Oxidative Stress and Exercise in Cardiopulmonary and Metabolic Disorders

Fisher‐Wellman, Kelsey H.

doi:10.1007/978-3-642-30018-9_169

Cited by 1 publication

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“…One of the most intriguing aspects of this study is the finding that the significant cytogenetic damage observed in the filtered air exposure scenario can most likely be attributed to the effects of the intermittent exercise that subjects were performing over a 4‐hr period while inside the chamber. The relationships between exercise‐induced oxidative stress and molecular changes and health effects have been analyzed in both animal and human studies [Powers et al, ; Fisher‐Wellman and Bloomer, ]. The association between muscular exercise and oxidative stress in humans was first reported more than 30 years ago [Dillard et al, ] when an attempt to ameliorate the adverse effects of ozone with the application of antioxidants proved to be unsuccessful.…”

Section: Discussionmentioning

confidence: 99%

Ozone inhalation leads to a dose‐dependent increase of cytogenetic damage in human lymphocytes

Holland

Davé

Venkat

et al. 2014

Environ and Mol Mutagen

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Ozone is an important constituent of ambient air pollution and represents a major public health concern. Oxidative injury due to ozone inhalation causes the generation of reactive oxygen species and can be genotoxic. To determine whether ozone exposure causes genetic damage in peripheral blood lymphocytes, we employed a well-validated cytokinesis-block micronucleus Cytome assay. Frequencies of micronuclei (MN) and nucleoplasmic bridges (NB) were used as indicators of cytogenetic damage. Samples were obtained from 22 non-smoking healthy subjects immediately before and 24-hr after controlled 4-hr exposures to filtered air, 100 ppb, and 200 ppb ozone while exercising in a repeated-measure study design. Inhalation of ozone at different exposure levels was associated with a significant dose-dependent increase in MN frequency (P < 0.0001) and in the number of cells with more than 1 MN per cell (P < 0.0005). Inhalation of ozone also caused an increase in the number of apoptotic cells (P = 0.002). Airway neutrophilia was associated with an increase in MN frequency (P = 0.033) independent of the direct effects of ozone exposure (P < 0.0001). We also observed significant increases in both MN and NB frequencies after exercise in filtered air, suggesting that physical activity is also an important inducer of oxidative stress. These results corroborate our previous findings that cytogenetic damage is associated with ozone exposure, and show that damage is dose-dependent. Further study of ozone-induced cytogenetic damage in airway epithelial cells could provide evidence for the role of oxidative injury in lung carcinogenesis, and help to address the potential public health implications of exposures to oxidant environments.

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Section: Discussionmentioning

confidence: 99%