Cardiac Cell Exposure to Electromagnetic Fields: Focus on Oxdative Stress and Apoptosis
Ilenia Martinelli,
Mathieu Cinato,
Sokhna Keita,
Dimitri Marsal,
Valentin Antoszewski,
Junwu Tao,
Oksana Kunduzova
Affiliations
Ilenia Martinelli
National Institute of Health and Medical Research (INSERM) U1297, CEDEX 4, 31432 Toulouse, France
Mathieu Cinato
National Institute of Health and Medical Research (INSERM) U1297, CEDEX 4, 31432 Toulouse, France
Sokhna Keita
National Institute of Health and Medical Research (INSERM) U1297, CEDEX 4, 31432 Toulouse, France
Dimitri Marsal
National Institute of Health and Medical Research (INSERM) U1297, CEDEX 4, 31432 Toulouse, France
Valentin Antoszewski
Unité Mixte de Recherche (UMR) 1297, Université Toulouse III Paul-Sabatier, 31062 Toulouse, France
Junwu Tao
Laboratoire Plasma et Conversion d’Energie (LAPLACE), National Polytechnic Institute of Toulouse, The Ecole Nationale Supérieure d’Electrotechnique, d’Electronique, d’Informatique, d’Hydraulique et des Télécommunications (ENSEEIHT), Toulouse University III, 31071 Toulouse, France
Oksana Kunduzova
National Institute of Health and Medical Research (INSERM) U1297, CEDEX 4, 31432 Toulouse, France
Exposure to electromagnetic fields (EMFs) is a sensitive research topic. Despite extensive research, to date there is no evidence to conclude that exposure to EMFs influences the cardiovascular system. In the present study, we examined whether 915 MHz EMF exposure affects myocardial antioxidative and apoptotic status in vitro and in vivo. No statistically significant difference in the apoptotic cell profile and antioxidant capacity was observed between controls and short-term EMF-exposed mouse cardiomyocytes and H9C2 cardiomyoblasts. Compared with sham-exposed controls, mice subjected to a 915 MHz EMF for 48 h and 72 h had no significant effect on structural tissue integrity and myocardial expression of apoptosis and antioxidant genes. Therefore, these results indicate that short-term exposure to EMF in cardiac cells and tissues did not translate into a significant effect on the myocardial antioxidant defense system and apoptotic cell death.
