Suppressive effect of hydroquinone, a benzene metabolite, on in vitro inflammatory responses mediated by macrophages, monocytes, and lymphocytes.

Suppressive effect of hydroquinone, a benzene metabolite, on in vitro inflammatory responses mediated by macrophages, monocytes, and lymphocytes.
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DOI:
10.1155/2008/298010
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发表时间:
2008
影响因子:
4.6
通讯作者:
Cho JY
Cho JY
中科院分区:
医学3区
文献类型:
--
作者:
Cho JY

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我们研究了对苯二酚对细胞因子释放、吞噬作用、NO产生、活性氧产生、细胞-细胞/细胞纤连蛋白粘附和淋巴细胞增殖的抑制作用。我们发现,氢醌抑制促炎细胞因子[肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和IL-6]的产生、毒性分子[一氧化氮(NO)和活性氧(ROS)]的分泌、FITC标记葡聚糖的吞噬摄取、共刺激分子的上调、CD 18和CD 29诱导的U937细胞-细胞粘附,以及来自骨髓和脾脏的淋巴细胞的增殖。考虑到(1)环境化学应激因素降低了慢性吸烟者和儿童对细菌和病毒感染的免疫反应,以及(2)石油工厂的工人患癌症的风险较高,我们的数据表明氢醌可能在病理上抑制单核细胞,巨噬细胞和淋巴细胞介导的炎症反应。
We investigated the inhibitory effects of hydroquinone on cytokine release, phagocytosis, NO production, ROS generation, cell-cell/cell fibronectin adhesion, and lymphocyte proliferation. We found that hydroquinone suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6], secretion of toxic molecules [nitric oxide (NO) and reactive oxygen species (ROS)], phagocytic uptake of FITC-labeled dextran, upregulation of costimulatory molecules, U937 cell-cell adhesion induced by CD18 and CD29, and the proliferation of lymphocytes from the bone marrow and spleen. Considering that (1) environmental chemical stressors reduce the immune response of chronic cigarette smokers and children against bacterial and viral infections and that (2) workers in petroleum factories are at higher risk for cancer, our data suggest that hydroquinone might pathologically inhibit inflammatory responses mediated by monocytes, macrophages, and lymphocytes.
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