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Journal of Environmental Pathology, Toxicology and Oncology
Facteur d'impact: 1.241 Facteur d'impact sur 5 ans: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Imprimer: 0731-8898
ISSN En ligne: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2014007260
pages 1-9

Effects of Nickel-Smelting Fumes on the Regulation of NIH/3T3 Cell Viability, Necrosis, and Expression of hMLH1 and RASSF1A

Jun Wang
Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China
Cui-Ping Yu
Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China
Xue-Ying Hu
Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China
Yong-Hui Wu
Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China

RÉSUMÉ

Nickel is widely used and distributed in various industries. This study investigated the effect of nickel-smelting fumes on the regulation of NIH/3T3 cell viability, apoptosis, and necrosis and the expression of the tumor suppressor genes hMLH1 and RASSF1A. Cell viability was determined using a methylthiazolyl tetrazolium colorimetric assay. NIH/3T3 cell viability was reduced after exposure to different concentrations of nickel-smelting fumes, but cell apoptosis and necrosis were induced. Moreover, cell morphology changed significantly after exposure to different concentrations of nickel-smelting fumes, as determined using an inverted microscope or transmission electron microscope. Real-time RT-PCR and Western blot analyses showed that exposure of cells to concentrations of ≥100 µg/mL of nickel-smelting fumes upregulated the expression of hMLH1 and RASSF1A compared to the negative controls. These data suggest that nickel-smelting fumes could be toxic to cells, upregulating the expression of hMLH1 and RASSF1A and in turn inducing cell apoptosis and necrosis.


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