长期暴露于颗粒状六价铬会诱发原代啮齿动物肺细胞 DNA 双链断裂并抑制同源重组修复

IF 3.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Biological Trace Element Research Pub Date : 2024-12-01 Epub Date: 2024-03-18 DOI:10.1007/s12011-024-04136-1
James T F Wise, Haiyan Lu, Idoia Meaza, Sandra S Wise, Aggie R Williams, Jamie Young Wise, Michael D Mason, John Pierce Wise
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引用次数: 0

摘要

六价铬[Cr(VI)]是一种已知的肺致癌物质,在人类肺细胞中,Cr(VI)诱发肺癌的驱动机制是染色体不稳定,这是由于长期接触六价铬会诱发 DNA 双链断裂,同时抑制这些断裂的修复。在北大西洋露脊鲸中,六价铬会诱发断裂,但不会抑制修复。目前还不清楚这种修复抑制作用是人类肺细胞特有的,还是发生在其他物种中,因为这种抑制作用只在人类和北大西洋露脊鲸中出现过。我们在啮齿动物细胞中评估了这些结果,因为啮齿动物是金属诱发肺癌的实验模型。我们使用了豚鼠肺成纤维细胞系 JH4 克隆 1 和大鼠肺成纤维细胞。将细胞暴露于两种不同的微粒六价铬化合物(0 至 0.5 微克/平方厘米)中 24 或 120 小时,并对细胞毒性、DNA 双链断裂和 DNA 双链断裂修复进行评估。在急性和长期暴露后,这两种微粒六价铬化合物都会引起细胞毒性和DNA双链断裂的浓度依赖性增加。值得注意的是,急性接触后,铬(VI)诱导的 DNA 双链断裂修复增加,而长期接触后,这些断裂的修复受到抑制。这些结果与人类肺细胞的结果一致,表明啮齿类动物细胞的反应与人类细胞相似,而鲸鱼细胞的反应则明显不同。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Prolonged Particulate Hexavalent Chromium Exposure Induces DNA Double-Strand Breaks and Inhibits Homologous Recombination Repair in Primary Rodent Lung Cells.

Hexavalent chromium [Cr(VI)] is a known lung carcinogen and a driving mechanism in human lung cells for Cr(VI)-induced lung cancer is chromosome instability, caused by prolonged Cr(VI) exposure inducing DNA double-strand breaks, while simultaneously inhibiting the repair of these breaks. In North Atlantic right whales, Cr(VI) induces breaks but does not inhibit repair. It is unclear if this repair inhibition is specific to human lung cells or occurs in other species, as it has only been considered in humans and North Atlantic right whales. We evaluated these outcomes in rodent cells, as rodents are an experimental model for metal-induced lung carcinogenesis. We used a guinea pig lung fibroblast cell line, JH4 Clone 1, and rat lung fibroblasts. Cells were exposed to two different particulate Cr(VI) compounds, ranging from 0 to 0.5 ug/cm2, for 24 or 120 h and assessed for cytotoxicity, DNA double-strand breaks, and DNA double-strand break repair. Both particulate Cr(VI) compounds induced a concentration-dependent increase in cytotoxicity and DNA double-strand breaks after acute and prolonged exposures. Notably, while the repair of Cr(VI)-induced DNA double-strand breaks increased after acute exposure, the repair of these breaks was inhibited after prolonged exposure. These results are consistent with outcomes in human lung cells indicating rodent cells respond like human cells, while whale cells have a markedly different response.

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来源期刊
Biological Trace Element Research
Biological Trace Element Research 生物-内分泌学与代谢
CiteScore
8.70
自引率
10.30%
发文量
459
审稿时长
2 months
期刊介绍: Biological Trace Element Research provides a much-needed central forum for the emergent, interdisciplinary field of research on the biological, environmental, and biomedical roles of trace elements. Rather than confine itself to biochemistry, the journal emphasizes the integrative aspects of trace metal research in all appropriate fields, publishing human and animal nutritional studies devoted to the fundamental chemistry and biochemistry at issue as well as to the elucidation of the relevant aspects of preventive medicine, epidemiology, clinical chemistry, agriculture, endocrinology, animal science, pharmacology, microbiology, toxicology, virology, marine biology, sensory physiology, developmental biology, and related fields.
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