Late preconditioning by ethanol is initiated via an oxidant-dependent signaling pathway

Yamaguchi, Takeshi; Dayton, Catherine; Ross, Christopher; Yoshikawa, Toshikazu; Gute, Dean C.; Korthuis, Ronald J.

doi:10.1016/s0891-5849(02)01292-3

Cited by 25 publications

(54 citation statements)

References 65 publications

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“…Mitochondrial Ca 2ϩ uptake upregulates energy metabolism, resulting in increased generation of reactive oxygen species, although the mechanism (70) and temporal pattern of oxidant production by excitotoxicity (69) remains uncertain. The antioxidant MnTBAP [Mn(III)tetra(4-carboxyphenyl)porphyrin] suppresses ischemic tolerance by ischemic (30) and nonischemic preconditioning (37,74) in nonneuronal tissue, consistent with oxygen radicals functioning as general mediators of preconditioning (66). Reactive oxygen speciesdependent hypoxic preconditioning in cardiomyocytes is suppressed by an anion channel blocker, 4,4Ј-diisothiocyanostilbene-2,2Ј-disulfonic acid (DIDS), implicating superoxide transfer to the cytosol via mitochondrial anion channels (68).…”

Section: N-methyl-d-aspartate; Camentioning

confidence: 91%

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Preconditioning of cortical neurons by oxygen-glucose deprivation: tolerance induction through abbreviated neurotoxic signaling

Tauskela

Brunette

Monette

et al. 2003

American Journal of Physiology-Cell Physiology

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Transient exposure of rat cortical cultures to nonlethal oxygen-glucose deprivation (OGD preconditioning) induces tolerance to otherwise lethal oxygen-glucose deprivation (OGD) or N-methyl-d-aspartate 24 h later. This study evaluates the role of cytosolic and mitochondrial Ca2+-dependent cellular signaling. Mechanistic findings are placed in context with other models of ischemic preconditioning or known neurotoxic pathways within cortical neurons. Tolerance to otherwise lethal OGD is suppressed by performing OGD preconditioning in the presence of the broad-scope catalytic antioxidants Mn(III)tetra(4-carboxyphenyl)porphyrin (MnTBAP) or Zn(II)tetra(4-carboxyphenyl)porphyrin [Zn(II)TBAP], but not by a less active analog, Mn(III)tetra(4-sulfonatophenyl)porphyrin, or a potent superoxide scavenger, Mn(III)tetra( N-ethyl-2-pyridyl)porphyrin chloride. Inhibitors of adenosine A1 receptors, nitric oxide synthase, mitogen-activated protein kinase, and poly(ADP-ribose) polymerase fail to suppress OGD preconditioning despite possible links with reactive oxygen species in other models of ischemic preconditioning. Preconditioning is suppressed by 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS), which has been ascribed elsewhere to inhibition of superoxide transport to the cytosol through mitochondrial anion channels. However, although it induces mitochondrial Ca2+ uptake, neuronal preconditioning is largely insensitive to mitochondrial uncoupling with carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone or 2,4-dinitrophenol. Un-couplers will prevent production of mitochondrial reactive oxygen species, implying nonmitochondrial targets by MnTBAP, Zn(II)TBAP, and DIDS. Emphasizing the importance of an increase in cytosolic Ca2+ during preconditioning, a Ca2+/calmodulin-dependent protein kinase II inhibitor, KN-62, suppresses development of subsequent tolerance. Summarizing, only those cellular transduction pathways that have the potential to be neurotoxic may be activated by preconditioning in cortical neurons. Finally, a marked decrease in extracellular glutamate is observed during otherwise lethal OGD in preconditioned cultures, suggesting that this end effector may represent a point of convergence across different preconditioning models.

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Section: N-methyl-d-aspartate; Camentioning

confidence: 91%

“…Consequently, MnTBAP likely suppresses preconditioning by mitochondrial-independent scavenging of oxygen radicals. In studies reporting inhibition of preconditioning by MnTBAP, a potential link with mitochondrial production of oxidants has not been investigated (30,37,74).…”

Section: Mitochondria-independent Preconditioningmentioning

confidence: 99%

Preconditioning of cortical neurons by oxygen-glucose deprivation: tolerance induction through abbreviated neurotoxic signaling

Tauskela

Brunette

Monette

et al. 2003

American Journal of Physiology-Cell Physiology

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“…Ethanol preconditioning (EtOH-PC) was induced by gavaging animals with a moderate dose of ethanol (volume ethanol in µl calculated from the relation: body weight (in g) × 0.6] + 0.3) 24 hrs before ischemia, as we have previously described (13,18). This volume of ethanol (95% in µl) was mixed in 0.3 ml of sterile distilled water before gavage.…”

Section: Production Of Ethanol Preconditioningmentioning

confidence: 99%

“…However, it is becoming increasingly apparent that these reactive molecules can also participate in a number of normal physiologic phenomena (16,17). Indeed, we have demonstrated a role for ethanol-induced NADPH oxidase-derived oxidants in the appearance of anti-adhesive and anti-inflammatory phenotype in postcapillary venules that becomes apparent on subsequent exposure to I/R (13,18,19). However, whether ethanol also exerts neuroprotective effects in stroke is unknown.…”

Section: Introductionmentioning

confidence: 98%

“…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%

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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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Antecedent Ethanol Ingestion Prevents Postischemic Leukocyte Adhesion and P-Selectin Expression by a Protein Kinase C?Dependent Mechanism

et al. 2005

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The aim of this study was to determine whether protein kinase C (PKC) contributed to the effects of ethanol ingestion to prevent P-selectin expression, leukocyte rolling (LR), and stationary leukocyte adhesion (LA) induced by subjecting the small bowel to ischemia and reperfusion (I/R) 24 hr later. I/R increased P-selectin expression, LR, and LA, effects that were largely abolished by antecedent ethanol consumption. Exposing the bowel to a specific but nonisoform-selective PKC inhibitor (chelerythrine or bisindolylmaleimide I) during the period of ethanol exposure did not alter the anti-inflammatory effects induced by ethanol ingestion 24 hr prior to I/R. Go-6976, a PKC inhibitor that exhibits a high degree of selectivity for the calcium-dependent PKC isoforms, markedly reduced the effectiveness of antecedent ethanol exposure to abrogate these postischemic inflammatory responses. Our data indicate that antecedent ethanol exposure prevents postischemic P-selectin expression, LR, and LA by a mechanism that involves activation of calcium-dependent PKC isotypes.

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Late preconditioning by ethanol is initiated via an oxidant-dependent signaling pathway

Cited by 25 publications

References 65 publications

Preconditioning of cortical neurons by oxygen-glucose deprivation: tolerance induction through abbreviated neurotoxic signaling

Preconditioning of cortical neurons by oxygen-glucose deprivation: tolerance induction through abbreviated neurotoxic signaling

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

Antecedent Ethanol Ingestion Prevents Postischemic Leukocyte Adhesion and P-Selectin Expression by a Protein Kinase C?Dependent Mechanism

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