Effects of reactive oxygen species on proliferation of Chinese hamster lung fibroblast (V79) cells

Kim, Bu-Yeo; Han, Min‐Joon; Chung, An‐Sik

doi:10.1016/s0891-5849(00)00514-1

Cited by 124 publications

(72 citation statements)

References 78 publications

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“…For instance, in fi broblasts, low concentrations of H 2 O 2 (<10 μM) stimulate cell proliferation; intermediate concentrations (~150 μM) cause growth arrest or senescence; and high levels of H 2 O 2 (>400 μM) induce rapid apoptosis [ 13 ]. Similar results were reported in vascular smooth muscle cells [ 10 ].…”

Section: Discussionsupporting

confidence: 68%

“…It is proposed that oxidative stress-induced apoptosis and senescence may act as mechanisms that protect the organism from further damages such as malignant transformation [ 8 , 9 ]. However, recent studies have indicated that appropriate levels of ROS generated within the cells may act as signaling molecules that regulate a wide range of cellular processes depending on cell types, such as cellular defense [ 2 ], and vascular functions [ 4 , 10 ], differentiation, and proliferation [11][12][13]. Most of the studies related to oxidative stress in the literature have used fully differentiated primary cells or cell lines.…”

Section: Cell Viability Proliferation and Cell Cycle Analysismentioning

confidence: 99%

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Effects of Oxidative Stress on Mouse Embryonic Stem Cell Proliferation, Apoptosis, Senescence, and Self-Renewal

Guo

Chakraborty

Rajan

et al. 2010

Stem Cells and Development

124

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Oxidative stress, associated with either normal metabolism or disease conditions, affects many cellular activities. Most of our knowledge in this fi eld is derived from fully differentiated cells. Embryonic stem cells (ESCs) have attracted enormous attention for their potential applications in cell therapy, but little is known about how the unique properties of ESCs are affected by oxidative stress. We have investigated the effects of oxidative stress induced by H 2 O 2 on several cellular activities of mouse ESCs. Like differentiated cells, ESCs are sensitive to H 2 O 2 -induced apoptosis when continuously exposed to H 2 O 2 at the concentrations above 150 μM. However, unlike differentiated cells, ESCs are resistant to oxidative stress induced senescence. This is demonstrated by the results that when subjected to a short-term sublethal concentration and duration of H 2 O 2 treatment, fi broblasts enter the senescent state with enlarged fl attened cell morphology concurrent with increased expression of senescence marker p21. On the contrary, ESCs neither show any sign of senescence nor express p21. Instead, ESCs enter a transient cell cycle arrest state, but they have remarkable recovery capacity to resume the normal cell proliferation rate without losing the ability of self-renewal and pluripotency. Our results further revealed that H 2 O 2 inhibits cell adhesion and the expression of cyclin D1, which are early events proceeding apoptosis and cell cycle arrest. In conclusion, our data suggest that ESCs are sensitive to H 2 O 2 toxicity, but may have unique mechanisms that prevent H 2 O 2 -induced senescence and protect self-renewal capacity.

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Section: Discussionsupporting

confidence: 68%

Section: Cell Viability Proliferation and Cell Cycle Analysismentioning

confidence: 99%

Effects of Oxidative Stress on Mouse Embryonic Stem Cell Proliferation, Apoptosis, Senescence, and Self-Renewal

Guo

Chakraborty

Rajan

et al. 2010

Stem Cells and Development

124

View full text Add to dashboard Cite

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“…In several apoptotic models, increased generation of ROS was described as an early event; in addition, enhanced ROS formation and impairment of the cellular anti-oxidant mechanisms may also lead to cellular apoptosis (23). However, ROS are able to play a role as mitogens to induce proliferation and protect cells from apoptosis induced by oxidative stresses (24,25). These data suggest a double-sided function of ROS.…”

Section: Discussionmentioning

confidence: 99%

Curcumin induces apoptosis in human lung adenocarcinoma A549 cells through a reactive oxygen species-dependent mitochondrial signaling pathway

Chen

Wang²,

Xu³

et al. 2009

Oncol Rep

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Abstract.Several studies have shown that curcumin can induce apoptosis and inhibit growth in human A549 lung adenocarcinoma cells. However, the mechanism is not completely understood yet. The present study was designed to investigate the effects of curcumin on A549 cells to better understand its apoptosis and apoptosis-related factors in vitro. The apoptosis induction, intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were examined by confocal fluorescence microscope and flow cytometry. The MAPK protein expression was examined by Western blot analysis. After treatment with curcumin, apoptosis were observed. Curcumin-induced apoptosis was accompanied by an increase of intracellular ROS level and a loss of MMP. In addition, induction of apoptosis was also accompanied by sustained phosphorylation and activation of JNK, p38 and ERK. However, pretreatment with MAPK inhibitors had no effect upon curcumin-induced apoptosis. GSH and NAC, an anti-oxidant agent, blocked the curcumin-induced ROS production, MMP loss and rescued cells from curcumininduced apoptosis. Our results indicated that curcumin induced apoptosis in A549 cells through a reactive oxygen speciesdependent mitochondrial signaling pathway and independent of MAPK signaling pathway.

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“…Alternatively, ROS can indirectly modulate molecules containing high thiol-disulfide oxidation potentials, such as thioredoxin or glutathione Stransferase (Adler et al, 1999a;Adler et al, 1999b;Saitoh et al, 1998) and thereby influence cellular processes. It has been shown that ROS play a significant role in mediation of inflammatory defense mechanisms (Darrah et al, 2000;Davies, 1995;Vazquez-Torres et al, 2000), regulation of transcription factors (Devary et al, 1991;Meyer et al, 1993), enzyme activity (Lopez-Ongil et al, 2000), cell proliferation (Preston et al, 2001;Kim et al, 2001) and various other crucial physiological signal transduction pathways (Finkel, 2000;Kamata and Hirata, 1999;Remacle et al, 1995;Suzuki et al, 1997). Exogenously applied oxidants, such as H 2 O 2 , can mimic cellular responses to physiological stimulants, including the stimulation of cell metabolism and growth via the insulin, epidermal growth factor (EGF) or platelet-derived growth factor (PDGF) receptors (Fantus et al, 1989;Gamou and Shimizu, 1995;Hayes and Lockwood, 1987;Heffetz et al, 1990;Knebel et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Manipulation of redox signaling in mammalian cells enabled by controlled photogeneration of reactive oxygen species

Posen

Kalchenko

Seger

et al. 2005

Journal of Cell Science

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Reactive oxygen species (ROS) comprise a group of noxious byproducts of oxidative processes which participate in the induction of many common diseases. However, understanding their role in the regulation of normal physiological redox signaling is currently evolving. Detailed study of the dynamic functions of ROS within the biological milieu is difficult because of their high chemical reactivity, short lifetime, minute concentrations and cytotoxicity at high concentrations. In this study, we show that increasing intracellular ROS levels, set off by controlled in situ photogeneration of a nontoxic bacteriochlorophyll-based sensitizer initiate responses in cultured melanoma cells. Using hydroethidine as detector, we determined light-dependent generation of superoxide and hydroxyl radicals in cell-free and cell culture models. Monitoring the ROS-induced responses revealed individual and differential behavior of protein kinases [p38, mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and Akt] as well as effects on the subcellular distribution of phosphorylated p38. Furthermore, alterations in morphology and motility and effects on cell viability as a function of time and photosensitizer doses were observed. Following mild ROS challenge, enzymatic and cellular changes were observed in the majority of the cells, without inducing extensive cell death. However, upon vigorous ROS challenge, a similar profile of the overall responses was observed, terminating in cell death. This study shows that precisely controlled photogeneration of ROS can provide simple, fine-tuned, noninvasive manipulation of ROS-sensitive cellular responses ranging from individual enzymes to gross behavior of target cells. The observations made with this tool enable a dynamic and causal correlation, presenting a new alternative for studying the role of ROS in cellular redox signaling.

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Effects of reactive oxygen species on proliferation of Chinese hamster lung fibroblast (V79) cells

Cited by 124 publications

References 78 publications

Effects of Oxidative Stress on Mouse Embryonic Stem Cell Proliferation, Apoptosis, Senescence, and Self-Renewal

Effects of Oxidative Stress on Mouse Embryonic Stem Cell Proliferation, Apoptosis, Senescence, and Self-Renewal

Curcumin induces apoptosis in human lung adenocarcinoma A549 cells through a reactive oxygen species-dependent mitochondrial signaling pathway

Manipulation of redox signaling in mammalian cells enabled by controlled photogeneration of reactive oxygen species

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