Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activ...

• Autor(es): Pereira, Susana P. ; Pereira, Gonçalo C. ; Pereira, Cláudia V. ; Carvalho, Filipa S. ; Cordeiro, Marília H. ; Mota, Paula C. ; Ramalho-Santos, J. ; Moreno, A. J. M. ; Oliveira, Paulo J.
• Data: 2013
• Identificador Persistente: http://hdl.handle.net/10316/25767
• Origem: Estudo Geral - Universidade de Coimbra
• Assunto(s): Bioenergetics; Dioxin; mitoKATP; Mitochondria; ROS; TCDD
• Tipo de Documento: Artigo
• Idioma: Inglês

Descrição

The environmental dioxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a Group 1 human carcinogen and teratogenic agent.We hypothesize that TCDD-induced oxidative stress may also interfere with mitochondrial ATP-sensitive potassium channels (mitoKATP), which are known to regulate and to be regulated by mitochondrial redox state. We investigated the effects of an acute treatment of male Wistar rats with TCDD (50 mg/kg i.p.) and measured the regulation of cardiac mitoKATP. While the function of cardiac mitochondria was slightly depressed, mitoKATP activity was 52% higher in animals treated with TCDD. The same effects were not observed in liver mitochondria isolated from the same animals. Our data also shows that regulation of mitochondrial ROS production by mitoKATP activity is different in both groups. To our knowledge, this is the first report to show that TCDD increases mitoKATP activity in the heart, which may counteract the increased oxidative stress caused by the dioxin during acute exposure. SPP and GCP are supported by a Portuguese Foundation for Science and Technology (FCT) Ph.D. fellowship (SFRH/BD/64247/ 2009 and SFRH/BD/36938/2007). The present work is supported by FCT grants PTDC-SAU-OSM-64084-2006 and PTDC/QUI-QUI/ 101409/2008 (to PO) and PEst-C/SAU/LA0001/2011 (to CNC) cofunded by FEDER, COMPETE and the Portuguese National Funds.