Exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin and tetraethyl lead affects lung mitochondria bioenergetics
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 o...
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Published in | Toxicology mechanisms and methods Vol. 20; no. 1; pp. 1 - 6 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
England
Informa UK Ltd
01.01.2010
Taylor & Francis |
Subjects | |
Online Access | Get full text |
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Summary: | 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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 1537-6516 1537-6524 |
DOI: | 10.3109/15376510903527916 |