Alcohol-induced oxidative stress

Das, Subir Kumar; Vasudevan, DM

doi:10.1016/j.lfs.2007.05.005

Cited by 509 publications

(405 citation statements)

References 143 publications

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“…Indeed, a critical role for ethanol in promoting apoptotic events in various cell lines and animal models has been well documented. [20][21][22][23][24][25][26][27][28][29] Also, ethanol stimulates the TRAIL-induced apoptosis in leukemic T-lymphocytes and colon cancer cells in vitro. 38,39 Despite these data, an interactive effect of ethanol and TRAIL in promoting PCa cell death has not been studied.…”

Section: Discussionmentioning

confidence: 99%

“…In a dose-dependent manner it promotes lead-induced oxidative stress and induces apoptosis in neuronal cells. [27][28][29] Ethanol also promotes apoptosis through inhibition of mitogenic growth factor signaling, glutathione depletion, DNA damage and endoplasmic reticulum stress. [30][31][32][33][34] Clinical studies examining the benefit of prostatic injection with ethanol for symptomatic BPH have demonstrated significant postsurgical improvements.…”

Section: Introductionmentioning

confidence: 99%

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Ethanol promotes cytotoxic effects of tumor necrosis factor-related apoptosis-inducing ligand through induction of reactive oxygen species in prostate cancer cells

Plante

Arscott

Folsom

et al. 2012

Prostate Cancer Prostatic Dis

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BACKGROUND: Effective treatment of prostate cancer (PCa) remains a major challenge due to chemoresistance to drugs including tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Ethanol and ethanol extracts are known apoptosis inducers. However, cytotoxic effects of ethanol on PCa cells are unclear. METHODS: In this study we utilized PC3 and LNCaP cell culture models. We used immunohistochemical analysis, western blot analysis, reactive oxygen species (ROS) measurement, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) Cell Proliferation Assay, Annexin-V staining and flow cytometry for quantification of apoptosis. In vitro soft agar colony formation and Boyden chamber invasion assays were used. Tumorigenicity was measured in a xenotransplantation mouse model. RESULTS: Here, we demonstrate that ethanol enhances the apoptosis-inducing potential of TRAIL in androgen-resistant PC3 cells and sensitizes TRAIL-resistant, androgen sensitive LNCaP cells to apoptosis through caspase activation, and a complete cleavage of poly (ADP)-ribose polymerase, which was in association with increased production of ROS. The cytotoxicity of ethanol was suppressed by an antioxidant N-acetyl cystein pretreatment. Furthermore, ethanol in combination with TRAIL increased the expression of cyclin-dependent kinase inhibitor p21 and decreased the levels of Bcl-2 and phosphorylated-AKT. These molecular changes were accompanied by decreased proliferation, anchorage-independent growth and invasive potential of PC3 and LNCaP cells. In vivo studies using a xenotransplantation mouse model with PC3 cells demonstrated significantly increased apoptosis in tumors treated with ethanol and TRAIL in combination. CONCLUSIONS: Taken together, use of ethanol in combination with TRAIL may be an effective strategy to augment sensitivity to TRAIL-induced apoptosis in PCa cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ethanol promotes cytotoxic effects of tumor necrosis factor-related apoptosis-inducing ligand through induction of reactive oxygen species in prostate cancer cells

Plante

Arscott

Folsom

et al. 2012

Prostate Cancer Prostatic Dis

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“…The amount and type of alcohol consumed and the frequency of its consumption can vary tremendously and can have divergent effects on an organism (1,2). The deleterious effects of alcohol, at least partly, involve alcohol induced oxidative injury that has been documented by measurement of oxidant radicals (3)(4)(5). The organism has developed a complex defense system which is composed of free radical scavenger molecules such as vitamins and antioxidative enzymes.…”

Section: Introductionmentioning

confidence: 99%

Trolox reduces the effect of ethanol on acetylcholine-induced contractions and oxidative stress in the isolated rabbit duodenum

Gonzálo

Grasa

et al. 2011

Rev. esp. enferm. dig.

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Trolox is a hydrophilic analogue of vitamin E and a free radical scavenger. Ethanol diminishes the amplitude of spontaneous contractions and acetylcholine (ACh)-induced contractions in rabbit duodenum. The aim of this work was to study the effect of trolox on the alterations induced by ethanol on contractility and lipid peroxidation in the duodenum. The duodenal contractility studies in vitro were carried out in an organ bath and the levels of malondialdehyde and 4-hydroxyalkenals (MDA+4-HAD) were measured by spectrophotometry. Trolox increased the reduction induced by ethanol on the amplitude of spontaneous contractions in longitudinal muscle but not in circular muscle. Trolox 4 mM decreased the effects of ethanol on ACh-induced contractions and on MDA+4-HDA concentrations. We conclude that trolox might prevent oxidative stress induced by ethanol in the duodenum. INTRODUCTIONAlcohol is a hydroxyl compound that can be present in the diet. The amount and type of alcohol consumed and the frequency of its consumption can vary tremendously and can have divergent effects on an organism (1,2). The deleterious effects of alcohol, at least partly, involve alcohol induced oxidative injury that has been documented by measurement of oxidant radicals (3-5). The organism has developed a complex defense system which is composed of free radical scavenger molecules such as vitamins and antioxidative enzymes.Ethanol induces inhibition of esophageal, gastric and intestinal contractility (6-9). The inhibition produced by ethanol is attributed to an inhibition of Ca 2+ influx in the canine jejunal circular muscle and in human and cat esophageal contractility (7,8). Alcohol also inhibits the motility of the sphincter of Oddi in vitro (10,11) and the colon (12). In a previous study, we demonstrated the inhibitory effects of ethanol on the spontaneous contractions and ACh-induced contractions in rabbit duodenum, which are reduced by Ca 2+ -activated K + channel antagonists (13). Ethanol also provokes an inhibition of gastric emptying and small intestinal transit that is mediated by type A CCK receptors or capsaicin-sensitive neural pathways (14-16). However, ethanol produces contractile actions in guinea pig gastric smooth muscle, which required extracellular calcium and are blocked by tyrosine kinase inhibitors (17).Trolox, a phenolic antioxidant, originally designed for food preservation, has a chromane structure similar to atocopherol or vitamin E (18,19). Trolox decreases hepatocellular damage during sepsis (20) and abrogates oxidative stress during cold small bowel storage (21).Although antioxidants can attenuate alcohol-induced injury, there is no single antioxidant that protects all organs during all modes of exposure (3). There is very little documentation available on the effect of trolox on intestinal motility. In addition, alcohol induces oxidative stress and REV ESP ENFERM DIG (Madrid) Vol. 103. N.° 8, pp. 396-401, 2011 Received: 10-01-11. Accepted: 18-03-11.

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“…of chronic, excessive alcohol exposure is associated with diverse organ damage across the liver, heart, pancreas, and brain, implicating several processes including acetaldehyde formation, disturbed calcium and iron regulation, epigenetic modifications, and oxidative stress (2,3). However, despite advances in understanding the consequences of excessive alcohol intake, a paucity of neural targets have been identified with translatable potential for pharmacotherapy.…”

mentioning

confidence: 99%

“…First, markers of greater oxidative stress (2,17,18) and predisposition to apoptosis (19)(20)(21) may be present in brain and other organs in AD, and oxidative stress and mitochondrial toxicity lead to elevated MAO-A levels in neuroblastoma and glioblastoma cell lines (4,(22)(23)(24). Second, a microarray analysis evaluating the effects of chronic alcohol vapor exposure in rodents reported a 2.5-fold elevation in MAO-A messenger (m)RNA in the prefrontal cortex (25).…”

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confidence: 99%

Greater Monoamine Oxidase A Binding in Alcohol Dependence

Matthews

Kish

et al. 2014

Biological Psychiatry

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Background-Alcohol dependence (AD) is a multiorgan disease in which excessive oxidative stress and apoptosis are implicated. Monoamine oxidase A (MAO-A) is an important enzyme on the outer mitochondrial membrane that participates in the cellular response to oxidative stress and mitochondrial toxicity. It is unknown whether MAO-A levels are abnormal in AD. We hypothesized that MAO-A V T , an index of MAO-A level, is elevated in the prefrontal cortex (PFC) during AD, because markers of greater oxidative stress and apoptosis are reported in the brain in AD and a microarray analysis reported greater MAO-A messenger RNA in the PFC of rodents exposed to alcohol vapor.

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Alcohol-induced oxidative stress

Cited by 509 publications

References 143 publications

Ethanol promotes cytotoxic effects of tumor necrosis factor-related apoptosis-inducing ligand through induction of reactive oxygen species in prostate cancer cells

Ethanol promotes cytotoxic effects of tumor necrosis factor-related apoptosis-inducing ligand through induction of reactive oxygen species in prostate cancer cells

Trolox reduces the effect of ethanol on acetylcholine-induced contractions and oxidative stress in the isolated rabbit duodenum

Greater Monoamine Oxidase A Binding in Alcohol Dependence

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