethanol treatment groups: WT-E group (wild-type), KV-E group (AA-supplemented), and KT-E group (AA-deficient). Mice were exposed to an acute dose of ethanol (6 g ethanol/kg) administered by gavage once a day for three days. The other three control groups, namely, WT-C, KV-C, and KT-C control groups, received an equal volume of water via oral administration. Analysis of changes in body weight showed that mice in the KT-E group had significant loss of body weight compared to the control, KV-E, and WT-E groups. Behavioral analysis revealed that alcohol exposure significantly increased alcohol sensitivity in the KT-E group, whereas the WT-E, KV-E, and control groups developed ethanol tolerance. Aspartate transaminase (AST) levels in the KT-E group were significantly higher than those in the control, KV-E, and WT-E groups. The number of large and binucleated hepatocytes was significantly higher in the KT-E group than in the KV-E and WT-E groups. In addition, cytochrome P450 2E1 (CYP2E1) was over expressed in the central vein in the KT-E group when compared to the KV-E and WT-E groups. Our current findings indicate that AA supplementation in SMP30 KO mice can alleviate alcohol-induced liver damage by down regulating CYP2E1 expression. These results suggest that reduced CYP2E1 expression is a novel How to cite this paper:

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

Cited by 55 publications

References 20 publications

Effects of Benzo(a)pyrene and Ethanol on Morphology and Antioxidant Status and Transaminases in Rat Liver

Effects of Benzo(a)pyrene and Ethanol on Morphology and Antioxidant Status and Transaminases in Rat Liver

Glycoprotein Isolated from Acanthopanax senticosus Protects against Hepatotoxicity Induced by Acute and Chronic Alcohol Treatment

Ascorbic Acid Attenuates Acute Ethanol-Induced Liver Injury in SMP30 Knockout Mice

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