Antioxidant defences and homeostasis of reactive oxygen species in different human mitochondrial DNA-depleted cell lines

Vergani, Lodovica, Floreani, Maura, Russell, Aaron, Ceccon, Mara, Napoli, Eleonore, Cabrelle, Anna, Valente, Lucia, Bragantini, Federica, Leger, Bertrand and Dabbeni-Sala, Federica 2004, Antioxidant defences and homeostasis of reactive oxygen species in different human mitochondrial DNA-depleted cell lines, European journal of biochemistry, vol. 271, no. 18, pp. 3646-3656, doi: 10.1111/j.1432-1033.2004.04298.x.

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Title Antioxidant defences and homeostasis of reactive oxygen species in different human mitochondrial DNA-depleted cell lines
Author(s) Vergani, Lodovica
Floreani, Maura
Russell, AaronORCID iD for Russell, Aaron
Ceccon, Mara
Napoli, Eleonore
Cabrelle, Anna
Valente, Lucia
Bragantini, Federica
Leger, Bertrand
Dabbeni-Sala, Federica
Journal name European journal of biochemistry
Volume number 271
Issue number 18
Start page 3646
End page 3656
Publisher Blackwell Publishing Ltd
Place of publication Oxford, England
Publication date 2004
ISSN 1742-464x
Keyword(s) A549 ρ0 cells
antioxidant defences
143 ρ0 cells
reactive oxygen species
rhabdomyosarcoma ρ0 cells
Summary Three pairs of parental (ρ+) and established mitochondrial DNA depleted (ρ0) cells, derived from bone, lung and muscle were used to verify the influence of the nuclear background and the lack of efficient mitochondrial respiratory chain on antioxidant defences and homeostasis of intracellular reactive oxygen species (ROS). Mitochondrial DNA depletion significantly lowered glutathione reductase activity, glutathione (GSH) content, and consistently altered the GSH2 : oxidized glutathione ratio in all of the ρ0 cell lines, albeit to differing extents, indicating the most oxidized redox state in bone ρ0 cells. Activity, as well as gene expression and protein content, of superoxide dismutase showed a decrease in bone and muscle ρ0 cell lines but not in lung ρ0 cells. GSH peroxidase activity was four times higher in all three ρ0 cell lines in comparison to the parental ρ+, suggesting that this may be a necessary adaptation for survival without a functional respiratory chain. Taken together, these data suggest that the lack of respiratory chain prompts the cells to reduce their need for antioxidant defences in a tissue-specific manner, exposing them to a major risk of oxidative injury. In fact bone-derived ρ0 cells displayed the highest steady-state level of intracellular ROS (measured directly by 2',7'-dichlorofluorescin, or indirectly by aconitase activity) compared to all the other ρ+ and ρ0 cells, both in the presence or absence of glucose. Analysis of mitochondrial and cytosolic/iron regulatory protein-1 aconitase indicated that most ROS of bone ρ0 cells originate from sources other than mitochondria.
Language eng
DOI 10.1111/j.1432-1033.2004.04298.x
Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2004, FEBS
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