Telomere shortening during aging: Attenuation by antioxidants and anti-inflammatory agents

•Age-related decline in telomerase activity can be retarded by dietary constituents.•Antioxidant and anti-infllammatory agents may slow the loss of telomere length.•The response of tumour cells to protective agents differs from that of normal cells. Telomeres are a repeated sequence -of bases found...

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Bibliographic Details
Published inMechanisms of ageing and development Vol. 164; pp. 61 - 66
Main Authors Prasad, Kedar N., Wu, Meixia, Bondy, Stephen C.
Format Journal Article
LanguageEnglish
Published Ireland Elsevier B.V 01.06.2017
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Summary:•Age-related decline in telomerase activity can be retarded by dietary constituents.•Antioxidant and anti-infllammatory agents may slow the loss of telomere length.•The response of tumour cells to protective agents differs from that of normal cells. Telomeres are a repeated sequence -of bases found at the ends of chromosomes. In humans, this sequence is TTAGGG, which is repeated over 2000 times. Telomeres protect the ends chromosomes from fusion with nearby chromosomes, and allow effective replication of DNA. Each time a cell divides, 25–200 base pairs are lost from the terminal sequence of chromosomes. By becoming truncated during cell division, telomeres protect essential genes from being shortened and thus inactivated. In addition, telomeres are sensitive to inflammation and oxidative stress, which can further promote telomere shortening. Reduction in the length of telomeres leads to the cessation of cell division and thus cellular senescence and apoptosis. This review discusses evidence for the role of oxidative stress and inflammation in regulating the length of telomeres in mammalian cells during senescence. Evidence is presented suggesting that antioxidants and anti-inflammatories can reduce the pace of shortening of telomere length during aging. The distinctive properties of transformed cells suggest that treatment with such materials will have a deleterious rather than a protective effect on such abnormal cells.
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ISSN:0047-6374
1872-6216
DOI:10.1016/j.mad.2017.04.004