Inflammatory bowel disease involves epithelial injury, ulceration, apoptosis, inflammation, and oxidative-stress dysregulation. Although bioelectromagnetic fields may modulate tissue responses, their effects on acute colitis remain unclear. This exploratory study assessed histological and molecular changes associated with combined radiofrequency electromagnetic field (RF-EMF) and pulsed magnetic field (PMF) exposure in acetic-acid-induced colitis.Thirty-two young female Wistar albino rats were allocated to Control, Colitis, Colitis+RF-EMF+PMF, or RF-EMF+PMF groups (n=8 each). Colitis was induced intrarectally with 4% acetic acid. Exposure comprised RF-EMF (27.12 MHz, 30 min/session, 12 cycles/day) and PMF (0.5 mT, continuous). After seven days, distal colonic specimens underwent semiquantitative histopathology, crypt morphometry, immunohistochemistry for CAS-3, IL-6, and TNF-α, and RT-qPCR for SIRT-1, NRF-2, and HO-1. Colitis caused histological injury, reduced crypt dimensions, increased CAS-3, IL-6, and TNF-α immunopositivity, and decreased SIRT-1, NRF-2, and HO-1 expression. Compared with untreated colitis, combined exposure increased crypt depth and width and reduced all three immunohistochemical markers (all Tukey-adjusted p<0.001). Overall histopathological injury was lower but not statistically significant (Dunn-adjusted p=0.068), whereas submucosal inflammatory infiltration decreased significantly (p=0.048). NRF-2 expression increased (Tukey-adjusted p=0.002); SIRT-1 and HO-1 increased numerically without statistical significance (p=0.057 and 0.134).Combined RF-EMF+PMF exposure was associated with preserved crypt architecture, reduced apoptotic and inflammatory immunopositivity, and increased NRF-2 expression. Absent barrier-function testing and incomplete RF dosimetry preclude conclusions regarding restored epithelial barrier function or established therapeutic efficacy.
The ongoing expansion of 5 G networks, using millimeter waves like the 26 GHz frequency band, calls for a better understanding of their potential health effects. In this context, the acute effects of 26 GHz exposure on heart rate variability (HRV), a non-invasive marker of autonomic nervous system activity, were evaluated in healthy young adults. Using a triple-blind, randomized crossover design, 31 participants were exposed to both real and sham 26 GHz 5 G new radio modulated radiofrequency fields in a controlled, shielded environment. Exposure levels were set to reflect realistic upper environmental values (2 V/m at the head and 1 V/m at the torso). Throughout pre-exposure, exposure, and post-exposure phases, HRV was continuously measured under resting eyes-open and eyes-closed conditions. Analysis revealed no statistically significant differences across time- or frequency-domain HRV parameters between real and sham exposures at any phase of exposure. These data suggest that short-term exposure to 26 GHz millimeter waves at environmentally relevant intensities does not alter cardiac autonomic regulation in resting healthy adults. This aligns with the known limited tissue penetration of millimeter waves and the absence of clearly identified biological mechanisms affecting deeper autonomic control at these frequencies. Still, as the exposure duration was relatively brief and the population limited to healthy young individuals, further studies are needed to investigate longer exposures, potential effects during autonomic modulation such as orthostatic maneuvers, and responses in more diverse or vulnerable groups. However, these findings contribute valuable information indicating that no measurable acute physiological changes were observed under the specific environmental exposure conditions investigated; these findings do not address possible long-term or cumulative effects.
BACKGROUND:Experimental findings on the biological effects of 0 Hz static magnetic fields (SMFs), representing the static component of the non-ionizing electromagnetic spectrum, remain inconsistent because of differences in field characteristics and exposure conditions. This study investigated the effects of moderate-intensity SMF exposure on cardiovascular and histopathological changes in an isoproterenol (ISO)-induced rat model of experimental heart failure (EHF) using a characterized system. METHODS:Twenty-eight male Wistar rats were randomly assigned to four groups (Control, EHF, SMF, and EHF+SMF; n = 7/group). Experimental heart failure was induced by intraperitoneal ISO administration (5 mg/kg/day) for 7 consecutive days. Rats in the SMF and EHF+SMF groups were exposed to moderate-intensity SMF for 2 h/day, 5 days/week, for 21 days. The exposure system was characterized by two- and three-dimensional magnetic field mapping. Hemodynamics, electrocardiography, serum cardiac biomarkers (brain natriuretic peptide [BNP] and cardiac troponin T [cTnT]), and myocardial histopathology were evaluated. RESULTS:Repeated ISO administration significantly reduced arterial pressure, produced selective electrocardiographic alterations, and induced myocardial inflammation and fibrosis. SMF exposure produced limited changes in hemodynamic, biochemical, and most electrocardiographic variables. Although BNP levels tended to decrease in the EHF+SMF group, neither BNP nor cTnT differed significantly from the untreated EHF group. In contrast, SMF exposure significantly reduced inflammatory cell infiltration, vascular congestion, and myocardial fibrosis. CONCLUSION:Prolonged moderate-intensity SMF exposure had limited systemic cardiovascular effects but significantly reduced myocardial histopathological injury. These findings support further investigation of SMF exposure as a biophysical approach for modulating myocardial structural injury in experimental heart failure.
