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首页> 外文期刊>Journal of biochemical and molecular toxicology >Linoleic acid amplifies polychlorinated biphenyl-mediated dysfunction of endothelial cells.
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Linoleic acid amplifies polychlorinated biphenyl-mediated dysfunction of endothelial cells.

机译：亚油酸会放大多氯联苯介导的内皮细胞功能障碍。

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摘要

Selected dietary lipids may increase the atherogenicity of environmental chemicals, such as polychlorinated biphenyls (PCBs), by cross-amplifying mechanisms leading to dysfunction of the vascular endothelium. To investigate this hypothesis, cultured endothelial cells were treated with 90 microM linoleic acid (18:2n-6), followed by either one of two PCBs, 3,3',4,4'-tetrachlorobiphenyl (PCB 77) or 2,2'4,4',5,5'-hexachlorobiphenyl (PCB 153). These PCBs were selected for their varying binding activities with the aryl hydrocarbon (Ah) receptor and differences in their induction of cytochrome P450. PCB 77 disrupted endothelial barrier function by allowing an increase in albumin transfer across endothelial monolayers. Prior cellular enrichment with 18:2 before PCB treatment further diminished endothelial barrier function, as compared to cells treated only with the PCB. This phenomenon appears to be mediated by increased oxidative stress, which is supported by enhanced 2,7-dichlorofluorescein fluorescence, activation data of the oxidative stress-sensitive nuclear transcription factor-kappaB (NF-kappaB), as well as an observed decrease in vitamin E content in the culture media. Similar to the endothelial permeability data, pre-enrichment of cells with 18:2 further increased the PCB-mediated induction of cytochrome P450 1A. In contrast to PCB 77, PCB 153 (or 18:2 plus PCB 153) had little or no effect on endothelial barrier function. Our results suggest that certain unsaturated fatty acids can potentiate PCB-mediated endothelial cell dysfunction and that oxidative stress and activation of the cytochrome P450 1A subfamily may be, in part, responsible for these metabolic events. These findings have implications for understanding the involvement of certain environmental contaminants in diseases that involve dysfunction of the vascular endothelium.
机译：通过交叉扩增机制，导致血管内皮功能障碍，选定的饮食脂质可能会增加环境化学物质（如多氯联苯（PCB））的动脉粥样硬化作用。为了研究这个假设，先用90 microM亚油酸（18：2n-6）处理培养的内皮细胞，然后再用两个PCBs中的一个进行处理：3,3'，4,4'-四氯联苯（PCB 77）或2,2 '4,4'，5,5'-六氯联苯（PCB 153）。选择这些PCB的原因在于它们与芳烃（Ah）受体的结合活性不同，以及它们诱导细胞色素P450的差异。 PCB 77通过增加跨内皮单层的白蛋白转移而破坏了内皮屏障功能。与仅用PCB处理的细胞相比，在PCB处理之前先用18：2富集细胞会进一步减少内皮屏障功能。这种现象似乎是由增加的2,7-二氯荧光素荧光，氧化应激敏感的核转录因子-kappaB（NF-kappaB）的活化数据以及观察到的维生素减少所支持的氧化应激所介导的电子内容在文化媒体上。与内皮通透性数据相似，以18：2进行的细胞预富集进一步增加了PCB介导的细胞色素P450 1A的诱导。与PCB 77相比，PCB 153（或18：2加PCB 153）对内皮屏障功能几乎没有影响。我们的结果表明，某些不饱和脂肪酸可以增强PCB介导的内皮细胞功能障碍，并且氧化应激和细胞色素P450 1A亚家族的激活可能部分负责这些代谢事件。这些发现对于理解某些环境污染物参与涉及血管内皮功能障碍的疾病具有重要意义。

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