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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Protein adducts of malondialdehyde and 4-hydroxynonenal contribute to trichloroethene-mediated autoimmunity via activating Th17 cells: Dose- and time-response studies in female MRL+/+ mice
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Protein adducts of malondialdehyde and 4-hydroxynonenal contribute to trichloroethene-mediated autoimmunity via activating Th17 cells: Dose- and time-response studies in female MRL+/+ mice

机译：丙二醛和4-羟基壬烯醛的蛋白质加合物通过激活Th17细胞促进三氯乙烯介导的自身免疫：雌性MRL + / +小鼠的剂量和时间响应研究

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Trichloroethene (TCE), a common occupational and environmental toxicant, is known to induce autoimmunity. Previous studies in our laboratory showed increased oxidative stress in TCE-mediated autoimmunity. To further establish the role of oxidative stress and to investigate the mechanisms of TCE-mediated autoimmunity, dose- and time-response studies were conducted in MRL+/+ mice by treating them with TCE via drinking water at doses of 0.5, 1.0 or 2.0. mg/ml for 12, 24 or 36 weeks. TCE exposure led to dose-related increases in malondialdehyde (MDA)-/hydroxynonenal (HNE)-protein adducts and their corresponding antibodies in the sera and decreases in GSH and GSH/GSSG ratio in the kidneys at 24 and 36 weeks, with greater changes at 36 weeks. The increases in these protein adducts and decreases in GSH/GSSG ratio were associated with significant elevation in serum anti-nuclear- and anti-ssDNA-antibodies, suggesting an association between TCE-induced oxidative stress and autoimmune response. Interestingly, splenocytes from mice treated with TCE for 24 weeks secreted significantly higher levels of IL-17 and IL-21 than did splenocytes from controls after stimulation with MDA-mouse serum albumin (MSA) or HNE-MSA adducts. The increased release of these cytokines showed a dose-related response and was more pronounced in mice treated with TCE for 36 weeks. These studies provide evidence that MDA- and or HNE-protein adducts contribute to TCE-mediated autoimmunity, which may be via activation of Th17 cells.
机译：众所周知，三氯乙烯（TCE）是一种常见的职业和环境毒物，可诱导自身免疫。我们实验室先前的研究表明，TCE介导的自身免疫中氧化应激增加。为了进一步确定氧化应激的作用并研究TCE介导的自身免疫的机制，在MRL + / +小鼠中通过以0.5、1.0或2.0的饮用水通过TCE处理，对它们进行了剂量和时间反应研究。毫克/毫升，持续12、24或36周。 TCE暴露导致血清中丙二醛（MDA）/羟壬醛（HNE）蛋白加合物及其相应抗体的剂量相关增加，并且在24和36周时肾脏中GSH和GSH / GSSG比值降低，变化更大在36周时。这些蛋白质加合物的增加和GSH / GSSG比的降低与血清抗核和抗SSDNA抗体的显着升高有关，表明TCE诱导的氧化应激与自身免疫反应之间存在关联。有趣的是，用MDA-小鼠血清白蛋白（MSA）或HNE-MSA加合物刺激后，经TCE处理24周的小鼠的脾细胞分泌的IL-17和IL-21水平明显高于对照组的脾细胞。这些细胞因子的释放增加显示出剂量相关的反应，并且在用TCE治疗36周的小鼠中更为明显。这些研究提供了MDA和/或HNE蛋白加合物有助于TCE介导的自身免疫的证据，可能是通过激活Th17细胞。

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