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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Telomere shortening and haemodialysis.

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          Abstract

          Increased oxidative stress is a well described feature of haemodialysis (HD). This is secondary to an increase in the production of reactive oxygen species and impaired antioxidant mechanisms. Telomeres are the specialized ends of eukaryotic chromosomes and consist of tandemly repeated DNA sequences. Telomeres shorten with each cell division and it is well known that telomere length in peripheral blood mononuclear cells (PBMCs) decreases with age. Telomere shortening rate is increased by oxidative stress. In this study we have examined a possible relationship between oxidative stress and telomere shortening in haemodialysis.

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          Oxidative stress shortens telomeres.

          Thomas von Zglinicki (2002)
          Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA. Oxidative damage is repaired less well in telomeric DNA than elsewhere in the chromosome, and oxidative stress accelerates telomere loss, whereas antioxidants decelerate it. I suggest here that oxidative stress is an important modulator of telomere loss and that telomere-driven replicative senescence is primarily a stress response. This might have evolved to block the growth of cells that have been exposed to a high risk of mutation.
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            The rate of telomere sequence loss in human leukocytes varies with age.

            R. Frenck, E H Blackburn, K Shannon (1998)
            A gradual loss of telomeric repeat sequences with aging previously has been noted in normal adult tissues, and this process has been implicated in cell senescence. No data exist that address the rate of telomere shortening in normal human cells within families or early in life. To address these questions, we measured telomere lengths in peripheral blood leukocytes (PBLs) from 75 members of 12 families and in a group of unrelated healthy children who were 5-48 months old. Here we report the surprising observation that rates of telomere attrition vary markedly at different ages. Telomeric repeats are lost rapidly (at a rate of >1 kilobase per year) from the PBLs of young children, followed by an apparent plateau between age 4 and young adulthood, and by gradual attrition later in life. These data suggest that the loss of telomeric repeats in hematopoietic cells is a dynamic process that is differentially regulated in young children and adults. Our results have implications for current models of how telomeric sequences are lost in normal somatic cells and suggest that PBLs are an excellent tissue to investigate how this process is controlled.
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              Telomere shortening in atherosclerosis.

              R Thompson, R Boultby, Nilesh J. Samani … (2001)
              Eukaryotic chromosomes end with telomeres, which shorten with cellular ageing. We investigated whether atherosclerosis is associated with systemic evidence of accelerated cellular ageing. We compared mean length of terminal restriction fragments (TRF), a measure of average telomere size, in leucocyte DNA of ten patients with severe coronary artery disease (CAD) with that of 20 controls without CAD. Adjusting for age and sex, cases had mean TRF lengths of 303 (SD 90) base pairs shorter than those of controls (p=0.002)-ie, equivalent in size to individuals with no CAD who are 8.6 years older. Although this is a pilot study, the findings could be relevant to the pathogenesis of atherosclerosis.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Blood Purif.
                Title: Blood purification
                Publisher: S. Karger AG
                ISSN: 0253-5068
                ISSN (Print): 0253-5068
                Publication date (Electronic): 2006
                Volume: 24
                Issue: 2
                Affiliations
                [1 ] Institute of Human Genetics and Institute for Ageing and Health, University of Newcastle upon Tyne, and Renal Unit, Newcastle upon Tyne Hospitals NHS Trust, Newcastle upon Tyne, UK.
                Article
                Publisher Item ID: 90517
                DOI: 10.1159/000090517
                PubMed ID: 16373996
                SO-VID: 0f6fdf8e-8c47-4bd2-8f2f-953e4adfebf4
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