NADPH oxidase inhibition prevents cocaine-induced up-regulation of xanthine oxidoreductase and cardiac dysfunction

Isabelle, Marc; Vergeade, Aurélia; Moritz, Fabienne; Dautreaux, Brigitte; Henry, Jean‐Paul; Lallemand, Françoise; Richard, Vincent; Mulder, Paul; Thuillez, Christian; Monteil, Christelle

doi:10.1016/j.yjmcc.2006.11.011

Cited by 47 publications

(56 citation statements)

References 34 publications

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“…However, DPI is a relatively non-specific inhibitor and it is possible that other flavoprotein reductase enzymes are contributing to nitric oxide formation. We show that apocynin, an inhibitor of the NADPH oxidase, a flavoprotein reductase [29], abolishes nitrite-induced cardioprotection. This novel finding may explain why DPI abolishes the protective effect of nitrite and identifies a component of another mechanism by which nitrite may confer its salubrious actions.…”

Section: Discussionmentioning

confidence: 77%

Nitrite confers protection against myocardial infarction: Role of xanthine oxidoreductase, NADPH oxidase and KATP channels

Baker

et al. 2007

Journal of Molecular and Cellular Cardiology

120

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Reduction of nitrite to nitric oxide during ischemia protects the heart against injury from ischemia/ reperfusion. However the optimal dose of nitrite and the mechanisms underlying nitrite-induced cardioprotection are not known. We determined the ability of nitrite and nitrate to confer protection against myocardial infarction in two rat models of ischemia/reperfusion injury and the role of xanthine oxidoreductase, NADPH oxidase, nitric oxide synthase and K ATP channels in mediating nitrite-induced cardioprotection. In vivo and in vitro rat models of myocardial ischemia/reperfusion injury were used to cause infarction. Hearts (n=6/group) were treated with nitrite or nitrate for 15 min prior to 30 min regional ischemia and 180 min reperfusion. Xanthine oxidoreductase activity was measured after 15 min aerobic perfusion and 30 min ischemia. Nitrite reduced myocardial necrosis and decline in ventricular function following ischemia/reperfusion in the intact and isolated rat heart in a dose or concentration-dependent manner with an optimal dose of 4 mg/kg in vivo and concentration of 10 μM in vitro. Nitrate had no effect on protection. Reduction in infarction by nitrite was abolished by inhibition of flavoprotein reductases and the molybdenum site of xanthine oxidoreductase, and was associated with an increase in activity of xanthine dehydrogenase and xanthine oxidase during ischemia. Inhibition of nitric oxide synthase had no effect on nitrite-induced cardioprotection. Inhibition of NADPH oxidase and K ATP channels abolished nitrite-induced cardioprotection. Nitrite but not nitrate protects against infarction by a mechanism involving xanthine oxidoreductase, NADPH oxidase and K ATP channels.

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Section: Discussionmentioning

confidence: 77%

Nitrite confers protection against myocardial infarction: Role of xanthine oxidoreductase, NADPH oxidase and KATP channels

Baker

et al. 2007

Journal of Molecular and Cellular Cardiology

120

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“…Xanthine oxidase (XO), a key enzyme of purine catabolism, is responsible for the generation of reactive oxygen species (ROS) via several pathways that include nitric oxide (NO) and calcium signaling 7, 8. Intracellular Ca 2+ handling is a critical regulator of action potential duration, and mechanical activity of cardiomyocytes via excitation‐contraction coupling 9.…”

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confidence: 99%

Xanthine Oxidase Inhibitor Allopurinol Prevents Oxidative Stress‐Mediated Atrial Remodeling in Alloxan‐Induced Diabetes Mellitus Rabbits

Yang

Zhao

Qiu

et al. 2018

JAHA

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BackgroundThere are several mechanisms, including inflammation, oxidative stress and abnormal calcium homeostasis, involved in the pathogenesis of atrial fibrillation. In diabetes mellitus (DM), increased oxidative stress may be attributable to higher xanthine oxidase activity. In this study, we examined the relationship between oxidative stress and atrial electrical and structural remodeling, and calcium handling abnormalities, and the potential beneficial effects of the xanthine oxidase inhibitor allopurinol upon these pathological changes.Methods and ResultsNinety rabbits were randomly and equally divided into 3 groups: control, DM, and allopurinol‐treated DM group. Echocardiographic and hemodynamic assessments were performed in vivo. Serum and tissue markers of oxidative stress and atrial fibrosis, including the protein expression were examined. Atrial interstitial fibrosis was evaluated by Masson trichrome staining. ICaL was measured from isolated left atrial cardiomyocytes using voltage‐clamp techniques. Confocal microscopy was used to detect intracellular calcium transients. The Ca2+ handling protein expression was analyzed by Western blotting. Mitochondrial‐related proteins were analyzed as markers of mitochondrial function. Compared with the control group, rabbits with DM showed left ventricular hypertrophy, increased atrial interstitial fibrosis, oxidative stress and fibrosis markers, ICaL and intracellular calcium transient, and atrial fibrillation inducibility. These abnormalities were alleviated by allopurinol treatment.ConclusionsAllopurinol, via its antioxidant effects, reduces atrial mechanical, structural, ion channel remodeling and mitochondrial synthesis abnormalities induced by DM‐related increases in oxidative stress.

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“…It has been discovered recently that cocaine administration is associated with severe oxidative stress in the heart (Moritz et al, 2003;Pacifici et al, 2003;Kovacic, 2005;Ren et al, 2006;Isabelle et al, 2007). Although there are several potential enzymatic sources of ROS existing in the heart, in an animal model of chronic cocaine administration, treatment with apocynin (an NADPH oxidase inhibitor) has been reported to be effective in reducing ROS generation and to restore the cardiac output, stroke volume, and fractional shortening, suggestive of the involvement of an NADPH oxidase (Isabelle et al, 2007).…”

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confidence: 99%

Chronic Cocaine-Induced Cardiac Oxidative Stress and Mitogen-Activated Protein Kinase Activation: The Role of Nox2 Oxidase

Fan¹,

Sawbridge²,

George³

et al. 2008

J Pharmacol Exp Ther

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Chronic cocaine exposure is associated with severe cardiac complications, but the mechanisms of cocaine cardiotoxicity remain unclear, and current therapies are unsatisfactory. We investigated the hypothesis of oxidative stress-mediated cardiotoxicity and the role of NADPH oxidase in this process in a mouse model of chronic escalating "binge" cocaine administration (milligrams per kilogram): days 1 to 4 at 3 ϫ 15 mg, days 5 to 8 at 3 ϫ 20 mg, days 9 to 12 at 3 ϫ 25 mg, and days 13 to 14 at 3 ϫ 30 mg. Compared with vehicle controls, chronic binge cocaine administration significantly increased the cardiac NADPH-dependent O 2 . production (1.96-Ϯ 0.4-fold) as detected by tiron (an O 2 . scavenger)-inhibitable lucigenin chemiluminescence and dihydroethidium fluorescence. Cocaine-induced reactive oxygen species (ROS) production was associated with significant increases (ϳ2-fold) in the protein expressions of Nox2 (an isoform of NADPH oxidase) and its regulatory subunits: p22 phox

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NADPH oxidase inhibition prevents cocaine-induced up-regulation of xanthine oxidoreductase and cardiac dysfunction

Cited by 47 publications

References 34 publications

Nitrite confers protection against myocardial infarction: Role of xanthine oxidoreductase, NADPH oxidase and KATP channels

Nitrite confers protection against myocardial infarction: Role of xanthine oxidoreductase, NADPH oxidase and KATP channels

Xanthine Oxidase Inhibitor Allopurinol Prevents Oxidative Stress‐Mediated Atrial Remodeling in Alloxan‐Induced Diabetes Mellitus Rabbits

Chronic Cocaine-Induced Cardiac Oxidative Stress and Mitogen-Activated Protein Kinase Activation: The Role of Nox2 Oxidase

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