小鼠吸入铜焊烟雾后,肺部肿瘤不再增大,肿瘤体积缩小。

IF 3.3 3区 医学 Q2 ONCOLOGY
Patti C Zeidler-Erdely, Vamsi Kodali, Lauryn M Falcone, Robert Mercer, Stephen S Leonard, Aleksandr B Stefaniak, Lindsay Grose, Rebecca Salmen, Taylor Trainor-DeArmitt, Lori A Battelli, Walter McKinney, Samuel Stone, Terence G Meighan, Ella Betler, Sherri Friend, Kristen R Hobbie, Samantha Service, Michael Kashon, James M Antonini, Aaron Erdely
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引用次数: 0

摘要

根据国际癌症研究机构的分类,焊接烟雾属于 1 类致癌物(对人类致癌)。焊接过程会产生富含铁(Fe)的可吸入烟雾,其中可能还含有铬(Cr)和镍(Ni)等已知致癌金属。流行病学证据表明,接触低碳钢(富含铁)和不锈钢(富含铁 + 铬 + 镍)焊接烟尘会增加患肺癌的风险,动物实验数据也支持这些结论。铜镍(CuNi)焊接工艺尚未在肺癌方面进行调查。然而,考虑到铜在致癌和癌症治疗中的作用,铜的研究很有意义。本研究采用两阶段小鼠生物测定法,研究了铜镍烟尘在体外诱导致癌机理关键特征和在体内促进肺肿瘤发生的潜力。雄性 A/J 小鼠以 3-甲基胆蒽(MCA;10 微克/克)为起始剂量,通过全身吸入的方式暴露于镍铜烟雾或空气中九周(低沉积-LD 和高沉积-HD),然后在 30 周时处死。在 BEAS-2B 细胞中,CuNi 烟雾会诱发微核,并导致 DNA 损伤(用 γ-H2AX 测量)。烟尘在细胞毒性和氧化应激方面表现出高反应性和剂量反应。在体内,MCA/CuNi HD 和 LD 能显著减少肺肿瘤和腺瘤的大小。暴露于 MCA/CuNi HD 可明显减少经粗略评估的肿瘤数量。总之,铜镍烟雾在体外表现出致癌物的特征,但在体内,接触铜镍烟雾会导致肿瘤变小、腺瘤减少、增生严重程度降低,而接触高密度铜镍烟雾则会导致总体肺部病变/肿瘤减少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Absence of lung tumor promotion with reduced tumor size in mice after inhalation of copper welding fumes.

Welding fumes are a Group 1 (carcinogenic to humans) carcinogen as classified by the International Agency for Research on Cancer. The process of welding creates inhalable fumes rich in iron (Fe) that may also contain known carcinogenic metals such as chromium (Cr) and nickel (Ni). Epidemiological evidence has shown that both mild steel (Fe-rich) and stainless steel (Fe-rich + Cr + Ni) welding fume exposure increases lung cancer risk, and experimental animal data support these findings. Copper-nickel (CuNi) welding processes have not been investigated in the context of lung cancer. Cu is intriguing, however, given the role of Cu in carcinogenesis and cancer therapeutics. This study examines the potential for a CuNi fume to induce mechanistic key characteristics of carcinogenesis in vitro and to promote lung tumorigenesis, using a two-stage mouse bioassay, in vivo. Male A/J mice, initiated with 3-methylcholanthrene (MCA; 10 µg/g), were exposed to CuNi fumes or air by whole-body inhalation for 9 weeks (low deposition-LD and high deposition-HD) and then sacrificed at 30 weeks. In BEAS-2B cells, the CuNi fume-induced micronuclei and caused DNA damage as measured by γ-H2AX. The fume exhibited high reactivity and a dose-response in cytotoxicity and oxidative stress. In vivo, MCA/CuNi HD and LD significantly decreased lung tumor size and adenomas. MCA/CuNi HD exposure significantly decreased gross-evaluated tumor number. In summary, the CuNi fume in vitro exhibited characteristics of a carcinogen, but in vivo, the exposure resulted in smaller tumors, fewer adenomas, less hyperplasia severity, and with HD exposure, less overall lung lesions/tumors.

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来源期刊
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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