Oxidative stress and antioxidant defenses in ethanol-induced cell injury

Koch, Osvaldo R.; Pani, Giovambattista; Borrello, Silvia; Colavitti, Renata; Cravero, Amerys; Farré, Stella M.; Galeotti, T.

doi:10.1016/j.mam.2004.02.019

Cited by 227 publications

(148 citation statements)

References 26 publications

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“…Indeed, reactive oxygen species (ROS) cause lipid peroxidation, a process that results in the degradation of cellular membranes and the generation of endogenous toxins, such as free radicals and over 200 species of electrophilic aldehydes [14]. These aldehydes mediate various toxic effects, such as GSH depletion, protein/DNA adduction and impaired cellular homeostasis, and they have been implicated in many pathological states, including neurodegenerative diseases [21] and alcoholic liver disease [22]. ALDH-mediated detoxification of aldehyde products of lipid peroxidation, therefore, represents a critical defense.…”

Section: Discussionmentioning

confidence: 99%

Expression and initial characterization of human ALDH3B1

Marchitti

Orlicky

Vasiliou

2007

Biochemical and Biophysical Research Communications

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Aldehyde dehydrogenases (ALDHs) are critical enzymes in the metabolism of endogenous and exogenous aldehydes. The human genome contains nineteen putatively functional ALDH genes; ALDH3B1 belongs to the ALDH3 family. While recent studies have linked the ALDH3B1 locus to schizophrenia, nothing was known, until now, about the properties and significance of the ALDH3B1 protein. The aim of this study was to characterize the ALDH3B1 protein. Human ALDH3B1 was baculovirus-expressed and found to be catalytically active towards medium-and long-chain aliphatic aldehydes and the aromatic aldehyde benzaldehyde. Western blot analyses indicate that ALDH3B1 is highly expressed in kidney and liver and moderately expressed in various brain regions. ALDH3B1-transfected HEK293 cells were significantly protected against cytotoxicity induced by the lipid-peroxidation product octanal when compared to vector-transfected cells. This study shows for the first time the functionality, expression and protective role of ALDH3B1 and indicates a potential physiological role of ALDH3B1 against oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Expression and initial characterization of human ALDH3B1

Marchitti

Orlicky

Vasiliou

2007

Biochemical and Biophysical Research Communications

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“…24,25) Levels of TG in serum or liver tissue increased from alcohol consumption due to several processes, including increased availability of free fatty acids and L-glycerophosphate, decreased secretion of VLDL into the serum, and decreased removal of TG and CHOL from serum due to diminished lipoprotein activity. 25,26) Furthermore, ADH, which primarily proceeds hepatic oxidation of ethanol to acetaldehyde, reduces NAD ϩ to NADH, and produces a striking redox change associated with metabolic disorders; reducing equivalents of NAD ϩ /NADH inhibit the TCA cycle and fatty acid oxidation, resulting in hepatic lipogenesis.…”

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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“…Reactive oxygen species can originate from endogenous sources such as leukocytes and immature spermatozoa [Aitken and West 1990;Kessopoulou et al 1992;Shekarriz et al 1995], as well as, exogenous sources such as industrial compounds, smoking, and alcohol [Acharya et al 2003;Agarwal and Saleh 2002;Kasahara et al 2002;Koch et al 2004;Kothari et al 2010;Saleh et al 2002b]. In infertile men, the mitochondrion is a major source of endogenous ROS production, which can result in DNA damage and apoptosis in spermatozoa [Barroso et al 2000;Koppers et al 2008].…”

Section: Introductionmentioning

confidence: 99%

Cytosolic and mitochondrial ROS: which one is associated with poor chromatin remodeling?

Kiani-Esfahani¹,

Bahrami²,

Tavalaee³

et al. 2013

Systems Biology in Reproductive Medicine

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The aim of this study was to determine if there are any associations between impaired chromatin packaging and the origin of reactive oxygen species (ROS) production. Cytosolic ROS, mitochondrial ROS, DNA protamination, and apoptosis were evaluated with dichlorofluoresceindiacetate (DCFH-DA), dihydrorhodamine 123 (DHR123), chromomycin A3 (CMA3), and YO-Pro-1 (Y1)/propidium iodide (PI), respectively, by flow cytometry (FCM) in 40 infertile individuals. Percentages DCF+ and R123+ sperm were positively associated with percentage CMA3+ sperm and negatively associated with percentage apoptotic sperm. No correlation was observed between CMA3+ sperm and the percentage of apoptotic sperm. Under protamination of sperm is not associated with the origin of ROS production, but their relationship may suggest an association with general physiological dysfunction of sperm. Furthermore, under protamination does make sperm prone to apoptosis. Rather, it is likely that apoptosis is induced by ROS production. Considering that these conclusions are derived from correlative analyses, additional studies including an interventive approach are required.

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Oxidative stress and antioxidant defenses in ethanol-induced cell injury

Cited by 227 publications

References 26 publications

Expression and initial characterization of human ALDH3B1

Expression and initial characterization of human ALDH3B1

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

Cytosolic and mitochondrial ROS: which one is associated with poor chromatin remodeling?

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