Abstract
Environmental pollutants such as TCDD and tetraethyl lead are extremely toxic and related with pulmonary disease development. Lung mitochondria are primary cellular targets for dioxins exposure-induced toxicity. TCDD showed a delay in the repolarization after a phosphorylative cycle and a decrease on state 3 respiration, suggesting alterations at the phosphorylative system level. The ATPase activity showed no differences between control and lung mitochondria incubated with TCDD, implying alterations in other components of the phosphorylative system. Tetraethyl lead also showed a delay in the repolarization after a phosphorylative cycle and a decrease on RCR. These data suggest that lung mitochondria incubated with TCDD and tetraethyl lead showed impaired mitochondrial function, reflecting the loss of oxidative phosphorylation capacity.
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Acknowledgements
J. P. Teodoro and F. V. Duarte are recipients of a fellowship from Science and Technology Foundation (SFRH/BD/38467/2007 and SFRH/BD/38372/2007, respectively).
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.