Reactive oxygen species: Destroyers or messengers?

Bartosz, Grzegorz

doi:10.1016/j.bcp.2008.11.009

Cited by 322 publications

(220 citation statements)

References 75 publications

(56 reference statements)

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“…ROS were traditionally thought of as toxic byproducts in cells, which damaged cellular macromolecules and led cells to apoptosis (Shackelford et al, 1999). However, in recent years, several studies have shown that ROS can function as signaling molecules that regulate numerous cellular processes, including proliferation (Sundaresan et al, 1995;Behrend et al, 2003;Menon and Goswami, 2007;Bartosz, 2009). This dual function of ROS is based on differences in their concentrations, pulse duration and subcellular localization (Laurent et al, 2005;Bartosz, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…However, in recent years, several studies have shown that ROS can function as signaling molecules that regulate numerous cellular processes, including proliferation (Sundaresan et al, 1995;Behrend et al, 2003;Menon and Goswami, 2007;Bartosz, 2009). This dual function of ROS is based on differences in their concentrations, pulse duration and subcellular localization (Laurent et al, 2005;Bartosz, 2009). High concentration of ROS in G1/S phase led to cell senescence or apoptosis and, on the contrary, low ROS facilitated cell cycle progression and activation of cell cycle regulators, such as, CDK4/6, cyclin D1, RB, p21 and E2F1 (Laurent et al, 2005;Menon and Goswami, 2007;Sarsour et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

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Functional interaction of Ugene and EBV infection mediates tumorigenic effects

et al. 2011

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Epstein-Barr virus (EBV) infection is associated with many human neoplasms, in which EBV-derived latent membrane protein-1 (LMP1) appears to be critical, but its exact oncogenic mechanism remains to be defined. To this end, our initial microarray analyses identified a LMP1-inducible gene, Ugene, originally characterized as a binding partner for uracil DNA glycosylase 2, which is highly expressed in malignant colon cancer. In this report, it was found that Ugene, designated herein as LMP1-induced protein (LMPIP), was induced, in a time-dependent manner, in EBV-infected peripheral blood mononuclear cells and LMP1-transfected 293 cells. Functionally, when compared with mock-transfected cells, overexpression of LMPIP in nasopharyngeal carcinoma (NPC) cell lines resulted in a decrease in reactive oxygen species production and maintained mitochondria membrane potential (Dw) loss induced by H 2 O 2 . The NPC cells transfected with LMPIP also showed a decrease in G1 population and an increase in the cell population in sub-G1 and multiploid phase, concomitant with increased levels of cell cycle activators, including cyclin D1 and CDK4. In contrast, silencing of LMPIP expression in the NPC tumor cell lines with short hairpin RNA interference revealed significantly decreased cell population at G1/S phase, while the number of cells in multiploid phase increased. Significantly, NPC cells with LMPIP knock-down also showed a decrease in tumorigenic and transforming activity induced by ectopic LMP1 expression, as determined by analyses of soft agar foci and tumor size in nude mice. Further, elevated LMPIP expression was also noted in cytoplasm and nuclei in EBVinfected NPC tumor cell mass and non-EBV-infected tumor cell lines. These results suggested that LMPIP may have an important mediator role in EBV-mediated neoplasm and may serve as a new target for therapy of tumors induced by EBV infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

et al. 2011

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“…This condition, which is responsible for cell damage, can be induced by many diseases and a number of toxic agents (5).…”

Section: Introductionmentioning

confidence: 99%

The oxygen radicals involved in the toxicity induced by parthenolide in MDA-MB-231 cells

et al. 2014

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Abstract.It has been shown that the sesquiterpene lactone parthenolide lowers the viability of MDA-MB-231 breast cancer cells, in correlation with oxidative stress. The present report examined the different radical species produced during parthenolide treatment and their possible role in the toxicity caused by the drug. Time course experiments showed that in the first phase of treatment (0-8 h), and in particular in the first 3 h, parthenolide induced dichlorofluorescein (DCF) signal in a large percentage of cells, while dihydroethidium (DHE) signal was not stimulated. Since the effect on DCF signal was suppressed by apocynin and diphenyleneiodonium (DPI), two inhibitors of NADPH oxidase (NOX), we suggest that parthenolide rapidly stimulated NOX activity with production of superoxide anion (O 2•-

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“…ROS take part in the signal transduction pathways of several growth and trophic factors, cytokines and G-proteincoupled receptors (Bartosz, 2009) and regulate proliferation, differentiation, migration and apoptosis in a wide variety of cells (Sauer et al, 2001;Bedard and Krause, 2007;Dumollard et al, 2007). ROS can signal to the nucleus and control gene expression to regulate cell metabolism appropriately (Finley and Haigis, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…However, it has also been suggested that ROS exert mitogenic effects (Bartosz, 2009). Such discrepancies may be associated with different experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

Effect of inhibitors of NADPH oxidase complex and mitochondrial ATP‐sensitive potassium channels on generation of dopaminergic neurons from neurospheres of mesencephalic precursors

Rodríguez‐Pallares

Joglar

Díaz-Ruiz

et al. 2010

Developmental Dynamics

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Reactive oxygen species signaling has been suggested to regulate stem cell development. In the present study, we treated neurospheres of rat mesencephalic precursors with inhibitors of the NADPH oxidase complex and mitochondrial ATP-sensitive potassium (mitoKATP) channel blockers during the proliferation and/or the differentiation periods to study the effects on generation of dopaminergic neurons. Treatment with low doses (100 or 250 mM) of the NADPH inhibitor apocynin during the proliferation period increased the generation of dopaminergic neurons. However, higher doses (1 mM) were necessary during the differentiation period to induce the same effect. Treatment with general (glibenclamide) or mitochondrial (5-hydroxydecanoate) KATP channel blockers during the proliferation and differentiation periods increased the number of dopaminergic neurons. Furthermore, neither increased proliferation rate nor apoptosis had a major role in the observed increase in generation of dopaminergic neurons, which suggests that the redox state is able to regulate differentiation of precursors into dopaminergic neurons. Developmental Dynamics 239:3247-3259,

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Reactive oxygen species: Destroyers or messengers?

Cited by 322 publications

References 75 publications

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

The oxygen radicals involved in the toxicity induced by parthenolide in MDA-MB-231 cells

Effect of inhibitors of NADPH oxidase complex and mitochondrial ATP‐sensitive potassium channels on generation of dopaminergic neurons from neurospheres of mesencephalic precursors

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