How can age and lifestyle variables affect DNA damage, repair capacity and endogenous biomarkers of oxidative stress?

Soares, Jorge Pinto; Silva, Amélia M.; Fonseca, Sandra; Oliveira, Maria Manuel; Peixoto, Francisco; Gaivão, Isabel; Mota, Maria Paula

doi:10.1016/j.exger.2015.01.001

Cited by 23 publications

(24 citation statements)

References 40 publications

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“…Recent cross-sectional studies in humans on this topic are equivocal since one study showed an age-related increase in both DNA damage and repair (Soares et al 2015), while another showed an age-related decrease in DNA repair capacity (Løhr et al 2015). Such mixed results emphasise the need for comprehensive longitudinal studies investigating age-related changes in both DNA damage and repair capacities.…”

Section: Discussionmentioning

confidence: 99%

Environmental conditions can modulate the links among oxidative stress, age, and longevity

Marasco

Stier

Boner

et al. 2017

Mechanisms of Ageing and Development

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* Joint first authorsHighlights  We exposed zebra finch females to challenging environmental conditions  We examined treatment effects on age-related changes in oxidative stress (OS)  Levels of damage to DNA and proteins increased with chronological age  The treatment produced a higher age-related increase in the level of damage to DNA  We found treatment-specific links among OS and longevity Corresponding author: Pat.Monaghan@glasgow.ac.uk 2 AbstractUnderstanding the links between environmental conditions and longevity remains a major focus in biological research. We examined within-individual changes between early-and midadulthood in the circulating levels of four oxidative stress markers linked to ageing, using zebra finches (Taeniopygia guttata): a DNA damage product (8-hydroxy-2'-deoxyguanosine; 8-OHdG), protein carbonyls (PC), non-enzymatic antioxidant capacity (OXY), and superoxide dismutase activity (SOD). We further examined whether such within-individual changes differed among birds living under control (ad lib food) or more challenging environmental conditions (unpredictable food availability), having previously found that the latter increased corticosterone levels when food was absent but improved survival over a three year period. Our key findings were: (i) 8-OHdG and PC increased with age in both environments, with a higher increase in 8-OHdG in the challenging environment; (ii) SOD increased with age in the controls but not in the challenged birds, while the opposite was true for OXY; (iii) control birds with high levels of 8-OHdG died at a younger age, but this was not the case in challenged birds. Our data clearly show that while exposure to the potentially damaging effects of oxidative stress increases with age, environmental conditions can modulate the pace of this age-related change.

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Section: Discussionmentioning

confidence: 99%

Environmental conditions can modulate the links among oxidative stress, age, and longevity

Marasco

Stier

Boner

et al. 2017

Mechanisms of Ageing and Development

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“…If the antioxidant defense is overwhelmed, elevated oxidative stress can cause DNA damage and increase the risk of various cancer types [11]. ROS production, stress responses and therefore genomic stability can be affected by life style factors [12, 13]. …”

Section: Introductionmentioning

confidence: 99%

Role of PTEN in Oxidative Stress and DNA Damage in the Liver of Whole-Body Pten Haplodeficient Mice

Bankoglu

Tschopp²,

Schmitt

et al. 2016

PLoS ONE

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Type 2 diabetes (T2DM) and obesity are frequently associated with non-alcoholic fatty liver disease (NAFLD) and with an elevated cancer incidence. The molecular mechanisms of carcinogenesis in this context are only partially understood. High blood insulin levels are typical in early T2DM and excessive insulin can cause elevated reactive oxygen species (ROS) production and genomic instability. ROS are important for various cellular functions in signaling and host defense. However, elevated ROS formation is thought to be involved in cancer induction. In the molecular events from insulin receptor binding to genomic damage, some signaling steps have been identified, pointing at the PI3K/AKT pathway. For further elucidation Phosphatase and Tensin homolog (Pten), a tumour suppressor phosphatase that plays a role in insulin signaling by negative regulation of PI3K/AKT and its downstream targets, was investigated here. Dihydroethidium (DHE) staining was used to detect ROS formation in immortalized human hepatocytes. Comet assay and micronucleus test were performed to investigate genomic damage in vitro. In liver samples, DHE staining and western blot detection of HSP70 and HO-1 were performed to evaluate oxidative stress response. DNA double strand breaks (DSBs) were detected by immunohistostaining. Inhibition of PTEN with the pharmacologic inhibitor VO-OHpic resulted in increased ROS production and genomic damage in a liver cell line. Knockdown of Pten in a mouse model yielded increased oxidative stress levels, detected by ROS levels and expression of the two stress-proteins HSP70 and HO-1 and elevated genomic damage in the liver, which was significant in mice fed with a high fat diet. We conclude that PTEN is involved in oxidative stress and genomic damage induction in vitro and that this may also explain the in vivo observations. This further supports the hypothesis that the PI3K/AKT pathway is responsible for damaging effects of high levels of insulin.

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“…But, if the damage accumulates throughout the entire lifespan, as a by-product of normal cellular processes or a consequence of inefficient repair systems, this could lead to the diseases associated with the elderly [31], [38]. On the other hand, Soares et al [39] highlighted the impact of the lifestyle (diet, environment, lifestyle among others factors of life-stage as physiological and/ or metabolic process) has an important role in the accumulation of oxidative damage or in the OS increase apart from growing older. The F 2 -dihomo-IsoPs have not been used previously as a biomarker of aging; they have been associated mainly with diseases in the elderly, adolescents, and children.…”

Section: Discussionmentioning

confidence: 99%

Snapshot situation of oxidative degradation of the nervous system, kidney, and adrenal glands biomarkers-neuroprostane and dihomo-isoprostanes-urinary biomarkers from infancy to elderly adults

et al. 2017

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We analyzed biomarkers of lipid peroxidation of the nervous system -F2-dihomo-isoprostanes, F3-neuroprostanes, and F4-neuroprostanes- in urine samples from 158 healthy volunteers ranging from 4 to 88 years old with the aim of analyzing possible associations between their excretion values and age (years). Ten biomarkers were screened in the urine samples by UHPLC-QqQ-MS/MS. Four F2-dihomo-isoprostanes (ent−7-(R)−7-F2t-dihomo-isoprostane, ent−7-epi−7-F2t-dihomo-isoprostane, 17-F2t-dihomo-isoprostane, 17-epi−17-F2t-dihomo-isoprostane), and one DPA-neuroprostane (4-F3t-neuroprostane) were detected in the samples. On the one hand, we found a significant, positive correlation (Rho: 0.197, P=0.015) between the age increase and the amount of total F2-dihomo-IsoPs. On the other hand, the values were significantly higher in the childhood group (4–12 years old), when compared to the adolescence group (13–17 years old) and the young adult group (18–35 years old). Surprisingly, no significant differences were found between the middle-aged adults (36–64 years old) and the elderly adults (65–88 years old). We display a snapshot situation of excretory values of oxidative stress biomarkers of the nervous system, using healthy volunteers representative of the different stages of human growth and development. The values reported in this study could be used as a basal or starting point in clinical interventions related to aging processes and/or pathologies associated with the nervous system.

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How can age and lifestyle variables affect DNA damage, repair capacity and endogenous biomarkers of oxidative stress?

Cited by 23 publications

References 40 publications

Environmental conditions can modulate the links among oxidative stress, age, and longevity

Environmental conditions can modulate the links among oxidative stress, age, and longevity

Role of PTEN in Oxidative Stress and DNA Damage in the Liver of Whole-Body Pten Haplodeficient Mice

Snapshot situation of oxidative degradation of the nervous system, kidney, and adrenal glands biomarkers-neuroprostane and dihomo-isoprostanes-urinary biomarkers from infancy to elderly adults

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