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Shortwave UV‐Induced Damage as Part of the Solar Damage Spectrum Is Not a Major Contributor to Mitochondrial Dysfunction
Author(s) -
Gebhard Daniel,
Matt Katja,
Burger Katharina,
Bergemann Jörg
Publication year - 2014
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21561
Subject(s) - mitochondrial dna , tfam , dna damage , mitochondrion , mitophagy , biology , dna repair , microbiology and biotechnology , genetics , dna , gene , apoptosis , autophagy
Because of the absence of a nucleotide excision repair in mitochondria, ultraviolet (UV)‐induced bulky mitochondrial DNA (mtDNA) lesions persist for several days before they would eventually be removed by mitophagy. Long persistence of this damage might disturb mitochondrial functions, thereby contributing to skin ageing. In this study, we examined the influence of shortwave UV‐induced damage on mitochondrial parameters in normal human skin fibroblasts. We irradiated cells with either sun‐simulating light (SSL) or with ultraviolet C to generate bulky DNA lesions. At equivalent antiproliferative doses, both irradiation regimes induced gene expression of mitochondrial transcription factor A (TFAM) and matrix metallopeptidase 1 (MMP‐1). Only irradiation with SSL, however, caused significant changes in mtDNA copy number and a decrease in mitochondrial respiration. Our results indicate that shortwave UV‐induced damage as part of the solar spectrum is not a major contributor to mitochondrial dysfunction.