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首页> 外文期刊>Journal of applied toxicology >Effects of DDT and triclosan on tumor-cell binding capacity and cell-surface protein expression of human natural killer cells
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Effects of DDT and triclosan on tumor-cell binding capacity and cell-surface protein expression of human natural killer cells

机译：滴滴涕和三氯生对人自然杀伤细胞肿瘤细胞结合能力和细胞表面蛋白表达的影响

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1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (DDT) and triclosan (TCS) are organochlorine (OC) compounds that contaminate the environment, are found in human blood and have been shown to decrease the tumor-cell killing (lytic) function of human natural killer (NK) cells. NK cells defend against tumor cells and virally infected cells. They bind to these targets, utilizing a variety of cell surface proteins. The present study examined concentrations of DDT and TCS that decrease lytic function for alteration of NK binding to tumor targets. Levels of either compound that caused loss of binding function were then examined for effects on expression of cell-surface proteins needed for binding. NK cells exposed to 2.5 μM DDT for 24 h (which caused a greater than 55% loss of lytic function) showed a decrease in NK binding function of about 22%, and a decrease in CD16 cell-surface protein of 20%. NK cells exposed to 5 μM TCS for 24 h showed a decrease in ability to bind tumor cells of 37% and a decrease in expression of CD56 of about 34%. This same treatment caused a decrease in lytic function of greater than 87%. These results indicated that only a portion of the loss of NK lytic function seen with exposures to these compounds could be accounted for by loss of binding function. They also showed that loss of binding function is accompanied by a loss of cell-surface proteins important in binding function.
机译：1,1,1-三氯-2,2-双（4-氯苯基）乙烷（DDT）和三氯生（TCS）是污染环境的有机氯（OC）化合物，存在于人的血液中，并已证明能减少人类自然杀伤（NK）细胞的肿瘤细胞杀伤（裂解）功能。 NK细胞防御肿瘤细胞和病毒感染的细胞。它们利用多种细胞表面蛋白与这些靶标结合。本研究检查了DDT和TCS的浓度，这些浓度会降低裂解功能以改变NK与肿瘤靶标的结合。然后检查引起结合功能丧失的任一化合物的水平对结合所需的细胞表面蛋白表达的影响。暴露于2.5μMDDT中24小时的NK细胞（导致裂解功能损失超过55％）显示出NK结合功能降低约22％，CD16细胞表面蛋白降低20％。暴露于5μMTCS 24小时的NK细胞与肿瘤细胞结合的能力下降了37％，CD56表达下降了约34％。相同的处理导致裂解功能下降超过87％。这些结果表明，仅暴露于这些化合物的NK裂解功能丧失的一部分可以归因于结合功能的丧失。他们还表明结合功能的丧失伴随着对结合功能重要的细胞表面蛋白的丧失。

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