title: Effects of nickel-smelting fumes on the regulation of NIH/3T3 cell viability, necrosis, and expression of hMLH1 and RASSF1A.
abstract: 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.
authors.affiliation: Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China.
authors.forename: Cui-Ping
authors.initials: CP
authors.lastname: Yu
authors.affiliation: Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China.
authors.forename: Xue-Ying
authors.initials: XY
authors.lastname: Hu
authors.affiliation: Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, Heilongjiang Province, China.
authors.forename: Yong-Hui
authors.initials: YH
authors.lastname: Wu
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism*; D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D005786:Gene Expression Regulation / Q000187:drug effects; D007220:Industrial Waste / Q000009:adverse effects; D051379:Mice; D046529:Microscopy, Electron, Transmission; D023421:Models, Animal; D000070957:MutL Protein Homolog 1; D041681:NIH 3T3 Cells; D009336:Necrosis / Q000209:etiology / Q000473:pathology; D009532:Nickel / Q000633:toxicity*; D009687:Nuclear Proteins / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000378:metabolism*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D000393:Air Pollutants; D007220:Industrial Waste; C501485:Mlh1 protein, mouse; D009687:Nuclear Proteins; C496882:RASSF1 protein, mouse; D012333:RNA, Messenger; D025521:Tumor Suppressor Proteins; D009532:Nickel; D000070957:MutL Protein Homolog 1