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Mol. Cells 2009; 27(5): 557-562

Published online May 15, 2009

https://doi.org/10.1007/s10059-009-0071-6

© The Korean Society for Molecular and Cellular Biology

Effects of the NADPH Oxidase p22phox C242T Polymorphism on Endurance Exercise Performance and Oxidative DNA Damage in Response to Aerobic Exercise Training

Il-Young Paik, Chan-Ho Jin, Hwa-Eun Jin, Young-Il Kim, Su-Youn Cho, Hee-Tae Roh, Ah-Ram Suh, and Sang-Hoon Suh

Received: December 30, 2009; Revised: March 17, 2009; Accepted: March 18, 2009

Abstract

We examined the effects of the NADPH oxidase p22phox C242T polymorphism on endurance exercise per-formance and oxidative DNA damage in response to acute and chronic exercises. One hundred three subjects were recruited, among which 26 healthy subjects (CC: 12, TC: 12, and TT: 2) were studied during rest, exercise at 85% VO2max, and recovery before and after 8 weeks of treadmill running. Lymphocyte DNA damage increased significantly in response to exercise (p < 0.05). There were no significant differences in plasma MDA, SOD concentrations and lymphocyte DNA damage between CC genotype and T allele group, but significant endurance training differences were observed. Endurance training increased exercise time to exhaustion in both the CC genotype and T allele groups (p < 0.05) but no significant difference was found between groups. The results of the current study with young, healthy, Korean men are interpreted to mean that 1) the majority had the CC genotype of the NADPH oxidase p22phox C242T polymorphism (82.5%: CC, 15.5%: TC, 1.9%: TT), 2) acute exercise increased lymphocyte DNA damage, 3) endurance training significantly increased exercise time to exhaustion, and alleviated lymphocyte DNA damage, and 4) The NADPH oxidase p22phox C242T polymorphism, however, did not alter lymphocyte DNA damage or exercise performance at rest, immediately after exercise, or during recovery.

Keywords endurance training, exercise performance, gene polymorphism, NADPH oxidase, oxidative DNA damage

Article

Research Article

Mol. Cells 2009; 27(5): 557-562

Published online May 31, 2009 https://doi.org/10.1007/s10059-009-0071-6

Copyright © The Korean Society for Molecular and Cellular Biology.

Effects of the NADPH Oxidase p22phox C242T Polymorphism on Endurance Exercise Performance and Oxidative DNA Damage in Response to Aerobic Exercise Training

Il-Young Paik, Chan-Ho Jin, Hwa-Eun Jin, Young-Il Kim, Su-Youn Cho, Hee-Tae Roh, Ah-Ram Suh, and Sang-Hoon Suh

Received: December 30, 2009; Revised: March 17, 2009; Accepted: March 18, 2009

Abstract

We examined the effects of the NADPH oxidase p22phox C242T polymorphism on endurance exercise per-formance and oxidative DNA damage in response to acute and chronic exercises. One hundred three subjects were recruited, among which 26 healthy subjects (CC: 12, TC: 12, and TT: 2) were studied during rest, exercise at 85% VO2max, and recovery before and after 8 weeks of treadmill running. Lymphocyte DNA damage increased significantly in response to exercise (p < 0.05). There were no significant differences in plasma MDA, SOD concentrations and lymphocyte DNA damage between CC genotype and T allele group, but significant endurance training differences were observed. Endurance training increased exercise time to exhaustion in both the CC genotype and T allele groups (p < 0.05) but no significant difference was found between groups. The results of the current study with young, healthy, Korean men are interpreted to mean that 1) the majority had the CC genotype of the NADPH oxidase p22phox C242T polymorphism (82.5%: CC, 15.5%: TC, 1.9%: TT), 2) acute exercise increased lymphocyte DNA damage, 3) endurance training significantly increased exercise time to exhaustion, and alleviated lymphocyte DNA damage, and 4) The NADPH oxidase p22phox C242T polymorphism, however, did not alter lymphocyte DNA damage or exercise performance at rest, immediately after exercise, or during recovery.

Keywords: endurance training, exercise performance, gene polymorphism, NADPH oxidase, oxidative DNA damage

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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