G2 arrest, binucleation, and single‐parameter DNA flow cytometric analysis

Ronot, Xavier; Hecquet, Christiane; Larno, S; Hainque, Bernard; Adolphe, M

doi:10.1002/cyto.990070310

Cited by 19 publications

(8 citation statements)

References 16 publications

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“…They can result from an arrest in the G 2 phase of the cell cycle (24) and can be induced by chemicals (14,25) and radiation (26). BSDE elicited a dosedependent increase in BNCs in NHBE cells ( Table 2) similar to that observed in the phenotypically altered progeny of NHBE cells exposed to fractionated doses of α-particles (26).…”

Section: Discussionmentioning

confidence: 67%

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

Catallo

Kennedy

Henk

et al. 2001

Environ Health Perspect

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Adverse health effects of airborne toxicants, especially small respirable particles and their associated adsorbed chemicals, are of growing concern to health professionals, governmental agencies, and the general public. Areas rich in petrochemical processing facilities (e.g., eastern Texas and southern California) chronically have poor air quality. Atmospheric releases of products of incomplete combustion (e.g., soot) from these facilities are not subject to rigorous regulatory enforcement. Although soot can include respirable particles and carcinogens, the toxicologic and epidemiologic consequences of exposure to environmentally relevant complex soots have not been well investigated. Here we continue our physico-chemical analysis of butadiene soot and report effects of exposure to this soot on putative targets, normal human bronchial epithelial (NHBE) cells. We examined organic extracts of butadiene soot by gas chromatography-mass spectrometry (GC-MS), probe distillation MS, and liquid chromatography (LC)-MS-MS. Hundreds of aromatic hydrocarbons and polycyclic aromatic hydrocarbons with molecular mass as high as 1,000 atomic mass units were detected, including known and suspected human carcinogens (e.g., benzo(a)pyrene). Butadiene soot particles also had strong, solid-state free-radical character in electron spin resonance analysis. Spin-trapping studies indicated that fresh butadiene soot in a buffered aqueous solution containing dimethylsulfoxide (DMSO) oxidized the DMSO, leading to CH(3)* radical formation. Butadiene soot DMSO extract (BSDE)-exposed NHBE cells displayed extranuclear fluorescence within 4 hr of exposure. BSDE was cytotoxic to > 20% of the cells at 72 hr. Morphologic alterations, including cell swelling and membrane blebbing, were apparent within 24 hr of exposure. These alterations are characteristic of oncosis, an ischemia-induced form of cell death. BSDE treatment also produced significant genotoxicity, as indicated by binucleated cell formation. The combination of moderate cytotoxicity and genotoxicity, as occurred here, can be pro-carcinogenic.

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Section: Discussionmentioning

confidence: 67%

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

Catallo

Kennedy

Henk

et al. 2001

Environ Health Perspect

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“…Measurement of the mitotic index and the percentage of binucleate cells allowed us to determine the precise cell distribution in G2 and/or M phase, since flow cytometric analysis cannot be used for this purpose as G0/1 binucleate cells and G2+M cells give equal fluorescent intensities after specific DNA staining (Kerker et al, 1982;Ronot et al, 1986). However, no significant modification of the mitotic index was observed for chondrocytes, HeLa cells, and L 929.…”

Section: Discussionmentioning

confidence: 95%

“…However, this transitory similar distribution was due to two different phenomena: either inhibition by cellular contact in the control or a specific antiproliferative action of D-penicillamine for treated cells affecting cell number since, after 72 h, a slight accumulation in the G2 + M phase was again observed. Measurement of the mitotic index and the percentage of binucleate cells allowed us to determine the precise cell distribution in G2 and/or M phase, since flow cytometric analysis cannot be used for this purpose as G0/1 binucleate cells and G2+M cells give equal fluorescent intensities after specific DNA staining (Kerker et al, 1982;Ronot et al, 1986). However, no significant modification of the mitotic index was observed for chondrocytes, HeLa cells, and L 929.…”

Section: Discussionmentioning

confidence: 99%

Differential effect of D‐penicillamine on the cell kinetic parameters of various normal and transformed cellular types

Friteau

Jaffray

Ronot

et al. 1988

Journal Cellular Physiology

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The cell-growth-inhibitory and phase-specific effects of D-penicillamine on cell-cycle progression were investigated using cell-proliferation patterns, quantitative cell-cycle analysis by flow cytometry, and determination of the mitotic index and binucleate cell fraction of normal (rabbit articular chondrocytes, L 809, rabbit fibroblasts) and transformed (HeLa, L 929) cells. D-penicillamine treatment resulted in an inhibition of growth within a dose range of 5 x 10(-4) M to 7.5 x 10(-3) M. Examination of DNA by flow cytometric analysis revealed that rabbit articular chondrocytes were preferentially arrested in the G0/1 phase of the cell cycle, whereas the other cell lines were blocked in the G2 + M phase; the increase in the proportion of cells with G2 + M DNA content was partially due to an enhancement of binucleate cells, resulting in a cytokinesis perturbation for HeLa and L 929 cells. These results showed that D-penicillamine affects cell proliferation through different events according to cell type.

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“…On the contrary, the greater the potential of a drug to induce damage or alterations of DNA, the higher the frequency of G2 arrest (Ronot et al, 1986). Drug DNA interaction could result in the inactivation or alteration of some genes, which in turn could lead to the failure of synthesis of certain proteins required for the transition of cells through G2 to mitosis, leading to an unbalanced growth.…”

Section: Biological Interpretation Derived From Mathematical Analysismentioning

confidence: 99%

Flow cytometric analysis of the cell cycle: Mathematical modeling and biological interpretation

Pierrez¹,

Ronot

1992

Acta Biotheor

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Estimation of the repartition of asynchronous cells in the cell cycle can be explained by two hypotheses: the cells are supposed to be distributed into three groups: cells with a 2c DNA content (G0/1 phase), cells with a 4c DNA content (G2 + M phase) and cells with a DNA content ranging from 2c to 4c (S phase); there is a linear relationship between the amount of fluorescence emitted by the fluorescent probe which reveals the DNA and the DNA content. According to these hypotheses, the cell cycle can be represented by the following equation: [formula: see text] All the solutions for this equation are approximations. Non parametric methods (or graphical methods: rectangle, peak reflect) only use one or two phase(s) of the cell cycle, the remaining phase(s) being estimated by exclusion. In parametric methods (Dean & Jett, Baisch II, Fried), the DNAT(x) distribution is supposed to be known and is composed of two gaussians (representative of G0/1 and G2 + M) and a P(x,y) function representative of S phase. Despite the generality, these models are not applicable to all sample types, particularly heterogeneous cell populations with various DNA content. In addition, the cell cycle is dependent on several regulation points (transition from quiescence to proliferation, DNA synthesis initiation, mitosis induction) and biological perturbations can also lead to cytokinesis perturbations. Before the emergence of flow cytometry, the current view of cell cycle resided in the assessment of cell proliferation (increase in cell number) or the kinetic of molecules incorporation (DNA precursors).(ABSTRACT TRUNCATED AT 250 WORDS)

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G2 arrest, binucleation, and single‐parameter DNA flow cytometric analysis

Cited by 19 publications

References 16 publications

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

Differential effect of D‐penicillamine on the cell kinetic parameters of various normal and transformed cellular types

Flow cytometric analysis of the cell cycle: Mathematical modeling and biological interpretation

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