BCL-2 is involved in preventing oxidant-induced cell death and in decreasing oxygen radical production

Amstad, Paul; Liu, Hui; Ichimiya, Masato; Berezesky, Irene K.; Trump, Benjamin F.; Buhimschi, Irina; Gutiérrez, Peter L.

doi:10.1179/135100001101536535

Cited by 59 publications

(34 citation statements)

References 48 publications

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“…Ink4a À/À and wild-type mice showed similar levels of Bcl-2 protein as measured by intracellular staining and flow cytometry (data not shown), indicating that resistance to oxidative stress and DNA damage is not mediated by increased Bcl-2 expression. This is relevant since Bcl-2 plays a major role in the control of T-cell apoptosis, and increased Bcl-2 expression can mediate resistance to apoptosis induced by diverse stimuli, including oxidative stress (Amstad et al, 2001).…”

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confidence: 99%

The tumor suppressor p16Ink4a regulates T lymphocyte survival

et al. 2006

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In contrast to other cell cycle inhibitors, the tumor suppressor p16 Ink4a is not detectable or expressed at very low levels in embryonic and adult mouse tissues, and therefore it has often been considered as a specialized checkpoint protein that does not participate in the control of normal cell cycle progression. However, Ink4a À/À mice possess increased thymus size and cellularity, thus suggesting the involvement of p16 Ink4a in the control of thymocyte proliferation. In this study, we found increased numbers of CD8 and CD4 T lymphocytes in thymus and spleen from Ink4a À/À mice. Unexpectedly, this was not related to an increase in T-cell division rates, which were similar in lymphoid organs of Ink4a À/À and wild-type mice. In contrast, T-cell apoptosis rates were significantly decreased in thymus and spleen from Ink4a À/À mice. Moreover, whereas p16 Ink4a -deficient and wild-type T cells were equally sensitive to Fas or TCR-mediated apoptosis, the former were clearly more resistant to apoptosis induced by oxidative stress or gamma irradiation. Our results indicate that p16 Ink4a function is associated with Tcell apoptosis, and subsequently contributes to the control of T-cell population size in lymphoid organs.

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confidence: 99%

The tumor suppressor p16Ink4a regulates T lymphocyte survival

et al. 2006

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“…[9]). Further, Bcl-2 has been shown to protect from oxidative stress via upregulation of antioxidant enzymes and by elevating the concentration of cellular thiols [10][11][12][13][14].…”

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confidence: 99%

Mechanisms of cell death induction by L-amino acid oxidase, a major component of ophidian venom

et al. 2006

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L-amino acid oxidase (LAAO) from the Malayan pit viper induces both necrosis and apoptosis in Jurkat cells. Cell death by necrosis is attributed to H 2 O 2 produced by oxidation of α-amino acids. In the presence of catalase that effectively scavenges H 2 O 2, a switch to apoptosis is observed. The major factors contributing to apoptosis are proposed to be: (i) generation of toxic intermediates from fetal calf serum (ii) binding and internalization of LAAO. The latter process appears to be mediated by the glycan moiety of the enzyme as desialylation reduces cytotoxicity. D-amino acid oxidase (DAAO), which catalyzes the same reaction as LAAO but lacks glycosylation, triggers necrosis as a consequence of H 2 O 2 production but not apoptosis in the presence of catalase. Thus induction of cell death by LAAO appears to involve both the generation of H 2 O 2 and the molecular interaction of the glycan moiety of the enzyme with structures at the cell surface.S. R. Ande, P. R. Kommoju contributed equally to this work.

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“…Enhanced oxidative stress and susceptibility to oxidants and altered levels of antioxidant enzymes occurred in the brains of Bcl-2-deficient mice. 89 Bcl-2 acted to inhibit oxidant-induced cell death, at least in part through an antioxidant pathway, involving glutathione; 90 whereas, acute oxidative stress reduced Bcl-2 expression. 91 Our results demonstrated markedly decreased Bcl-2 protein concentration in striatum following rotenone injection.…”

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Cerebrolysin protects against rotenone-induced oxidative stress and neurodegeneration

Abdel-Salam¹,

Mohammed²,

Youness³

et al. 2014

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Abstract:We investigated the effect of cerebrolysin, a peptide mixture used for promoting memory and recovery from cerebral stroke, on the development of oxidative stress and nigrostriatal cell injury induced by rotenone administration in rats. Rotenone 1.5 mg/kg was given subcutaneously three times weekly either alone or in combination with cerebrolysin at 21.5, 43, or 86 mg/kg. Rats were euthanized 14 days after starting the rotenone injection. Lipid peroxidation (malondialdehyde), reduced glutathione (GSH), nitric oxide (nitrite) concentrations, paraoxonase 1 (PON1), and acetylcholinesterase (AChE) activities -as well as the monocyte chemoattractant protein-1 (MCP-1) and the antiapoptotic protein Bcl-2 -were measured in the brain. Histopathology, tyrosine hydroxylase, inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and cleaved caspase-3 immunohistochemistry were also performed. Rotenone caused a significantly elevated oxidative stress and proinflammatory response in the different brain regions. Malondialdehyde and nitric oxide concentrations were significantly increased, while GSH markedly decreased in the cerebral cortex, striatum, hippocampus, and in the rest of the brain. PON1 and AChE activities significantly decreased with respect to the control levels after rotenone application. Striatal Bcl-2 was significantly decreased while MCP-1 increased following rotenone injection. Rotenone caused prominent iNOS, TNF-α, and caspase-3 immunostaining in the striatum and resulted in markedly decreased tyrosine hydroxylase immunoreactivity in the substantia nigra and striatum. Cerebrolysin coadministered with rotenone decreased lipid peroxidation, increased GSH, and inhibited the elevation of nitric oxide induced by rotenone. Cerebrolysin also decreased the rotenone-induced decline in the PON1 and AChE activities and the rotenone-mediated changes in the striatal Bcl-2 and MCP-1 levels. The drug reduced iNOs, TNF-α, and caspase 3 expressions and increased the tyrosine hydroxylase immunoreactivity in the striatum. Cerebrolysin markedly prevented the development of neuronal damage in the cortex and striatum. These data suggest that cerebrolysin may have potential therapeutic effect in Parkinson's disease.

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BCL-2 is involved in preventing oxidant-induced cell death and in decreasing oxygen radical production

Cited by 59 publications

References 48 publications

The tumor suppressor p16Ink4a regulates T lymphocyte survival

The tumor suppressor p16Ink4a regulates T lymphocyte survival

Mechanisms of cell death induction by L-amino acid oxidase, a major component of ophidian venom

Cerebrolysin protects against rotenone-induced oxidative stress and neurodegeneration

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