Short-term exposure of nontumorigenic human bronchial epithelial cells to carcinogenic chromium(VI) compromises their respiratory capacity and alters their bioenergetic signature. [artículo]
Por: Cerveira, Joana F [Instituto de Investigación imas12]
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Colaborador(es): Instituto de Investigación imas12.
Editor: FEBS open bio, 2014Descripción: 4:594-601.Recursos en línea: Acceso libre Resumen: Previous studies on the impact of hexavalent chromium [Cr(VI)] on mammalian cell energetics revealed alterations suggestive of a shift to a more fermentative metabolism. Aiming at a more defined understanding of the metabolic effects of Cr(VI) and of their molecular basis, we assessed the impact of a mild Cr(VI) exposure on critical bioenergetic parameters (lactate production, oxygen consumption and intracellular ATP levels). Cells derived from normal human bronchial epithelium (BEAS-2B cell line), the main in vivo target of Cr(VI) carcinogenicity, were subjected for 48 h to 1 μM Cr(VI). We could confirm a shift to a more fermentative metabolism, resulting from the simultaneous inhibition of respiration and stimulation of glycolysis. This shift was accompanied by a decrease in the protein levels of the catalytic subunit (subunit β) of the mitochondrial H+-ATP synthase (β-F1-ATPase) and a concomitant marked increase in those of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). The corresponding alteration in the β-F1-ATPase/GAPDH protein ratio (viewed as a bioenergetic signature) upon Cr(VI) exposure was in agreement with the observed attenuation of cellular respiration and enhancement of glycolytic flux. Altogether, these results constitute a novel finding in terms of the molecular mechanisms of Cr(VI) effects.
Abbreviations: Cr(III), trivalent chromium; Cr(IV), tetravalent chromium; Cr(V), pentavalent chromium; Cr(VI), hexavalent chromium; DCF, 2′,7′-dichlorofluorescein; 2-DG, 2-deoxyglucose; 2,4-DNP, 2,4-dinitrophenol; EDTA, ethylenediaminetetracetic acid; ETC, mitochondrial electron transport chain; β-F1-ATPase, catalytic subunit (subunit β) of the mitochondrial H+-ATP synthase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IARC, International Agency for Research on Cancer; OCR, oxygen consumption rate; OXPHOS, oxidative phosphorylation; PBS, phosphate-buffered saline; PI, propidium iodide; ROS, reactive oxygen species; TCA, tricarboxylic acid
Keywords: Chromate lung cancer, Warburg effect, Aerobic glycolysis, Cellular respiration, Cellular bioenergetic index, Cellular energy status
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Artículo
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Navegando Hospital Universitario 12 de Octubre Estantes Cerrar el navegador de estanterías
Formato Vancouver:
Cerveira JF, Sánchez Aragó M, Urbano AM, Cuezva JM. Short-term exposure of nontumorigenic human bronchial epithelial cells to carcinogenic chromium(VI) compromises their respiratory capacity and alters their bioenergetic signature. FEBS Open Bio. 2014 Jun 26;4:594-601.
PMID: 25161867
PMC4141194
Contiene 54 referencias
Previous studies on the impact of hexavalent chromium [Cr(VI)] on mammalian cell energetics revealed alterations suggestive of a shift to a more fermentative metabolism. Aiming at a more defined understanding of the metabolic effects of Cr(VI) and of their molecular basis, we assessed the impact of a mild Cr(VI) exposure on critical bioenergetic parameters (lactate production, oxygen consumption and intracellular ATP levels). Cells derived from normal human bronchial epithelium (BEAS-2B cell line), the main in vivo target of Cr(VI) carcinogenicity, were subjected for 48 h to 1 μM Cr(VI). We could confirm a shift to a more fermentative metabolism, resulting from the simultaneous inhibition of respiration and stimulation of glycolysis. This shift was accompanied by a decrease in the protein levels of the catalytic subunit (subunit β) of the mitochondrial H+-ATP synthase (β-F1-ATPase) and a concomitant marked increase in those of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). The corresponding alteration in the β-F1-ATPase/GAPDH protein ratio (viewed as a bioenergetic signature) upon Cr(VI) exposure was in agreement with the observed attenuation of cellular respiration and enhancement of glycolytic flux. Altogether, these results constitute a novel finding in terms of the molecular mechanisms of Cr(VI) effects.
Abbreviations: Cr(III), trivalent chromium; Cr(IV), tetravalent chromium; Cr(V), pentavalent chromium; Cr(VI), hexavalent chromium; DCF, 2′,7′-dichlorofluorescein; 2-DG, 2-deoxyglucose; 2,4-DNP, 2,4-dinitrophenol; EDTA, ethylenediaminetetracetic acid; ETC, mitochondrial electron transport chain; β-F1-ATPase, catalytic subunit (subunit β) of the mitochondrial H+-ATP synthase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IARC, International Agency for Research on Cancer; OCR, oxygen consumption rate; OXPHOS, oxidative phosphorylation; PBS, phosphate-buffered saline; PI, propidium iodide; ROS, reactive oxygen species; TCA, tricarboxylic acid
Keywords: Chromate lung cancer, Warburg effect, Aerobic glycolysis, Cellular respiration, Cellular bioenergetic index, Cellular energy status
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