Cardioprotective effect of chronic low dose ethanol drinking: Insights into the concept of ethanol preconditioning

Guiraud, Annabelle; Lorgeril, Michel de; Boucher, François; Berthonneche, Corinne; Rakotovao, Andry; Leiris, Joël de

doi:10.1016/j.yjmcc.2004.02.003

Cited by 56 publications

(37 citation statements)

References 40 publications

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“…Other investigators have shown that during ischemia-reperfusion, sustained translocation of PKC-⑀ is not necessary to induce cardioprotection (49,53). PKC-⑀ translocation may thus act as a trigger rather than a mediator of cardioprotection (15).…”

Section: Discussionmentioning

confidence: 95%

Attenuation of fatty acid-induced apoptosis by low-dose alcohol in neonatal rat cardiomyocytes

Sparagna¹,

Jones²,

Hickson-Bick³

2004

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Discussionmentioning

confidence: 95%

Attenuation of fatty acid-induced apoptosis by low-dose alcohol in neonatal rat cardiomyocytes

Sparagna¹,

Jones²,

Hickson-Bick³

2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Moderate ethanol consumption, defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) as an average consumption of one to two drinks per day (equivalent to peak blood alcohol levels of~10 mM ethanol), has long been known to be cardioprotective in a variety of animal models [16][17][18], and a contribution of purinergic signaling has been implicated in many of these studies.…”

Section: Introductionmentioning

confidence: 99%

The adenosine transporter, ENT1, in cardiomyocytes is sensitive to inhibition by ethanol in a kinase-dependent manner: implications for ethanol-dependent cardioprotection and nucleoside analog drug cytotoxicity

Ramadan

Naydenova

Stevanovic

et al. 2013

Purinergic Signalling

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The adenosine transporter 1 (ENT1) transports nucleosides, such as adenosine, and cytotoxic nucleoside analog drugs. ENT1 is well established to play a role in adenosinergic signaling in the cardiovascular system by modulating adenosine levels. Moderate ethanol consumption is cardioprotective and underlying mechanisms of action are not clear although adenosinergic signaling has been implicated. Here, we show that ethanol (5-200 mM) significantly reduces ENT1-dependent [ 3 H] 2-chloroadenosine uptake (by up to 27 %) in the cardiomyocyte cell line, HL-1. Inhibition or absence of ENT1 is known to be cardioprotective, suggesting that the interaction of ethanol with ENT1 may promote adenosinergic cardioprotective pathways in the cardiovasculature.Ethanol sensitivity of adenosine uptake is altered by pharmacological activation of PKA and PKC. Primary cardiomyocytes from PKCε-null mice have significantly greater sensitivity to inhibition (by approximately 37 %) of adenosine uptake by ethanol than controls. These data suggest that the presence of ethanol may compromise ENT1-dependent nucleoside analog drug cytotoxicity, and indeed, ethanol (5 mM) reduces the cytotoxic effects of gemcitabine (2 nM), an anti-cancer drug, in the human cancer cell line, HTB2. Thus, the pharmacological inhibition of ENT1 by ethanol may contribute to ethanol-dependent cardioprotection but compromise gemcitabine cytotoxicity.

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“…Studies conducted in cultured cell and intact animal models attributed these beneficial effects to the polyphenolic antioxidants present in red wine (4)(5)(6)(7). However, there is evidence that moderate consumption of ethanol alone also exerts protective effects against injury due to cerebral and myocardial ischemia (8)(9)(10)(11)(12). Furthermore, ethanol ingestion 24 hrs prior to ischemia/reperfusion (I/R) (ethanol preconditioning or EtOH-PC) completely prevented postischemic leukocyte-endothelial cell adhesive interactions by a mechanism that involves the ability for ethanol to activate an oxidant-dependent signaling pathway (13).…”

Section: Introductionmentioning

confidence: 99%

Ethanol preconditioning protects against ischemia/reperfusion-induced brain damage: Role of NADPH oxidase-derived ROS

Wang

Sun

Simonyi

et al. 2007

Free Radical Biology and Medicine

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Ethanol preconditioning (EtOH-PC) refers to a phenomenon in which tissues are protected from the deleterious effects of ischemia/reperfusion (I/R) by prior ingestion of ethanol at low to moderate levels. In this study, we tested whether prior (24 hrs) administration of ethanol as a single bolus that produced a peak plasma concentration of 42-46 mg/dl in gerbils would offer protective effects on neuronal damage due to cerebral I/R. In addition, we also tested whether reactive oxygen species (ROS)-derived from NADPH oxidase played a role as an initiator of these putative protective effects. Groups of gerbils were administered either ethanol or the same volume of water by gavage 24 hrs prior to transient global cerebral ischemia induced by occlusion of both common carotid arteries (CCA) for 5 min. In some experiments, apocynin, a specific inhibitor of NADPH oxidase, was administered (5 mg/kg body wt, i.p.) 10 min before ethanol administration. EtOH-PC ameliorated behavioral deficit induced by cerebral I/R and protected the brain against I/R-induced delayed neuronal death (DND), neuronal and dendritic degeneration, oxidative DNA damage, and glial cell activation. These beneficial effects were attenuated by apocynin treatment coincident with ethanol administration. Ethanol ingestion was associated with translocation of the NADPH oxidase subunit, p67 phox , from hippocampal cytosol fraction to membrane, increased NADPH oxidase activity in hippocampus within the first hour after gavage, and increased lipid peroxidation (4-hydroxy-2-nonenal, HNE) in plasma and hippocampus within the first 2 hrs after gavage. These effects were also inhibited by concomitant apocynin treatment. Our data are consistent with the hypothesis that antecedent ethanol ingestion at socially-relevant levels induces neuroprotective effects in I/R by a mechanism that is triggered by ROS produced through NADPH oxidase. Our results further suggest the possibility that preconditioning with other pharmacological agents that induce a mild oxidative stress may have similar therapeutic value for suppressing stroke-mediated damage in brain.

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Cardioprotective effect of chronic low dose ethanol drinking: Insights into the concept of ethanol preconditioning

Cited by 56 publications

References 40 publications

Attenuation of fatty acid-induced apoptosis by low-dose alcohol in neonatal rat cardiomyocytes

Attenuation of fatty acid-induced apoptosis by low-dose alcohol in neonatal rat cardiomyocytes

The adenosine transporter, ENT1, in cardiomyocytes is sensitive to inhibition by ethanol in a kinase-dependent manner: implications for ethanol-dependent cardioprotection and nucleoside analog drug cytotoxicity

Ethanol preconditioning protects against ischemia/reperfusion-induced brain damage: Role of NADPH oxidase-derived ROS

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