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Effects of 3,3′,4,4′,5-pentachlorobiphenyl on human Kv1.3 and Kv1.5 channels
Article em En | WPRIM | ID: wpr-764042
Biblioteca responsável: WPRO
ABSTRACT
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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Texto completo: 1 Índice: WPRIM Assunto principal: Atrofia / Carbono / Linfócitos B / Canais de Potássio / Terapia de Imunossupressão / Bifenilos Policlorados / Apoptose / Condrócitos / Sistema Endócrino / Coração Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: International Journal of Oral Biology Ano de publicação: 2019 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Assunto principal: Atrofia / Carbono / Linfócitos B / Canais de Potássio / Terapia de Imunossupressão / Bifenilos Policlorados / Apoptose / Condrócitos / Sistema Endócrino / Coração Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: International Journal of Oral Biology Ano de publicação: 2019 Tipo de documento: Article