Short‐term exposure of nontumorigenic human bronchial epithelial cells to carcinogenic chromium(VI) compromises their respiratory capacity and alters their bioenergetic signature

Cerveira, Joana; Sánchez‐Aragó, María; Urbano, Ana M.; Cuezva, José M.

doi:10.1016/j.fob.2014.06.006

Cited by 20 publications

(8 citation statements)

References 49 publications

(68 reference statements)

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“…Previous studies from our group suggested increased proliferation rates for BEAS-2B cells exposed to mild Cr(VI) concentrations (0.1-2 lM) (Costa et al 2010;Ferreira et al 2012;Cerveira et al 2014). By determining the doubling times of Cr(VI)-exposed cultures, we now confirmed that Cr(VI) produces a concentration-dependent increase in proliferation rate (Fig.…”

Section: Cr(vi) Stimulates Cellular Proliferationsupporting

confidence: 79%

“…It is well established, though, that Cr(VI) is an inducer of oxidative, genotoxic and proteotoxic stress, through the generation of the above-mentioned reactive species, some of them potent oxidizers (Fornace et al 1981;Tsapakos and Wetterhahn 1983;Myers 2012;Urbano et al 2012;Li et al 2015). Cr(VI)induced deregulated cellular energetics, as shown by us (Rodrigues et al 2009;Goncalves et al 2011;Ferreira et al 2012;Cerveira et al 2014) and others (Liu et al 2010;Myers et al 2010;Molina-Jijon et al 2011;Xiao et al 2012a;Abreu et al 2014), likely constitutes an additional major stressor.…”

Section: Introductionmentioning

confidence: 94%

“…Since the aim of this study was to explore the hypothesis that incubation with Cr(VI) protects cells from further stress and not to carry out a comprehensive investigation on this protective effect, all subsequent experiments were conducted with a single Cr(VI) concentration, thus considerably reducing the overall cost of the study. Taking into account the results just described, as well as the cytotoxicity data obtained in previous studies by our group (Costa et al 2010;Cerveira et al 2014), as well as by the group of Caglieri and co-workers (Caglieri et al 2008), 1 lM Cr(VI) was the concentration chosen. Importantly, Caglieri and co-workers showed that, in the cell line used throughout this study, the intracellular chromium levels after a 24 h exposure to this concentration were Fig.…”

Section: Cr(vi) Confers Resistance Against Acute Thermal Shockmentioning

confidence: 99%

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Hexavalent chromium, a lung carcinogen, confers resistance to thermal stress and interferes with heat shock protein expression in human bronchial epithelial cells

et al. 2018

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Exposure to hexavalent chromium [Cr(VI)], a lung carcinogen, triggers several types of cellular stresses, namely oxidative, genotoxic and proteotoxic stresses. Given the evolutionary character of carcinogenesis, it is tempting to speculate that cells that survive the stresses produced by this carcinogen become more resistant to subsequent stresses, namely those encountered during neoplastic transformation. To test this hypothesis, we determined whether pre-incubation with Cr(VI) increased the resistance of human bronchial epithelial cells (BEAS-2B cells) to the antiproliferative action of acute thermal shock, used here as a model for stress. In line with the proposed hypothesis, it was observed that, at mildly cytotoxic concentrations, Cr(VI) attenuated the antiproliferative effects of both cold and heat shock. Mechanistically, Cr(VI) interfered with the expression of two components of the stress response pathway: heat shock proteins Hsp72 and Hsp90α. Specifically, Cr(VI) significantly depleted the mRNA levels of the former and the protein levels of the latter. Significantly, these two proteins are members of heat shock protein (Hsp) families (Hsp70 and Hsp90, respectively) that have been implicated in carcinogenesis. Thus, our results confirm and extend previous studies showing the capacity of Cr(VI) to interfere with the expression of stress response components.

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Section: Cr(vi) Stimulates Cellular Proliferationsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 94%

Section: Cr(vi) Confers Resistance Against Acute Thermal Shockmentioning

confidence: 99%

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Hexavalent chromium, a lung carcinogen, confers resistance to thermal stress and interferes with heat shock protein expression in human bronchial epithelial cells

et al. 2018

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“…The resultant intermediates further react with H 2 O 2 to generate a spectrum of reactive oxygen species (ROS) containing hydroxyl radicals, singlet oxygen, superoxide, and hydrogen peroxide via the Fenton pathway. 12 – 15 Consequently, excessive ROS interaction with these intermediates may give rise to oxidative stress and DNA damage, including chromium–DNA adducts, DNA strand breaks, and DNA–protein cross-links (DPCs), all of which are unstable factors of mutagenic effects. 16 , 17 Therefore, the International Agency for Research on Cancer (IARC) has classified Cr(VI) as a group I carcinogen.…”

Section: Introductionmentioning

confidence: 99%

Carcinogenicity of chromium and chemoprevention: a brief update

Song

et al. 2017

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Chromium has two main valence states: hexavalent chromium (Cr[VI]) and trivalent chromium (Cr[III]). Cr(VI), a well-established human carcinogen, can enter cells by way of a sulfate/phosphate anion-transport system, and then be reduced to lower-valence intermediates consisting of pentavalent chromium (Cr[V]), tetravalent chromium (Cr[IV]) or Cr(III) via cellular reductants. These intermediates may directly or indirectly result in DNA damage or DNA–protein cross-links. Although Cr(III) complexes cannot pass easily through cell membranes, they have the ability to accumulate around cells to induce cell-surface morphological alteration and result in cell-membrane lipid injuries via disruption of cellular functions and integrity, and finally to cause DNA damage. In recent years, more research, including in vitro, in vivo, and epidemiological studies, has been conducted to evaluate the genotoxicity/carcinogenicity induced by Cr(VI) and/or Cr(III) compounds. At the same time, various therapeutic agents, especially antioxidants, have been explored through in vitro and in vivo studies for preventing chromium-induced genotoxicity/carcinogenesis. This review aims to provide a brief update on the carcinogenicity of Cr(VI) and Cr(III) and chemoprevention with different antioxidants.

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“…Beas-2B cells were plated in 6 well plates at an initial density of 300 cells per well [99]. The medium was refreshed with incinerated thermoplastic-containing AEGM, and 0.5 μM B[a]P or DMSO vehicle as control treatments.…”

Section: Clonogenic Assaymentioning

confidence: 99%

Carbon nanotube filler enhances incinerated thermoplastics-induced cytotoxicity and metabolic disruption in vitro

et al. 2020

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Background: Engineered nanomaterials are increasingly being incorporated into synthetic materials as fillers and additives. The potential pathological effects of end-of-lifecycle recycling and disposal of virgin and nano-enabled composites have not been adequately addressed, particularly following incineration. The current investigation aims to characterize the cytotoxicity of incinerated virgin thermoplastics vs. incinerated nano-enabled thermoplastic composites on two in vitro pulmonary models. Ultrafine particles released from thermally decomposed virgin polycarbonate or polyurethane, and their carbon nanotube (CNT)-enabled composites were collected and used for acute in vitro exposure to primary human small airway epithelial cell (pSAEC) and human bronchial epithelial cell (Beas-2B) models. Post-exposure, both cell lines were assessed for cytotoxicity, proliferative capacity, intracellular ROS generation, genotoxicity, and mitochondrial membrane potential. Results: The treated Beas-2B cells demonstrated significant dose-dependent cellular responses, as well as parent matrix-dependent and CNT-dependent sensitivity. Cytotoxicity, enhancement in reactive oxygen species, and dissipation of ΔΨm caused by incinerated polycarbonate were significantly more potent than polyurethane analogues, and CNT filler enhanced the cellular responses compared to the incinerated parent particles. Such effects observed in Beas-2B were generally higher in magnitude compared to pSAEC at treatments examined, which was likely attributable to differences in respective lung cell types. Conclusions: Whilst the effect of the treatments on the distal respiratory airway epithelia remains limited in interpretation, the current in vitro respiratory bronchial epithelia model demonstrated profound sensitivity to the test particles at depositional doses relevant for occupational cohorts.

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Short‐term exposure of nontumorigenic human bronchial epithelial cells to carcinogenic chromium(VI) compromises their respiratory capacity and alters their bioenergetic signature

Cited by 20 publications

References 49 publications

Hexavalent chromium, a lung carcinogen, confers resistance to thermal stress and interferes with heat shock protein expression in human bronchial epithelial cells

Hexavalent chromium, a lung carcinogen, confers resistance to thermal stress and interferes with heat shock protein expression in human bronchial epithelial cells

Carcinogenicity of chromium and chemoprevention: a brief update

Carbon nanotube filler enhances incinerated thermoplastics-induced cytotoxicity and metabolic disruption in vitro

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