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SPORTS AND EXERCISE MEDICINE AND HEALTH

DNA damage in mononuclear cells following maximal exercise in sedentary and physically active lean and obese men

, , , , , & show all
Pages 1073-1082 | Published online: 06 Aug 2020
 

Abstract

We evaluated the impact of maximal exercise on oxidative stress and DNA damage in peripheral blood mononuclear cells (PBMC) from sedentary and exercised lean and obese men. PBMC were collected before, immediately and 1-h after exercise and exposed to hydrogen peroxide (H2O2; 25 and 50 µM, 4 h). A leukocytosis was induced by maximal exercise immediately and 1-h after exercise in all groups. However, a lymphopenia was observed 1-h after exercise in the Sedentary obese group. In the control condition, low DNA damage index concomitant to increases in intracellular glutathione content (GSH) was identified immediately after exercise in all groups. However, higher DNA damage index and lipid peroxidation occurred 1-h after the bout in Sedentary and Exercised Obese groups. PBMC exposed to both H2O2 25 and 50 µM experienced higher DNA damage and lipid peroxidation index immediately after exercise in all groups. Both lipid peroxidation and DNA damage index remained higher in PBMC of Sedentary Lean, Sedentary Obese, and Exercised obese groups obtained 1-h after exercise in both H2O2 25 and 50 µM, with the highest values identified in PBMC from Sedentary Obese group. However, increases in GSH content were identified in treated PBMC from sedentary and exercised lean groups as well as exercised obese group 1-h after exercise. Habitual exercise confers increased resistance of PBMC to DNA damage induced by oxidative stress, reducing the detrimental effects of obesity.

Keywords: Exercise, physical activity, DNA damage, obesity, mutagenesis, oxidative stress

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

We are grateful to the Brazilian agencies Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)– Finance Code 001, CAPES (CAPES-PNPD - 23038007200/11-08) and Conselho Nacional de Desenvolvimento Cientifico e Tecnológico (CNPq) for financial support. AP, VMA and PRTR also thank CNPq for fellowships.

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