A total of 32 electrohypersensitivity (EHS) self‑reporting patients were serially included in the present prospective study for oxidative stress and antioxidative stress response assessment. All thiobarbituric acid‑reactive substances (TBARs) were measured in the plasma, particularly malondialdehyde (MDA) for lipid peroxidation; additional measurements included total thiol group molecules, reduced glutathione (GSH), oxidized glutathione (GSSG) for oxidative stress assessment and nitrotyrosine, a marker of peroxynitrite‑induced oxidative/nitrosative stress. In addition, the activity of Cu‑Zn superoxide dismutase (SOD1) was measured in red blood cells (RBCs) and glutathione reductase (GR) and glutathione peroxidase (GPx) in RBCs and plasma. Depending of the biomarker considered, 30‑50% of EHS self‑reporting patients presented statistically significantly increased TBARs, MDA, GSSG and NTT mean plasmatic level values in comparison with normal values obtained in healthy controls (P<0.0001). By contrast, there were no plasmatic level values above the upper normal limits for GSH, GSH/GSSG ratio, total glutathione (GluT) and GSH/GluT ratio, and values for these GSH‑associated biomarkers were statistically significantly decreased in 20‑40% of the patients (P<0.0001). Furthermore, in RBCs, mean SOD1 and GPx activities were observed to be statistically significantly increased in ~60% and 19% (P<0.0001) of the patients, respectively, while increased GR activity in RBCs was observed in only 6% of the patients. The present study reports for the first time, to the best of our knowledge, that overall ~80% of EHS self‑reporting patients present with one, two or three detectable oxidative stress biomarkers in their peripheral blood, meaning that these patients‑as is the case for cancer, Alzheimer's disease or other pathological conditions‑present with a true objective new pathological disorder.
EHS | electromagnetic fields | EMFIS | glutathione | inflammation-associated biomarker | malondialdehyde | nitrotyrosine | oxidative stress | SOd1