Oxidative damage to DNA and replicative lifespan in cultured adrenocortical cells

Hornsby, Peter J.; Harris, Sandra E.

doi:10.1016/0014-4827(87)90429-0

Cited by 35 publications

(16 citation statements)

References 50 publications

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“…An extension of replicative life span in bovine adrenocortical cells after selenium supplementation (20 nM) has been reported by Hornsby et al [204]. Also, in hepatocytes high doses of Se (0.5 and 2.5 μM) were found to be able to extend telomere length, prolonging the cellular life span, too [205].…”

Section: The Role Of Trace Elements and Micronutrients In Agingsupporting

confidence: 56%

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

et al. 2017

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Aging is a complex phenomenon and its impact is becoming more relevant due to the rising life expectancy and because aging itself is the basis for the development of age-related diseases such as cancer, neurodegenerative diseases and type 2 diabetes. Recent years of scientific research have brought up different theories that attempt to explain the aging process. So far, there is no single theory that fully explains all facets of aging. The damage accumulation theory is one of the most accepted theories due to the large body of evidence found over the years. Damage accumulation is thought to be driven, among others, by oxidative stress. This condition results in an excess attack of oxidants on biomolecules, which lead to damage accumulation over time and contribute to the functional involution of cells, tissues and organisms. If oxidative stress persists, cellular senescence is a likely outcome and an important hallmark of aging. Therefore, it becomes crucial to understand how senescent cells function and how they contribute to the aging process. This review will cover cellular senescence features related to the protein pool such as morphological and molecular hallmarks, how oxidative stress promotes protein modifications, how senescent cells cope with them by proteostasis mechanisms, including antioxidant enzymes and proteolytic systems. We will also highlight the nutritional status of senescent cells and aged organisms (including human clinical studies) by exploring trace elements and micronutrients and on their importance to develop strategies that might increase both, life and health span and postpone aging onset.

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Section: The Role Of Trace Elements and Micronutrients In Agingsupporting

confidence: 56%

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

et al. 2017

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“…Previous studies have shown an extension of replicative lifespan for human fibroblasts cultured under low oxygen environments (Packer and Fuehr 1977;Saito et al 1995). Other reports have found that antioxidant addition such as vitamin E, N-acetylcysteine, selenite, 2-mercaptoethylamine, or a-phenyl-t-butylnitrone (PBN) can extend the cellular proliferation limit of cultured human or bovine cells (Chen et al 1995;Golczewski 1984;Haendeler et al 2004;Hornsby and Harris 1987;von Zglinicki et al 2000). Alternatively, elevated oxygen tensions or reactive oxygen species (ROS) are toxic to normal human fibroblasts and reduces their proliferative lifespan in vitro (Balin et al 1977;Haendeler et al 2004;Honda and Matsuo 1983;Packer and Fuehr 1977).…”

Section: Discussionmentioning

confidence: 97%

Low oxygen delays fibroblast senescence despite shorter telomeres

2007

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It has been widely accepted that telomere shortening acts as a cell division counting mechanism that beyond a set critical length signals cells to enter replicative senescence. In this study, we demonstrate that by simply lowering the oxygen content of the cell culture environment 10-fold (20-2%) extends the replicative lifespan of fetal bovine fibroblasts at least five-times (30-150 days). Although, low oxygen fibroblasts display a slightly slower rate (P > 0.05) of telomere attrition than their high oxygen counterparts (171 bp versus 182 bp/PD), late passage fibroblasts (>50 PD) that have extended their replicative capacity under low oxygen conditions exhibited significantly (P < 0.05) shorter telomere lengths (11,135 +/- 467 bp) compared to senescent cells (25-34 PD) cultured under high oxygen conditions (14,827 +/- 1173 bp). There was a significant increase (P < 0.05) in chromosomal abnormalities with continual cell division under both high and low oxygen environments, however, fibroblasts displayed a significant reduction (P < 0.001) in chromosomal abnormalities at low oxygen tensions compared to those under 20% oxygen. These apparent protective effects on telomere shortening, delayed senescence and reduced chromosomal aberrations may be attributed to the up-regulation of telomerase activity observed for fibroblasts cultured under low oxygen. These results are consistent with the idea that a critically short telomere length may not be the sole trigger of replicative senescence, but may be regulated by the integrity of telomere structure itself and/or the amount of oxidative DNA damage in the cell.

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“…Moreover, selenium supplementation has been reported to increase replicative life span in bovine adrenocortical cells (18). To examine this relationship in a human cellular model for replicative senescence, we have used previously validated growth media for WI-38 fibroblasts with various selenium concentrations mimicking adequate, deficient, and supplemented dietary intake (see "Experimental Procedures").…”

Section: Selenium Levels Extend the Replicative Life Span Of Wi-38mentioning

confidence: 99%

“…These studies suggest that low selenium levels lead to a weakening of the antioxidant defense and show that the concentration of blood selenium is an important predictor of longevity in elderly patients, although the molecular mechanisms and selenoproteins involved remain to be elucidated. At a cellular level, only studies performed in 1987 (18), before many selenoproteins were identified and characterized, report an extension of the replicative life span of bovine adrenocortical cells with 20 nM selenium supplementation of the culture medium.…”

mentioning

confidence: 99%

Interplay between Selenium Levels, Selenoprotein Expression, and Replicative Senescence in WI-38 Human Fibroblasts

Legrain

Touat-Hamici

Chavatte

2014

Journal of Biological Chemistry

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Background: Selenoproteins are important enzymes for antioxidant defense, redox homeostasis, and redox signaling. Results: We report that, in WI-38 human fibroblasts, replicative senescence is controlled by selenium levels and selectively modulates selenoprotein expression. Conclusion: Our data indicate that the selenoproteome is regulated at the translational and mRNA levels in WI-38 cells. Significance: We have characterized a strong interplay between selenium levels, selenoprotein expression, and replicative senescence.

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Oxidative damage to DNA and replicative lifespan in cultured adrenocortical cells

Cited by 35 publications

References 50 publications

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

Low oxygen delays fibroblast senescence despite shorter telomeres

Interplay between Selenium Levels, Selenoprotein Expression, and Replicative Senescence in WI-38 Human Fibroblasts

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