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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Hyperosmolality in the form of elevated NaCl but not urea causes DNA damage in murine kidney cells
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Hyperosmolality in the form of elevated NaCl but not urea causes DNA damage in murine kidney cells

机译：高渗的NaCl而不是尿素以高渗形式引起鼠肾细胞DNA损伤

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摘要

This study demonstrates, by using neutral comet assay and pulsed field gel electrophoresis, that hyperosmotic stress causes DNA damage in the form of double strand breaks (dsb). Different solutes increase the rate of DNA dsb to different degrees at identical strengths of hyperosmolality. Hyperosmolality in the form of elevated NaCl (HNa) is most potent in this regard, whereas hyper- osmolality in the form of elevated urea (HU) does not cause DNA dsb. The amount of DNA dsb increases significantly as early as 1S min after the onset of HNa. By using neutral comet and DNA ladder assays. we show that this rapid induction of DNA damage is not attributable to apoptosis. We demonstrate that renal inner med- ullary cells are able to efficiently repair hyperosmotic DNA damage within 48 h after exposure to hyperosmolality. DNA repair corre- lates with cell survival and is repressed by 25 μM LY294002. an inhibitor of DNA-activated protein kinases. These results strongly suggest that the hyperosmotic stress resistance of renal inner medullary cells is based not only on adaptations that protect cellular proteins from osmotic damage but, in addition, on adap- tations that compensate DNA damage and maintain genomic integrity.
机译：这项研究通过使用中性彗星试验和脉冲场凝胶电泳证明，高渗胁迫以双链断裂（dsb）的形式引起DNA损伤。在相同的高渗浓度下，不同的溶质会不同程度地提高DNA dsb的比率。在这方面，NaCl（HNa）升高的高渗性最有效，而尿素（HU）升高的高渗透性不会引起DNA dsb。 DNA dsb的数量早在HNa发病后1S分钟就显着增加。通过使用中性彗星和DNA阶梯分析。我们表明，DNA损伤的这种快速诱导并非归因于细胞凋亡。我们证明，肾内髓质细胞能够在暴露于高渗血症后48小时内有效修复高渗DNA损伤。 DNA修复与细胞存活有关，并被25μMLY294002抑制。 DNA活化蛋白激酶的抑制剂。这些结果强烈表明，肾内髓质细胞的高渗应激抗性不仅基于保护细胞蛋白免受渗透性损害的适应，而且还基于补偿DNA损害并保持基因组完整性的适应。

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