Sulfide-hemoglobin interactions in the sulfide-tolerant salt marsh resident, the California killifish Fundulus parvipinnis

Bagarinao, Teodora; Vetter, Russell D.

doi:10.1007/bf00296642

Cited by 31 publications

(15 citation statements)

References 47 publications

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“…Sulfhemoglobin has also been reported in fish living in a sulfide-rich environment in vitro but rarely in vivo, in agreement with different independent conclusions that sulfhemoglobin is not a significant factor in cases of sulfide poisoning [42,43]. Moreover, conversion of fish hemoglobin to sulfhemoglobin also required sulfide concentrations (1-15 mM) as high as those required for vertebrate hemoglobins [42,43]. These results explain why the formation of sulfhemoglobin has not been observed in annelids from sulfide-rich environments [44][45][46].…”

Section: Sulfide and Hemoglobinsupporting

confidence: 50%

“…Furthermore, although in vitro treatment of purified vertebrate hemoglobin with sulfide leads to sulfhemoglobin formation, treatment of native blood does not produce sulfhemoglobin, suggesting the presence of a protecting factor [41]. Sulfhemoglobin has also been reported in fish living in a sulfide-rich environment in vitro but rarely in vivo, in agreement with different independent conclusions that sulfhemoglobin is not a significant factor in cases of sulfide poisoning [42,43]. Moreover, conversion of fish hemoglobin to sulfhemoglobin also required sulfide concentrations (1-15 mM) as high as those required for vertebrate hemoglobins [42,43].…”

Section: Sulfide and Hemoglobinmentioning

confidence: 58%

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The sulfide binding function of annelid hemoglobins: relic of an old biosystem?

Bailly

Vinogradov

2005

Journal of Inorganic Biochemistry

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Section: Sulfide and Hemoglobinsupporting

confidence: 50%

Section: Sulfide and Hemoglobinmentioning

confidence: 58%

The sulfide binding function of annelid hemoglobins: relic of an old biosystem?

Bailly

Vinogradov

2005

Journal of Inorganic Biochemistry

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“…H 2 S reversibly inhibits the electron transport chain via cytochrome c oxidase [7][8][9], which is mechanistically similar to cyanide poisoning [9,10]. Supraphysiological concentrations of H 2 S may have other toxic consequences as well, including opening of the mitochondrial permeability transition pore [11,12], increasing production of reactive oxygen species (including superoxide) [11][12][13][14], and out-competing oxygen for hemoglobin binding [15][16][17].…”

Section: The Discovery Of Hydrogen Sulfide As a Physiological Mediatormentioning

confidence: 99%

Development of Hydrogen Sulfide-Based Therapeutics for Cardiovascular Disease

Predmore

Lefer

2010

J. of Cardiovasc. Trans. Res.

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The physiological role of the gaseous signaling molecule hydrogen sulfide (H(2)S) was first realized in the mid-1990s with the work of Abe and Kimura. Since then, it has become evident that this endogenous gas is extremely important in the homeostasis of the cardiovascular system and the pathogenesis of cardiovascular disease. Several biotechnology companies have developed and are developing H(2)S-based therapeutic compounds, and there are ongoing clinical trials investigating the therapeutic potential of H(2)S. Several organic and chemical compounds that are known H(2)S donors have the potential to be developed into effective H(2)S-based therapeutic agents. This review will provide a historical and current perspective on the role(s) of H(2)S in the cardiovascular system and the current state of development and future outlook of H(2)S-based therapies for cardiovascular disease.

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“…However, at supraphysiological concentrations, H 2 S can be toxic and potentially lethal. H 2 S can reversibly inhibit the electron-transport chain [32–34], open the mitochondrial permeability transition pore [35,36], increase production of reactive oxygen species (ROS) [35–38] and outcompete oxygen for hemoglobin binding [39–41]. …”

Section: Mechanisms Of H2s Cardioprotection In Pre- and Post-conditioningmentioning

confidence: 99%

Hydrogen sulfide-mediated myocardial pre- and post-conditioning

Predmore¹,

Lefer²

2011

Expert Review of Clinical Pharmacology

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Coronary artery disease is a major cause of morbidity and mortality in the Western world. Acute myocardial infarction, resulting from coronary artery atherosclerosis, is a serious and often fatal consequence of coronary artery disease, resulting in cell death in the myocardium. Pre-and postconditioning of the myocardium are two treatment strategies that reduce the amount of cell death significantly. Hydrogen sulfide has recently been identified as a potent cardioprotective signaling molecule, which is a highly effective pre-and post-conditioning agent. The cardioprotective signaling pathways involved in hydrogen sulfide-based pre-and post-conditioning will be explored in this article. Keywordsacute myocardial infarction; apoptosis; ischemia/reperfusion injury; myocardial protection; oxidative stress Acute myocardial infarction (AMI) is a serious and often fatal consequence of coronary artery disease. With AMI, the best course of action to limit myocardial infarct size is a timely restoration of blood flow to the ischemic myocardium by either thrombolysis or percutaneous angioplasty [1,2]. Unfortunately, the blockage is rarely recanalized before a considerable amount of damage is done to the myocardium, subsequently leading to persistent heart failure in a large percentage of patients [1,2].Pre-and post-conditioning and pharmacological treatments to mimic these interventions have been shown to be effective in limiting infarct size in the setting of myocardial ischemia/reperfusion (MI/R) injury in both animals and humans [3]. When coupled with timely reperfusion, pre-and post-conditioning attenuate myocardial infarct size and postischemic left ventricular dysfunction more than reperfusion alone [3]. Both pre-and post-conditioning can be achieved in numerous ways to induce physiological changes that result in increased cytoprotection after reperfusion of the ischemic heart [3].

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Sulfide-hemoglobin interactions in the sulfide-tolerant salt marsh resident, the California killifish Fundulus parvipinnis

Abstract: JournalofPhysiolosy B --comparatnre % E L

Cited by 31 publications

References 47 publications

The sulfide binding function of annelid hemoglobins: relic of an old biosystem?

The sulfide binding function of annelid hemoglobins: relic of an old biosystem?

Development of Hydrogen Sulfide-Based Therapeutics for Cardiovascular Disease

Hydrogen sulfide-mediated myocardial pre- and post-conditioning

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