Reactive Oxygen Species and Apoptosis

Bauer, Georg; Dormann, Sabine; Schulz, Adriana; Sarán, Manfred

doi:10.1007/978-3-642-57075-9_11

Cited by 7 publications

(8 citation statements)

References 259 publications

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“…The known interdependencies of ROS (for review see Bauer, 2000;Bauer et al, 2000) allowed to speculate that alternatively to direct apoptosis induction by hydrogen peroxide, several other hydrogen peroxidedependent signaling pathways were conceivable. These were (1) the iron-catalysed Haber-Weiss reaction; (2) .…”

Section: Resultsmentioning

confidence: 99%

“…The balance between cellular reactive oxygen species (ROS) generation and the cellular antioxidant tone prevents ROS-dependent damage and induction of apoptosis (for review see Bauer et al, 2000). Whereas transformed and nontransformed fibroblasts are both exposed to intracellular ROS derived from mitochondria (Fridovich, 1995;Boveris and Chance, 1973;Cadenas and Davies, 2000), only transformed cells are characterized by substantial extracellular ROS generation (Irani et al, 1997;Bauer, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Proapoptotic and redox state-related signaling of reactive oxygen species generated by transformed fibroblasts

Schimmel¹,

Bauer²

2002

Oncogene

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Oncogenic transformed fibroblasts are characterized by extracellular superoxide anion generation through a membrane-associated NADPH oxidase. After cellular glutathione depletion, extracellular reactive oxygen species (ROS) generated by transformed fibroblasts exhibit a strong apoptosis-inducing potential. As apoptosis induction under glutathione depletion is inhibited by catalase, the NADPH oxidase inhibitor apocynin, superoxide dismutase, the hydroxyl radical scavenger terephthalate and the iron chelator deferoxamine, the metal-catalysed Haber-Weiss reaction seems to be the responsible signaling mechanism. In contrast to extracellular ROS, intracellular ROS play no role for apoptosis induction in glutathione-depleted transformed fibroblasts initially, since a high level of intracellular catalase scavenges intracellular hydrogen peroxide. Intracellular catalase seems to be induced by extracellular hydrogen peroxide, as pretreatment of transformed fibroblasts with exogenous catalase downmodulates endogenous catalase and renders glutathione-depleted transformed cells susceptible for the effect of endogenous hydrogen peroxide. In contrast to transformed fibroblasts, nontransformed glutathione-depleted fibroblasts do not generate substantial extracellular ROS, but apoptosis is efficiently induced in these cells by intracellular ROS. Our data show that extracellular ROS of transformed fibroblasts exhibit redox-related signaling and at the same time represent a potential apoptosis-inducing hazard through the metalcatalysed Haber-Weiss reaction.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Proapoptotic and redox state-related signaling of reactive oxygen species generated by transformed fibroblasts

Schimmel¹,

Bauer²

2002

Oncogene

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“…Biologically produced NO originates from oxygen and Larginine in the reaction catalyzed by NO synthase. NO, a long-lived radical with a wide range of actions, is known as a regulator of a variety of biological processes [27]. The NO level was determined according [28], NO release was defined using the Greyss reagent (by NO 2 concentration in the cultural medium).…”

Section: In Vitromentioning

confidence: 99%

Synthesis, structure and cytotoxicity of 3-C, N, S, Se substituted benzo[b]selenophene derivatives

Arsenyan

Paegle

Belyakov

et al. 2011

European Journal of Medicinal Chemistry

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“…1G), which generates hydroxyl radicals by spontaneous Fenton chemistry and leads to the activation of the mitochondrial pathway of apoptosis induction. GOX-mediated oxidative stress provides a very strong proapoptotic signal that induces strong apoptosis within the first few hours after the addition of GOX and massive necrotic cell death at later time points (3,24). To reduce the possible impact of necrosis on the outcome of our experiment, we determined the percentage of apoptotic C6 cells at 2 and 2.5 h after the addition of GOX.…”

Section: Cells and Transfectionmentioning

confidence: 99%

Protein X of Borna Disease Virus Inhibits Apoptosis and Promotes Viral Persistence in the Central Nervous Systems of Newborn-Infected Rats

Poenisch

Burger

Staeheli

et al. 2009

J Virol

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Borna disease virus (BDV) is a neurotropic member of the order Mononegavirales with noncytolytic replication and obligatory persistence in cultured cells and animals. Here we show that the accessory protein X of BDV represents the first mitochondrion-localized protein of an RNA virus that inhibits rather than promotes apoptosis induction. Rat C6 astroglioma cells persistently infected with wild-type BDV were significantly more resistant to death receptor-dependent and -independent apoptotic stimuli than uninfected cells or cells infected with a BDV mutant expressing reduced amounts of X. Confocal microscopy demonstrated that X colocalizes with mitochondria and expression of X from plasmid DNA rendered human 293T and mouse L929 cells resistant to apoptosis induction. A recombinant virus encoding a mutant X protein unable to associate with mitochondria (BDV-X A6A7 ) failed to block apoptosis in C6 cells. Furthermore, Lewis rats neonatally infected with BDV-X A6A7 developed severe neurological symptoms and died around day 30 postinfection, whereas all animals infected with wild-type BDV remained healthy and became persistently infected. TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) staining revealed a significant increase in the number of apoptotic cells in the brain of BDV-X A6A7 -infected animals, whereas the numbers of CD3 ؉ T lymphocytes were comparable to those detected in animals infected with wild-type BDV. Our data thus indicate that inhibition of apoptosis by X promotes noncytolytic viral persistence and is required for the survival of cells in the central nervous system of BDV-infected animals.

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Reactive Oxygen Species and Apoptosis

Cited by 7 publications

References 259 publications

Proapoptotic and redox state-related signaling of reactive oxygen species generated by transformed fibroblasts

Proapoptotic and redox state-related signaling of reactive oxygen species generated by transformed fibroblasts

Synthesis, structure and cytotoxicity of 3-C, N, S, Se substituted benzo[b]selenophene derivatives

Protein X of Borna Disease Virus Inhibits Apoptosis and Promotes Viral Persistence in the Central Nervous Systems of Newborn-Infected Rats

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