Phosphorylation of Histone H2AX Generated by Linear Alkylbenzene Sulfonates and its Suppression by UVB Exposure
Phosphorylation of Histone H2AX Generated by Linear Alkylbenzene Sulfonates and its Suppression by UVB Exposure
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DOI：
10.1111/php.12268
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发表时间：
2014-07
影响因子：
3.3
通讯作者：
T. Kubota;T. Toyooka;Xiaoxu Zhao;Y. Ibuki
中科院分区：
文献类型：
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作者：
T. Kubota;T. Toyooka;Xiaoxu Zhao;Y. Ibuki
我们之前证明了非离子表面活性剂壬基酚聚乙氧基化物（NPEOs）诱导组蛋白H2 AX（γ-H2 AX）的磷酸化，伴随着DNA双链断裂（DSB），并且暴露于紫外线（UV）降解NPEOs，这有时会增强其DNA损伤能力。在这项研究中，我们发现，线性烷基苯磺酸盐（LAS），一般的阴离子表面活性剂，也产生DSB与γ-H2 AX，这种能力被UVB照射减弱。在人乳腺癌细胞系MCF-7中，LAS处理细胞后立即以剂量依赖性方式产生γ-H2 AX，这归因于DSB的形成，与细胞周期阶段无关。暴露于UVB的LAS产生γ-H2 AX的能力显着降低。HPLC分析表明，LAS是各种烷基链长度的混合物，在各个保留时间处检测到其峰。UVB使LAS的所有峰均匀地降低，没有峰迁移到其他保留时间，这表明UVB可能降解LAS的苯环，但不缩短烷基链。UVB是LAS降解的重要环境因素，表现出诱导DSB的能力，DSB是最严重的DNA损伤类型。
We previously demonstrated that the nonionic surfactants, nonylphenol polyethoxylates (NPEOs) induced the phosphorylation of histone H2AX (γ‐H2AX), accompanied by DNA double‐strand breaks (DSBs), and that exposure to ultraviolet (UV) degraded NPEOs, which sometimes enhanced their DNA‐damaging ability. In this study, we showed that linear alkylbenzene sulfonates (LAS), general anion surfactants, also generated DSBs with γ‐H2AX, and this ability was attenuated by UVB exposure. In the human breast adenocarcinoma cell line, MCF‐7, γ‐H2AX was generated in a dose‐dependent manner immediately after cells were treated with LAS, and this was attributed to the formation of DSBs and was independent of cell cycle phases. The ability to generate γ‐H2AX was markedly reduced in LAS exposed to UVB. HPLC analysis revealed that LAS were a mixture of various alkyl chain lengths, the peaks of which were detected at individual retention times. UVB evenly decreased all peaks of LAS, without migration of peaks to other retention times, which indicated that UVB may degrade the benzene ring of LAS, but did not shorten the alkyl chains. UVB is an important environmental factor in the degradation of LAS exhibiting the ability to induce DSBs, the most serious type of DNA damage.