Metabolic, Apoptotic and Fibro-Inflammatory Profiles of the Heart Exposed to Environmental Electromagnetic Fields

Abstract

Environmental stress can disturb the integrative functioning of the cardiovascular system and trigger a number of adaptive and/or maladaptive cell responses. Concomitant with the expanding use of mobile communication systems, public exposure to electromagnetic fields (EMFs) raises the question of the impact of 900 MHz EMFs on cardiovascular health. Therefore, in this study, we experimentally investigated whether 915 MHz EMF exposure influenced cardiac metabolic, antioxidant, apoptotic, and fibro-inflammatory profiles in a mouse model. Healthy mice were sham-exposed or exposed to EMF for 14 days. Western blot analysis using whole cardiac tissue lysates demonstrated that there was no significant change in the expression of oxidative phosphorylation (OXPHOS) complexes between the control and EMF-exposed mice. In addition, the myocardial expression of fibro-inflammatory cytokines, antioxidant enzymes, and apoptosis-related markers remained unchanged in the EMF-challenged hearts. Finally, the structural integrity of the cardiac tissues was preserved among the groups. These findings suggest that the apoptotic, antioxidant, metabolic, and fibro-inflammatory profiles of the heart remained stable under conditions of EMF exposure in the analyzed mice.

Keywords: antioxidants; apoptosis; electromagnetic stressor; fibrosis; inflammation.

Figure 1

Mitochondrial OXPHOS system in mice subjected to 915 MHz EMF for 14 days. (A) Representative Western blot image and (B) quantification of MitoProfile Total OXPHOS protein expression levels in control and EMF-exposed mice after 14 days. The results are presented as means ± SEM.

Figure 2

Cardiac mRNA expression of apoptosis-associated genes in mice exposed to EMFs. (A,B) qRT-PCR quantification of the mRNA-expression levels of BAX and BCL-2 in control and EMF-exposed mice after 14 days. The results are presented as means ± SEM.

Figure 3

Myocardial levels of apoptosis-related proteins in EMF-challenged hearts. (A) Representative Western blot images and (B–D) quantification of protein expression levels of caspase-8, BCL-2, and BAX in cardiac tissue from mice subjected to 14 days of EMFs. The results are presented as means ± SEM.

Figure 4

Cardiac expression of SOD2 in EMF-exposed mice. (A) Representative Western blot image and (B) quantification of SOD2 protein expression level. (C,D) qRT-PCR quantification of the expression level of SOD2 and catalase in mice exposed to 915 MHz EMFs and control mice after 14 days. The results are presented as means ± SEM.

Figure 5

Pro-inflammatory profiling in cardiac tissue from EMF-exposed mice. (A,B) qRT-PCR results regarding IL-6 and CCL2 in control group, and mice subjected to EMFs for 14 days. The results are presented as means ± SEM.

Figure 6

Cardiac tissue integrity in EMF-challenged mouse hearts. (A) Representative images showing Sirius red staining of cardiac sections in control and EMF-exposed mice for 14 days (scale bar: 2.5 mm) and (B) quantification of (A). (C–E) qRT-PCR analysis of fibrosis-associated genes including collagen type I, collagen type III and TGF β-1 and (F) ratio of heart weight to body weight in control and EMF-exposed groups. The results are presented as means ± SEM.

Figure 7

Electromagnetic computation of SAR of six phantoms in GTEM. The impact of EMF on the mouse body was calculated using a standardized unit known as the SAR. The electromagnetic simulations for the six phantoms were conducted using HFSS software. The whole-body SAR was determined as the volume integration of absorption power using MATLAB codes.