Influence of Acute Exercise on DNA Repair and PARP Activity before and after Irradiation in Lymphocytes from Trained and Untrained Individuals

Abstract

Several studies indicate that acute exercise induces DNA damage, whereas regular exercise increases DNA repair kinetics. Although the molecular mechanisms are not completely understood, the induction of endogenous reactive oxygen species (ROS) during acute exhaustive exercise due to metabolic processes might be responsible for the observed DNA damage, while an adaptive increase in antioxidant capacity due to regular physical activity seems to play an important protective role. However, the protective effect of physical activity on exogenously induced DNA damage in human immune cells has been poorly investigated. We asked the question whether individuals with a high aerobic capacity would have an enhanced response to radiation-induced DNA damage. Immune cells are highly sensitive to radiation and exercise affects lymphocyte dynamics and immune function. Therefore, we measured endogenous and radiation-induced DNA strand breaks and poly (ADP-ribose) polymerase-1 (PARP1) activity in peripheral blood mononuclear cells (PBMCs) from endurance-trained (maximum rate of oxygen consumption measured during incremental exercise V’O2max > 55 mL/min/kg) and untrained (V’O2max < 45 mL/min/kg) young healthy male volunteers before and after exhaustive exercise. Our results indicate that: (i) acute exercise induces DNA strand breaks in lymphocytes only in untrained individuals, (ii) following acute exercise, trained individuals repaired radiation-induced DNA strand breaks faster than untrained individuals, and (iii) trained subjects retained a higher level of radiation-induced PARP1 activity after acute exercise. The results of the present study indicate that increased aerobic fitness can protect immune cells against radiation-induced DNA strand breaks.

Changes in γH2AX and H4K16ac levels are involved in the biochemical response to a competitive soccer match in adolescent players

“…An increase in serum 8-OHdG level, such as observed in this study, may also result from the release of DNA from damaged cells 47 . Other studies have also documented physical activity-induced increases in 8-OHdG concentrations 25,26 .…”

“…Although the role of γH2AX in the response to DNA damage produced by a wide range of chemical and physical agents, such as high doses of ionizing radiation and oxidative stress, is well established 49 , the link between γH2AX and physical activity is still very poorly documented. While there are reports documenting an impact of physical activity on DNA damage 26 or exercise-dependent kinetics of DNA damage repair mechanisms 25 , they focus on other, non-epigenetic components of the DDR pathway.…”

“…We focused on those epigenetic markers for two reasons. First, although the relationship between exercise and DNA damage has been addressed in several studies 24 , 25 , there is still lack of information concerning epigenetic aspects of the exercise-induced DDR pathway, especially in the sport science field. Second, the data for this study were collected under real competitive conditions, in the presence of a wide range of environmental stressors.…”

Regular, Intense Exercise Training as a Healthy Aging Lifestyle Strategy: Preventing DNA Damage, Telomere Shortening and Adverse DNA Methylation Changes Over a Lifetime

“…Training status (e.g., high cardiorespiratory fitness) also appears to be a vital factor when it comes to adaptation. Acute exercise seems to protect immune cells against radiation-induced DNA strand breaks in trained subjects (Moreno-Villanueva et al, 2019). Therefore, it can be said that incorporating acute exercise, especially acute aerobic exercise as a healthy aging strategy might be beneficial.…”

Targeted Antioxidants in Exercise-Induced Mitochondrial Oxidative Stress: Emphasis on DNA Damage

“…Although complex, it has been proposed that the increase in RONS (and potentially the macromolecular damage itself) can trigger the up-regulation of transcription factors, and activate redox signals resulting in the enhanced capacity of the organism to overcome greater stress. Ultimately, over time these exercise-mediated signals trigger adaptations to RONS handling by influencing antioxidant enzyme capacity and DNA repair [ 15 , 16 , 17 , 18 , 19 ].…”