Nitroxyl affords thiol-sensitive myocardial protective effects akin to early preconditioning

Pagliaro, Pasquale; Mancardi, Daniele; Rastaldo, Raffaella; Penna, Cláudia; Gattullo, D; Miranda, Katrina M.; Feelisch, Martin; Wink, David A.; Kass, David A.; Paolocci, Nazareno

doi:10.1016/s0891-5849(02)01179-6

Cited by 193 publications

(207 citation statements)

References 53 publications

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“…The methods were similar to those previously described [45,[50][51][52][53][54]. In brief, each animal was anesthetized.…”

Section: Isolated Heart Perfusionmentioning

confidence: 99%

“…Since in isolated hearts, pre and postconditioning are known to reduce the release of lactatedehydrogenase (LDH) during reperfusion, the release of LDH was measured during the 2 hours of reperfusion as previously described [45,49,51,53]. Infarct areas were also assessed at the end of the experiment with the nitro-blu-tetrazolium technique (Sigma-Aldrich) as described [45,49,51,53,54].…”

Section: Assessment Of Myocardial Injurymentioning

confidence: 99%

“…Infarct areas were also assessed at the end of the experiment with the nitro-blu-tetrazolium technique (Sigma-Aldrich) as described [45,49,51,53,54]. The necrotic mass was expressed as a percentage of total left ventricular mass (i.e., risk area).…”

Section: Assessment Of Myocardial Injurymentioning

confidence: 99%

“…Therefore a vicious cycle is likely to be established in the so-called ROS-induced ROS release (RIRR) [26,27,34]; thus inducing ROS stress and reperfusion injury [for reviews see 46,50]. Survival mechanisms in the heart can be triggered by short, non-lethal periods of ischemia and reperfusion, applied either before (preconditioning) or immediately after (postconditioning, PostC) the index ischemia [3,10,20,25,33,[44][45][46]62]. Both in vivo and in vitro ischemic-and pharmacologicalpreconditioning triggering require protective ROS signaling.…”

Section: Introductionmentioning

confidence: 99%

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Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Penna

Perrelli

Tullio

et al. 2011

Pflugers Arch - Eur J Physiol

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Postconditioning (PostC) modifies early post-ischemic pH, redox-environment and activity of enzymes. We hypothesized that early acidosis in PostC may affect superoxide-dismutase (SOD) and catalase(CAT) activities, may reduce 3-nitrotyrosine(3-NT)-and may increase S-nitrosylated (SNO)-protein levels, thus deploying its protective effects. To verify this hypothesis, we studied early (7 th min) and late (120 th min) phases of reperfusion a) endogenous-SOD and -CAT activities, and b) 3-NT-and SNO-protein levels. Isolated rat hearts underwent 30-min ischemia/120-min reperfusion(I/R) or PostC (5 cycles of 10-s I/R at the beginning of 120-min reperfusion) either with or without exogenous-CAT or -SOD infused during the initial 3-min of reperfusion. The effects of early reperfusion with acidic-buffer(AB, pH 6.8) on endogenous antioxidant-enzymes were also tested. Pressure, infarct-size and lactate-dehydrogenase release were also measured. At the 7 th min, PostC induced a significant decrease in SOD-activity with no major change in both Mn-and Cu/Zn-SOD levels, and in CAT-activity and level. PostC also reduced 3-NT and increased SNO levels. Exogenous-SOD, but not -CAT abolished PostCcardioprotection. In late reperfusion(120-min), I/R increased SOD-activity, but decreased CATactivity and Cu/Zn-SOD levels; these effects were reversed by PostC; 3-NT was not affected, but SNO was increased by PostC. AB reproduced PostC effects on antioxidant-enzymes.Conclusions: PostC downregulates endogenous-SOD and preserves -CAT activity, thus increasing SNO and reducing 3-NT levels. These effects are triggered by early post-ischemic acidosis. Yet acidosis-induced SOD-downregulation may limit denitrosylation; thus contributing to PostC-triggering. Hence, exogenous-SOD, but not -CAT, interferes with PostC-triggering.Persistent SOD-downregulation and SNO-increase may contribute to PostC and AB beneficial effects.

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“…The methods were similar to those previously described [45,[50][51][52][53][54]. In brief, each animal was anesthetized.…”

Section: Isolated Heart Perfusionmentioning

confidence: 99%

Section: Assessment Of Myocardial Injurymentioning

confidence: 99%

Section: Assessment Of Myocardial Injurymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Penna

Perrelli

Tullio

et al. 2011

Pflugers Arch - Eur J Physiol

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“…For example, the one-electron-reduced form of NO, known as nitroxyl or hyponitrous acid (HNO) is more reactive than NO, especially with nucleophilic thiols and thus mediates their oxidation. Nitroxyl is known to have cardioprotective properties offering a similar degree of protection to ischemic preconditioning [18]. In the absence of thiols, nitroxyl (HNO) may dimerise to H 2 N 2 O 2 , which can then decompose to nitrous oxide (N 2 O), which has well established anaesthetic and analgesic effects.…”

Section: Molecular Species That Alter Cellular Redoxmentioning

confidence: 99%

Redox signalling in cardiovascular disease

Charles

Eaton

2008

Proteomics Clinical Apps

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Oxidative stress has almost universally and unequivocally been implicated in the pathogenesis of all major diseases, including those of the cardiovascular system. Oxidative stress in cells and cardiovascular biology was once considered only in terms of injury, disease and dysfunction. However, it is now appreciated that oxidants are also produced in healthy tissues, and they function as signalling molecules transmitting information throughout the cell. Conversely, when cells move to a more reduced state, as can occur when oxygen is limiting, this can also result in alterations in the function of biomolecules and subsequently cells. At the centre of this 'redox signalling' are oxidoreductive chemical reactions involving oxidants or reductants post translationally modifying proteins. These structural alterations allow changes in cellular redox state to be coupled to alterations in cell function. In this review, we consider aspects of redox signalling in the cardiovascular system, focusing on the molecular basis of redox sensing by proteins and the array of post-translational oxidative modifications that can occur. In addition, we discuss studies utilising proteomic methods to identify redox-sensitive cardiac proteins, as well as those using this technology more broadly to assess redox signalling in cardiovascular disease.

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N-Hydroxybenzenesulfonamide

Shenvi¹

2010

Encyclopedia of Reagents for Organic Synthesis

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Nitroxyl affords thiol-sensitive myocardial protective effects akin to early preconditioning

Cited by 193 publications

References 53 publications

Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Post-ischemic early acidosis in cardiac postconditioning modifies the activity of antioxidant enzymes, reduces nitration, and favors protein S-nitrosylation

Redox signalling in cardiovascular disease

N-Hydroxybenzenesulfonamide

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