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Mitochondrial Alterations in Fanconi Anemia Fibroblasts Following Ultraviolet A or Psoralen Photoactivation ¶
Author(s) -
Rousset Solange,
Nocentini Silvano,
Rouillard Danièlle,
Baroche Christiane,
Moustacchi Ethel
Publication year - 2002
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/0031-8655(2002)0750159maifaf2.0.co2
Subject(s) - reactive oxygen species , cardiolipin , chemistry , fanconi anemia , mitochondrion , psoralen , dna damage , oxygen , oxygen tension , cytosol , microbiology and biotechnology , biophysics , dna repair , dna , biology , biochemistry , membrane , enzyme , phospholipid , organic chemistry
The genetic disease Fanconi anemia (FA), generally considered to be a DNA repair defect, has also been related to a deficiency in cellular defense against reactive oxygen species (ROS). Results show that mitochondrial matrix densification occurs rapidly and transiently in FA fibroblasts following 8‐methoxypsoralen (8‐MOP) photoreaction or ultraviolet A (320 to 380 nm) (UVA) irradiation. This effect is oxygen dependent because it is more important under 20 than under 5% oxygen tension. In contrast, in normal fibroblasts very little, if any, densification of mitochondrial matrix is induced by treatments even at the highest oxygen tension. The changes in matrix density in FA cells are accompanied by some modifications in transmembrane potential, linked to a Fenton‐like reaction, and in mitochondrial cardiolipin content, differing from the responses of normal cells. These data are indicative of some sort of membrane damage induced by 8‐MOP photoreaction and UVA irradiation, to which FA cells appear to be particularly sensitive.