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How mitochondria record the effects of UV exposure and oxidative stress using human skin as a model tissue
Author(s) -
Mark A. BirchMachin,
Helen Swalwell
Publication year - 2009
Publication title -
mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.723
H-Index - 91
eISSN - 1464-3804
pISSN - 0267-8357
DOI - 10.1093/mutage/gep061
Subject(s) - mitochondrial dna , oxidative stress , mitochondrion , human skin , ageing , biology , dna damage , oxidative phosphorylation , skin cancer , mutation , genetics , gene , microbiology and biotechnology , dna , cancer , biochemistry
The accumulation of mitochondrial DNA (mtDNA) mutations has been proposed as an underlying cause of the ageing process and mutations have been associated with cancer in many tissues, including human skin. This involvement is linked to the key roles of mitochondrial function and mtDNA in oxidative stress production and as a mediator of apoptosis. We and others have pioneered the use of mtDNA damage as a highly sensitive biomarker of ultraviolet exposure in human skin and have also shown that the accumulation of an ageing-dependent mtDNA mutation is accelerated by exposure to sunlight, which is known to induce oxidative stress in skin. This is important as ultraviolet radiation (UVR)-induced gene mutations play a key role in the development of skin cancer and ageing in human skin. Novel applications of mtDNA as a biomarker of UVR-induced oxidative stress will also be highlighted in this review.

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