Theory of malignant cell transformation by superoxide fate coupled with cytoskeletal electron-transport and electron-transfer

Cavelier, German

doi:10.1054/mehy.1998.0821

Cited by 12 publications

(6 citation statements)

References 18 publications

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“…* P , 0.05, treatment stimulation index (SI) versus unstimulated SI (unstimulated SI 5 1). cytoskeleton (30), and in the regulation of cell cycle progression (31). These processes are thought to be due to effects of ROS on cyclins, cyclin-dependent kinases, and downstream signals that up-regulate the expression of transcription factors including nuclear factor (NF)-kB and AP-1 family members (31,32).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Lymphocyte Proliferation by Antioxidants in Chronic Beryllium Disease

Dobis

Sawyer²,

Gillespie³

et al. 2008

Am J Respir Crit Care Med

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Rationale: Occupational exposure to beryllium (Be) can result in chronic granulomatous inflammation characterized by the presence of Be-specific CD4 1 T cells. Studies show that oxidative stress plays a role in the pathogenesis of chronic inflammatory disorders. Objectives: We hypothesized that Be-induced oxidative stress modulates the proliferation of Be-specific CD4 1 T cells. Methods: Thirty-three subjects with chronic beryllium disease (CBD), 15 subjects with beryllium sensitization, and 28 healthy normal control subjects were consecutively enrolled from the Occupational and Environmental Health Clinic of the National Jewish Medical and Research Center. Measurements and Main Results: All studies were performed with Ficoll-Hypaque-isolated peripheral blood mononuclear cells from subsets of the study subjects. Decreased intracellular levels of the thiol antioxidants, glutathione and cysteine, were observed in peripheral blood mononuclear cells from subjects with beryllium sensitization and CBD, as compared with healthy control subjects. Beryllium stimulation decreased intracellular thiol antioxidants by more than 40%, accompanied by increased reactive oxygen species levels and the proliferation of Be-specific blood CD4 1 T cells from subjects with CBD. Be-induced T-cell proliferation was inhibited by treatment with the thiol antioxidant N-acetylcysteine or the catalytic antioxidant manganese(III) 5,10,15,20-tetrakis(4-benzoic acid)porphyrin (MnTBAP). MnTBAP treatment also inhibited T-cell proliferation in response to the unrelated, MHC class II-restricted antigen tetanus toxoid. Treatment of CBD blood lymphocytes, but not antigen-presenting cells, with MnTBAP decreased Be-induced T-cell proliferation by more than 40%. Conclusions: Beryllium can mediate a thiol imbalance leading to oxidative stress that may modulate the proliferation and clonal expansion of Be-specific blood CD4 1 T cells. These data suggest that Be-induced oxidative stress plays a role in the pathogenesis of granulomatous inflammation in CBD.

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Section: Discussionmentioning

confidence: 99%

Modulation of Lymphocyte Proliferation by Antioxidants in Chronic Beryllium Disease

Dobis

Sawyer²,

Gillespie³

et al. 2008

Am J Respir Crit Care Med

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“…Interestingly, ROS represent important signalling molecules, altering for instance DNA binding and transactivation properties of transcription factors [40], as well as actin cytoskeleton regulation and remodelling. Superoxide, for instance, could be transported through actin microfilaments from the plasma membrane, or from the mitochondria, towards the nucleus [41], specifically influencing the transport into the nucleus of transcription-related proteins [42]. It could be the case of the far upstream element binding protein 1 [43] that was significantly reduced in fibroblasts after serum withdrawal.…”

Section: Discussionmentioning

confidence: 99%

The effect of serum withdrawal on the protein profile of quiescent human dermal fibroblasts in primary cell culture

Boraldi

Annovi

Paolinelli-deVincenzi

et al. 2007

Proteomics

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The effect of serum deprivation on proliferating cells is well known, in contrast its role on primary cell cultures, at confluence, has not been deeply investigated. Therefore, in order to explore the response of quiescent cells to serum deprivation, ubiquitous mesenchymal cells, as normal human dermal fibroblasts, were grown, for 48 h after confluence, in the presence or absence of 10% FBS. Fibroblast behaviour (i.e. cell morphology, cell viability, ROS production and elastin synthesis) was evaluated morphologically and biochemically. Moreover, the protein profile was investigated by 2-DE and differentially expressed proteins were identified by MS. Serum withdrawal caused cell shrinkage but did not significantly modify the total cell number. ROS production, as evaluated by the dihydroethidium (DH2) probe, was increased after serum deprivation, whereas elastin synthesis, measured by a colorimetric method, was markedly reduced in the absence of serum. By proteome analysis, 41 proteins appeared to significantly change their expression, the great majority of protein changes were related to the cytoskeleton, the stress response and the glycolytic pathway. Data indicate that human dermal fibroblasts in primary cell culture can adapt themselves to environmental changes, without significantly altering cell viability, at least after a few days of treatment, even though serum withdrawal represents a stress condition capable to increase ROS production, to influence cell metabolism and to interfere with cell behaviour, favouring the expression of several age-related features.

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“…ROS are potentially mutagenic and may be involved in activation of protooncogene and inactivation of tumor suppressor genes (1,2). Thus, ROS are suspected to represent important human carcinogens (3,4). Oxidative signals, either external or internal, are thought to be detected by sensor molecules and mediated by cellular signal transduction systems, which eventually results in cell cycle arrest, senescence, or apoptosis in normal diploid fibroblast cells.…”

mentioning

confidence: 99%

Reactive Oxygen Species-induced Phosphorylation of p53 on Serine 20 Is Mediated in Part by Polo-like Kinase-3

Xie

Wang

et al. 2001

Journal of Biological Chemistry

135

114

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Theory of malignant cell transformation by superoxide fate coupled with cytoskeletal electron-transport and electron-transfer

Cited by 12 publications

References 18 publications

Modulation of Lymphocyte Proliferation by Antioxidants in Chronic Beryllium Disease

Modulation of Lymphocyte Proliferation by Antioxidants in Chronic Beryllium Disease

The effect of serum withdrawal on the protein profile of quiescent human dermal fibroblasts in primary cell culture

Reactive Oxygen Species-induced Phosphorylation of p53 on Serine 20 Is Mediated in Part by Polo-like Kinase-3

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