Hydrogen peroxide as a mediator of programmed cell death in the blastocyst

Pierce, G. Barry; Parchment, Ralph E.; Lewellyn, Andrea L.

doi:10.1111/j.1432-0436.1991.tb00880.x

Cited by 196 publications

(104 citation statements)

References 26 publications

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“…Reactive oxygen species (such as H 2 product 2',7'-dichlorofluorescein (DCF) [37]. The levels of ROS in heat-stressed cells, relative to the nonstressed controls, had higher DCF fluorescence values for all cell types tested (Fig.…”

Section: Effects Of Ced-9 Bcl-2 and Bcl-xl On The Generation Of Rosmentioning

confidence: 97%

“…Oxidative stress has been implicated in numerous biological processes and diseases, including cancer, tumor promotion, arthritis, heart disease, aging, and programmed cell death in both plants and animals [1][2][3][4]. Thus, aerobic organisms need to mitigate the deleterious reactive oxygen species (ROS) that are generated during the normal course of aerobic metabolism to avoid oxidative damage.…”

Section: Introductionmentioning

confidence: 99%

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Bcl-2 family members inhibit oxidative stress-induced programmed cell death in Saccharomyces cerevisiae

Chen

Dunigan

Dickman

2003

Free Radical Biology and Medicine

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Section: Effects Of Ced-9 Bcl-2 and Bcl-xl On The Generation Of Rosmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Bcl-2 family members inhibit oxidative stress-induced programmed cell death in Saccharomyces cerevisiae

Chen

Dunigan

Dickman

2003

Free Radical Biology and Medicine

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“…The toxic effect of Na 2 N 2 O 3 was pronounced several hours after the treatment of the cells. Delayed cell death induced by exposure to oxidative stress has been described in a number of other cell systems and has usually been attributed to apoptosis (49,50). The cytotoxicity of Na 2 N 2 O 3 was ⅐ OH-dependent as suggested by the protective effect of ascorbic acid, ␣-(4-pyridyl-1-oxide)-N-tert-butylnitrone, and Me 2 SO, which are efficient scavengers of ⅐ OH (Fig.…”

Section: Effects Of Ph On the Cytotoxicity Of Na 2 N 2 O 3 -mentioning

confidence: 99%

Formation of Nitroxyl and Hydroxyl Radical in Solutions of Sodium Trioxodinitrate

Ivanova

Salama

Clancy

et al. 2003

Journal of Biological Chemistry

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Despite its negative redox potential, nitroxyl (HNO) can trigger reactions of oxidation. Mechanistically, these reactions were suggested to occur with the intermediate formation of either hydroxyl radical ( ⅐ OH) or peroxynitrite (ONOO ؊ ). In this work, we present further experimental evidence that HNO can generate ⅐ OH. Sodium trioxodinitrate (Na 2 N 2 O 3 ), a commonly used donor of HNO, oxidized phenol and Me 2 SO to benzene diols and ⅐ CH 3 , respectively. The oxidation of Me 2 SO was O 2 -independent, suggesting that this process reflected neither the intermediate formation of ONOO ؊ nor a redox cycling of transition metal ions that could initiate Fenton-like reactions. In solutions of phenol, Na 2 N 2 O 3 yielded benzene-1,2-diol and benzene-1,4-diol at a ratio of 2:1, which is consistent with the generation of free ⅐ OH. Ethanol and Me 2 SO, which are efficient scavengers of ⅐ OH, impeded the hydroxylation of phenol. A mechanism for the hydrolysis of Na 2 N 2 O 3 is proposed that includes dimerization of HNO to cis-hyponitrous acid (HO-N‫؍‬N-OH) with a concomitant azo-type homolytic fission of the latter to N 2 and ⅐ OH. The HNO-dependent production of ⅐ OH was with 1 order of magnitude higher at pH 6.0 than at pH 7.4. Hence, we hypothesized that HNO can exert selective toxicity to cells subjected to acidosis. In support of this thesis, Na 2 N 2 O 3 was markedly more toxic to human fibroblasts and SK-N-SH neuroblastoma cells at pH 6.2 than at pH 7.4. Scavengers of ⅐ OH impeded the cytotoxicity of Na 2 N 2 O 3 . These results suggest that the formation of HNO may be viewed as a toxicological event in tissues subjected to acidosis.The biochemistry of nitroxyl (HNO) has attracted considerable interest in recent years. In cells, the biosynthesis of HNO is believed to proceed via reduction of NO ⅐ by superoxide dismutase (1) and cytochrome c (2), and reduction of S-nitrosoglutathione by low molecular weight and protein thiols (3-5). It has been suggested that HNO can affect the etiology of various pathophysiological conditions such as inflammation and neurodegenerative diseases, especially when H 2 O 2 and transition metal ions are present (6, 7). Similar to NO ⅐ and NO ϩ , HNO is a potent inducer of the antioxidant protein heme oxygenase 1 (8), exhibits vasorelaxant properties (9), and modulates the activity of thiol-containing proteins, such as aldehyde dehydrogenase (10, 11) and the N-methyl-D-aspartate receptor (12, 13). In in vivo experiments, Paolocci et al. (14) observed that HNO exerts positive inotropic and lusitropic action, which unlike NO ⅐ and nitrates is independent and additive to ␤-adrenergic stimulation and increases the release of plasma calcitonin gene-related peptide; these results suggest that donors of HNO are potential prodrugs for the treatment of heart failure (14). At high doses, HNO has been shown to induce DNA singlestrand breakage (15, 16) and a concentration-dependent cytotoxicity in murine thymocytes (16). This cytotoxicity was associated with activation of the nuclear nick sen...

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“…H 2 O 2 has been implicated in the redox regulation of several physiological processes that include signal transduction (1,2), response to oxidative stress (3)(4)(5), development (6), cell proliferation (7)(8)(9), and apoptosis (6,10). Mitochondria are considered the major cellular sources of H 2 O 2 and, accordingly, these organelles may increase the cytosolic steady-state level of oxidants and lead to the activation of c-jun N-terminal kinases, which are critical-and sometimes suf cient-to induce apoptosis (11,12).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Production of Hydrogen Peroxide Regulation by Nitric Oxide and the Role of Ubisemiquinone

Boveris

Cadenas

2000

IUBMB Life

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Hydrogen peroxide as a mediator of programmed cell death in the blastocyst

Cited by 196 publications

References 26 publications

Bcl-2 family members inhibit oxidative stress-induced programmed cell death in Saccharomyces cerevisiae

Bcl-2 family members inhibit oxidative stress-induced programmed cell death in Saccharomyces cerevisiae

Formation of Nitroxyl and Hydroxyl Radical in Solutions of Sodium Trioxodinitrate

Mitochondrial Production of Hydrogen Peroxide Regulation by Nitric Oxide and the Role of Ubisemiquinone

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