In vivo antioxidant status, DNA damage, mutation and DNA repair capacity in cultured lymphocytes from healthy 75- to 80-year-old humans

King, Carolyn M.; Bristow-Craig, H.E; Gillespie, E. S.; Barnett, Yvonne

doi:10.1016/s0027-5107(97)00072-9

Cited by 62 publications

(18 citation statements)

References 40 publications

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“…24 The mean ceruloplasmin levels in elderly (45.19 ± 6.61 mg%) and middle-aged group (33.16 ± 4.75 mg%) were significantly higher than that of young controls (29.52 ± 4.42 mg%) -(table 3, figure 3). Our findings were in agreement with those obtained by Daimon et al and king et al 25,26 It has been known that the antioxidants are under homeostatic control. A decrease in a particular antioxidant can be compensated by an increase in a different one.…”

Section: Discussionsupporting

confidence: 94%

Oxidative stress in ageing

Fasna¹,

Geetha

Maliekkal

2017

Int J Res Med Sci

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Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.

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Section: Discussionsupporting

confidence: 94%

Oxidative stress in ageing

Fasna¹,

Geetha

Maliekkal

2017

Int J Res Med Sci

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“…However, when older aged individuals were examined, basal levels of DNA damage in lymphocytes from donors 75-80 years old were similar to those of the 35-39 year-old group (494). There was also no significant difference between frequency of mutation at the hprt locus in the young and more aged populations, nor was there any difference in DNA repair capacity after hydrogen peroxide-induced DNA damage (629). These findings may possibly be explained by donor selection pressures resulting in an association of longevity with retention of DNA repair capacity.…”

Section: Mutations and Dna Repairmentioning

confidence: 65%

“…T cells with mutations measured at the hprt locus show a reduced proliferation rate in vitro and may therefore have a selective disadvantage (630). Together with the increased levels of anti-oxidants glutathione peroxidase, catalase and ceruloplasmin in the elderly (629), these data suggest that those individuals with best retention of DNA repair mechanisms and anti-oxidant defences form a group with extended longevity. Concordant with this idea, treatment with anti-oxidants may also decrease DNA damage in human lymphocytes.…”

Section: Mutations and Dna Repairmentioning

confidence: 95%

T cells and aging (update February 1999)

Pawelec

1999

Front Biosci

113

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T cell immunosenescence 218effects of dysregulated immune responses in the elderly by supplementation or other approaches may result in an enhancement of their quality of life, and significant reductions in the cost of medical care in old age. FACTORS CONTRIBUTING TO IMMUNO-SENESCENCE HematopoiesisDysregulated hematopoiesis is seen in elderly individuals, raising the possibility that this could contribute to altered immune function in the aged. Hematopoiesis in man may be compromised because of a severely reduced capacity to produce colony stimulating factors (44) and increased production of pro-inflammatory factors such as IL 6 (45), because lower numbers of progenitor cells are present in the BM (46) and because of an age-related decline in proliferative potential of putative haematopoietic stem cells (HSC) (47). In mice, the repopulating potential of murine fetal liver-derived HSC is higher than that of adult BM-derived stem cells (48), suggesting possible aging of the HSC themselves. Normal cells with shorter telomeres possess less remaining replicative capacity than those with longer telomeres (see section 5.2). Accordingly, HSC from adult BM were found to have shorter telomeres than fetal liver-derived or umbilical cord-derived stem cells, consistent with aging of HSC (49). Telomere lengths decreased on culture despite low level expression of telomerase in these cells (50,51), although the rate of basepair loss per population doubling of cells in culture was lower during the first two weeks, when telomerase was upregulated, than in the next two, when it was downregulated (52). The telomerase expressed is therefore functionally active but may not be able to completely maintain telomere length in aging HSC cells. True embryonic stem cells (ESC), on the other hand, which may really be immortal, do retain high levels of telomerase activity (53). On the other hand, ESC from telomerase-knockout mice show gradual telomere shortening over many population doublings (PD) resulting in slowing and eventual cessation of growth (54). Certain animals which do not downregulate telomerase manifest a permanent growth phase and little or no senescence (55,56).

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“…Nonetheless, King et al (1997) found a simi-noma de México (Zaragoza Campus) approved the research protocol for this study.…”

Section: Subjects and Designmentioning

confidence: 99%

Aging-Related Oxidative Stress in Healthy Humans

Mendoza-Núñez

Ruíz-Ramos

Sánchez-Rodrı́guez

et al. 2007

Tohoku J. Exp. Med.

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MENDOZA-NÚÑEZ, V.M., RUIZ-RAMOS, M., SÁNCHEZ-RODRÍGUEZ, M.A., RETANA-UGALDE, R. and MUÑOZ-SÁNCHEZ, J.L. Aging-Related Oxidative Stress in Healthy Humans. Tohoku J. Exp. Med., 2007, 213 (3), 261-268 Oxidative stress has been reported to increase with aging; however, the scientifi c evidence is controversial. We therefore aimed to analyze the relationship between aging and some markers of oxidative stress. A crosssectional and comparative study was carried out in a sample of 249 healthy subjects: (i) 25-29 years (n = 22); (ii) 30-39 years (24); (iii) 40-49 years (30); (iv) 50-59 years (48); (v) 60-69 years (60), and (vi) 70 years (65). We measured lipoperoxides and total antioxidant status in plasma and superoxide dismutase and glutathione peroxidase activities in erythrocytes. There was an age-related increase in lipoperoxides, which was evident in the comparison of the group of 25-29 years (0.22 ± 0.11 μ mol/l) with the group of 60-69 years (0.38 ± 0.18 μ mol/l, p < 0.01) and 70 years (0.42 ± 0.19, p < 0.001). Conversely, the total antioxidant status showed an age-related decrease (25-29 years, 1.4 ± 0.31 mmol/l vs 60-69 years, 1.1 ± 0.21 and 70 years, 1.1 ± 0.22, p < 0.05 for each). In erythrocytes, glutathione peroxidase activity showed an age-related decrease (25-29 years, 7,966 ± 1,813 UI/l vs 60-69 years, 6,193 ± 2,235 and 70 years, 6,547 ± 2,307, p < 0.001 for each), whereas superoxide dismutase activity was similar in all age groups. Importantly, there was no age-related change in oxidative stress markers in subjects of < 60 years. These fi ndings suggest that age of 60 years may be associated with increased oxidative stress.aging; oxidative stress; superoxide dismutase; lipoperoxides; antioxidant enzymes

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In vivo antioxidant status, DNA damage, mutation and DNA repair capacity in cultured lymphocytes from healthy 75- to 80-year-old humans

Cited by 62 publications

References 40 publications

Oxidative stress in ageing

Oxidative stress in ageing

T cells and aging (update February 1999)

Aging-Related Oxidative Stress in Healthy Humans

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