3,3 ',4,4 ',5-五氯联苯对人体Kv1.3和Kv1.5通道的影响

Jong-Hui Kim, Soobeen Hwang, Seo-in Park, S. Jo
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引用次数: 1

摘要

在可能破坏动物和人类内分泌系统的环境化学物质中,多氯联苯(PCBs)是一类令人相当关注的化学物质。PCB由两个由单个碳键连接的六碳环组成,理论上,根据氯的数量和它们在联苯环上的位置,可以形成209个同系物。此外,3,3 ',4,4 ',5-五氯联苯(PCB126)暴露还会增加一氧化氮的产生和活化B细胞在软骨细胞中的结合活性的核因子kappa轻链增强剂,从而作为软骨细胞凋亡的启动物,导致胸腺萎缩和免疫抑制。本研究确定了PCB126的心脏和免疫异常是否由Kv1.3和Kv1.5通道引起。PCB126不影响Kv1.3和Kv1.5通道的稳态电流和峰值电流。然而,PCB126右移了人类Kv1.3通道的稳态激活曲线。这些结果表明,多氯联苯可以以一种不直接阻断电压依赖性钾通道(包括Kv1.3和Kv1.5)的方式影响心脏。
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Effects of 3,3’,4,4’,5-pentachlorobiphenyl on human Kv1.3 and Kv1.5 channels
Among the environmental chemicals that may be able to disrupt the endocrine systems of animals and humans are polychlorinated biphenyls (PCBs), a chemical class of considerable concern. PCB consists of two six-carbon rings linked by a single carbon bond, and theoretically, 209 congeners can form, depending on the number of chlorines and their location on the biphenyl rings. Furthermore, 3,3’,4,4’,5-pentachlorobiphenyl (PCB126) exposure also increases nitric oxide production and nuclear factor kappa-light-chain-enhancer of activated B cells binding activity in chondrocytes, thus contributing as an initiator of chondrocyte apoptosis and resulting in thymic atrophy and immunosuppression. This study identified whether cardiac and immune abnormalities from PCB126 were caused by the Kv1.3 and Kv1.5 channels. PCB126 did not affect either the steady-state current or peak current of the Kv1.3 and Kv1.5 channels. However, PCB126 right-shifted the steady-state activation curves of human Kv1.3 channels. These results suggest that PCBs can affect the heart in a way that does not block voltage-dependent potassium channels including Kv1.3 and Kv1.5 directly.
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