Exposure to cigarette tar inhibits ribonucleotide reductase and blocks lymphocyte proliferation
Exposure to cigarette tar inhibits ribonucleotide reductase and blocks lymphocyte proliferation
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DOI：
10.4049/jimmunol.165.12.6771
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发表时间：
2000-12-15
影响因子：
4.4
通讯作者：
Freed, BM
中科院分区：
文献类型：
--
作者：
McCue, JM;Link, KL;Freed, BM
吸烟会严重抑制肺部 T 细胞反应，这与呼吸道感染的易感性增加和特纳监测减少有关。人类 T 细胞接触香烟焦油或其主要酚类成分、对苯二酚和儿茶酚，会导致 DNA 合成立即停止，而不会产生细胞毒性。然而，人们对这种现象发生的机制知之甚少。在本报告中，我们证明对苯二酚和儿茶酚通过猝灭核糖核苷酸还原酶 M2 亚基中必需的酪氨酰自由基来抑制淋巴细胞增殖。
Cigarette smoking causes profound suppression of pulmonary T cell responses, which has been associated with increased susceptibility to respiratory tract infections and decreased turner surveillance. Exposure of human T cells to cigarette tar or its major phenolic components, hydroquinone and catechol, causes an immediate cessation of DNA synthesis without cytotoxicity. However, Little is known of the mechanisms by which this phenomenon occurs. In this report we demonstrate that hydroquinone and catechol Inhibit lymphocyte proliferation by quenching the essential tyrosyl radical in the M2 subunit of ribonucleotide reductase.