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Dibenzofuran-induced mitochondrial dysfunction: Interaction with ANT carrier.

F V Duarte¹, A P Gomes, J S Teodoro

¹CNC - Center for Neurosciences and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal; Department of Life Sciences, Faculty of Sciences and Technology, University of Coimbra, Apartado 3046, 3001-401 Coimbra, Portugal.

Toxicology in Vitro : an International Journal Published in Association with BIBRA

|September 7, 2013

Summary

Dibenzofuran (DBF) exposure disrupts mitochondrial function by interfering with the adenine nucleotide translocase (ANT). This pollutant impairs cellular energy production and inhibits the mitochondrial permeability transition (MPT), potentially contributing to disease.

Keywords:

Adenine nucleotide translocator (ANT)Cyclophilin D (CypD)Dibenzofuran (DBF)Mitochondria Mitochondrial permeability transition (MPT)

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Area of Science:

Environmental Toxicology
Mitochondrial Biology
Biochemistry

Background:

Environmental pollutants like dibenzofuran (DBF) are linked to diseases, including cancers.
Mitochondria are crucial for cellular energy and homeostasis; their dysfunction can lead to organ failure.
DBF is a persistent, bioaccumulative, and toxic pollutant of concern.

Purpose of the Study:

To investigate the effects of dibenzofuran (DBF) on isolated rat liver mitochondria.
To elucidate the specific molecular mechanisms by which DBF impacts mitochondrial function.

Main Methods:

Isolated rat liver mitochondria were exposed to DBF.
Mitochondrial function was assessed by measuring ADP phosphorylation, ATPase activity, and calcium-induced mitochondrial permeability transition (MPT).
Adenine nucleotide translocase (ANT) and Cyclophilin D (CypD) interactions were analyzed using co-immunoprecipitation.

Main Results:

DBF exposure increased the lag phase of ADP-induced depolarization and decreased ATPase activity, indicating interference with the phosphorylative system.
DBF increased the threshold for calcium-induced MPT and enhanced calcium retention capacity.
DBF was shown to interfere with ANT, reducing CypD binding and inhibiting MPT.

Conclusions:

Dibenzofuran (DBF) impairs mitochondrial bioenergetics and function by interacting with the adenine nucleotide translocase (ANT).
DBF's inhibition of the mitochondrial permeability transition (MPT) and its effects on ANT binding suggest a novel mechanism of toxicity.
Understanding these pollutant-induced mitochondrial dysfunctions may explain the progression of chronic diseases linked to environmental exposures.