Publication details

Base excision repair, aging and health span

Authors

XU Guogang HERZIG Maryane ROTREKL Vladimír WALTER Christi, A.

Year of publication 2008
Type Article in Periodical
Magazine / Source Mechanisms of ageing and development
MU Faculty or unit

Faculty of Medicine

Citation
Web https://www.sciencedirect.com/science/article/pii/S0047637408000675?via%3Dihub
Doi http://dx.doi.org/10.1016/j.mad.2008.03.001
Field Biochemistry
Keywords Base excision repair; Aging; DNA damage; Mutagenesis; Health span
Description DNA damage and mutagenesis are suggested to contribute to aging through their ability to mediate cellular dysfunction. The base excision repair (BER) pathway ameliorates a large number of DNA lesions that arise spontaneously. Many of these lesions are reported to increase with age. The specific BER protein that appears to limit activity varies among tissues. DNA polymerase-beta is reduced in brain from aged mice and rats while AP endonuclease is reduced in spermatogenic cells obtained from old mice. The differences in proteins that appear to limit BER activity among tissues may represent true tissue-specific differences in activity or may be due to differences in techniques, environmental conditions or other unidentified differences among the experimental approaches. Much remains to be addressed concerning the potential role of BER in aging and age-related health span.

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