Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/25767
Title: Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats
Authors: 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. 
Keywords: Bioenergetics; Dioxin; mitoKATP; Mitochondria; ROS; TCDD
Issue Date: 2013
Publisher: Elsevier Ltd.
Serial title, monograph or event: Environmental Pollution
Volume: 180
Abstract: 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.
URI: http://hdl.handle.net/10316/25767
DOI: 10.1016/j.envpol.2013.05.049
Rights: openAccess
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais

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