Table 3.
Physical exercise and DNA repair.
| Population | Determinations | Objective | Finding | Ref. |
|---|---|---|---|---|
| Fifty-seven healthy males (40 to 74 years) | Strength tests. Power tests. DNA damage. Assessment of repair capacity. Lipid peroxidation. TAC. |
This study aimed to determine the effects of a 16-week combined physical training program on DNA damage and DNA repair of human lymphocytes, taking into account the improvement of physical fitness. To investigate the role of OxS in these changes. |
Improvement in general physical performance in the experimental group. Decrease in DNA chain breaks and sites, sensitive to formamide-pyrimidine glycosylase, with a concomitant increase in antioxidant activity and a decrease in lipid peroxidation levels after physical training. There are no significant changes in the enzymatic activity of DNA glycosylase and 8-oxoguanine. |
[213] |
| Endurance-trained and young healthy males (age 20 to 36 years) | Simple DNA single break detection. Poly detection (ADP-ribose) and phosphorylation of the H2AX histone (γh2ax). |
Determine the general effect of acute exhaustive exercise and physical aptitude (aerobic capacity) on DNA damage, radiosensitivity, and PLP1 activity induced by radiation in immune cells isolated from trained and non-healthy trained volunteers. | Acute exercise induces DNA strand breaks in lymphocytes in untrained individuals. During acute exercise, trained subjects repaired radiation-induced DNA strand breaks more rapidly than untrained subjects. Trained subjects maintained higher levels of radiation-induced PARP1 activity after acute stress. |
[214] |
| Thirty-two healthy Caucasian males (40 to 74 years) | Assessment of strand break DNA (SB) and oxidative damage to DNA. Evaluation of sites sensitive to FPG. Assessment of repair capacity with the comet assay. The activity of OGG1. TAC. Determination of the hOGG1 (Ser326Cys) polymorphism. |
To investigate the possible influence of genetic polymorphisms of hOGG1 on DNA damage and repair activity OGG1 enzyme in response to 16 weeks of combined physical training. | At baseline, there were no differences in DNA damage and OGG1 activity between the groups. With 16 weeks of physical exercise, there was a decrease in DNA strand breaks in both groups, as well as a decrease in FPG-sensitive sites and an increase in TAC in WTG. |
[215] |
| Fourteen (apparently healthy recreationally active males (age 22 ± 2 years, stature 178 ± 6 cm, mass 83 ± 8 kg, BMI 26.2 ± 2) | DNA single-strand breaks and FPG-sensitive sites. Detection of double-strand breaks via histone γ-H2AX and 53BP1. Lipid hydroperoxides. Soluble antioxidants. EPR. |
Characterization of the interplay of exercise and hypoxia about DNA damage repair. Quantification of the effects of exercise in hypoxia on single- and double-strand DNA damage using the comet assay in conjunction with γ-H2AX and colocalized repair protein 53BP1. |
Increase in γ-H2AX and 53BP1 foci after high-intensity exercise, with markers, increased in hypoxia. Although normoxia resulted in a marked increase in foci detection, hypoxia challenge resulted in a 2.5- and 3.5-fold increase in γ-H2AX and 53BP1 foci, respectively, after exercise. | [216] |
| Sixty-one T2DM subjects, aged (mean ± SD: 50.3 ± 4.2) | Glycemic status. DNA damage (Comet assay). Oxidative DNA damage. OGG1 protein expression. TAC. |
Elucidation of the mechanism of action of yoga on T2DM-related DNA damage in terms of its effect on oxidative DNA damage and DNA repair markers. | The yoga group showed a significant reduction in DNA damage, oxidative DNA damage marker, and fasting blood sugar compared to the control. The beneficial effect of yoga on DNA damage in T2DM subjects was found to be mediated by the mitigation of oxidative DNA damage and enhancement of DNA repair. |
[217] |
TAC: Total antioxidant capacity; OxS: Oxidative stress; γH2AX: H2AX histone; PLP1: Polymerase poly; PARP: Poly(ADP-ribose) polymerase; FPG: Formamidopyrimidine DNA glycosylase; OGG1: 8-Oxoguanine DNA glycosylase; WTG: Wild-type group; BMI: Body mass index; 53BP1: 53-Binding protein 1; EPR: Electron paramagnetic resonance spectroscopy; T2DM: Diabetes mellitus type 2.