Static electric field exposure decreases white blood cell count in peripheral blood through activating hypothalamic-pituitary-adrenal axis.

With the development of ultra-high-voltage (UHV) direct-current (DC) transmission, the health risk from the static electric field (SEF) generated by UHV DC transmission lines has drawn public attention. To investigate the effect of SEF exposure on white blood cell (WBC) count, mice were exposed to 56.3 kV/m SEF. Results revealed that total WBC count and lymphocyte count significantly decreased and serum levels of corticotropin-releasing hormone, adrenocorticotropic hormone and corticosterone (CORT) significantly increased after the exposure of 7d and 14d. All indices above recovered after the exposure of 21d. Analysis showed that the exposure of 7d and 14d could activate hypothalamic-pituitary-adrenal (HPA) axis. The increased CORT could bind to the glucocorticoid receptor (GR) in lymphocytes, and then promote the migration and apoptosis of lymphocytes. After the exposure of 21d, the magnitude of HPA axis activation declined through CORT-mediated negative feedback and the regulation of stress-related neural circuitry, so WBC count recovered.

Can static electric fields increase the activity of nitric oxide synthase and induce oxidative stress and damage of spleen?

With the rapid development of ultra-high-voltage (UHV) direct-current (DC) transmissions, the impact of static electric fields (SEF) in the vicinity of overhead UHV DC transmission lines on health has aroused much public concern. This study explored the effects of 56.3kV/m SEF on the spleen of mice. Results showed that SEF exposure of 21days significantly increased malonic dialdehyde content, superoxide dismutase activity, calcineurin activity, nitric oxide synthase (NOS) activity, and the mRNA expression levels of tumor necrosis factor-α (TNF-α) and nuclear factor-κB (NF-κB) in the spleen and caused the separation of nucleus and nuclear membrane, the disappearance of mitochondrial membrane, and the deficiency of mitochondrial cristae in splenic lymphocytes. By analysis and discussion, it was deduced that SEF could induce oxidative stress of the spleen by increasing the activity of NOS. Oxidative stress could further cause ultrastructural changes of splenic lymphocytes. Moreover, oxidative stress could cause the increase of the mRNA expression levels of TNF-α and NF-κB, which contributed to the occurrence of spleen inflammation.

Testosterone synthesis in testicular Leydig cells after long-term exposure to a static electric field (SEF).

China's clean energy and resources are mainly located in the west and north while electric load center is concentrated in the middle and east. Thus, these resources and energy need to be converted into electrical energy in situ and transported to electric load center through ultra-high voltage direct current (UHVDC) transmissions. China has built 25,000 km UHVDC transmission lines of 800 kV and 1100 kV, near which the impact of electric field on health has attracted public attention. Previous studies showed that time-varying electromagnetic field exposure could disturb testosterone secretion. To study the effect of non-time-varying electric field caused by direct current transmission lines on testosterone synthesis, male ICR mice were continually (24 h/d) exposed to static electric field of 56.3 ± 1.4 kV/m. Results showed that on the 3rd day of exposure and on the 7th day after ceasing the exposure of 28 d, serum testosterone level and testicular oxidative stress indicators didn't change significantly. On the 28th day of exposure, serum testosterone levels, testicular glutathione peroxidase (GSH-Px) activity, the mRNA and protein levels of testicular StAR, PBR, CYP11A1 decreased significantly, and testicular malondialdehyde (MDA) content increased significantly. Meanwhile, electron-dense edges and vacuolation appeared in lipid droplets of Leydig cells. The gap between inner mitochondrial membrane (IMM) and outer mitochondrial membrane (OMM) enlarged, which would cause the swelling of mitochondria, the rupture and deficiency of mitochondrial membranes. Analysis showed that testicular oxidative stress could induce the damage of mitochondrial structure in Leydig cells, which would decrease the rate of cholesterol transport from cytoplasm to mitochondria. Since cholesterol is the necessary precursor of testosterone synthesis, testosterone synthesis was inhibited. The decrease of the mRNA and protein expression levels of StAR and PBR in testes could diminish the cholesterol transported from OMM to IMM. The decrease of the mRNA and protein expression levels of CYP11A1 could reduce the pregnenolone required in testosterone synthesis and inhibit testosterone synthesis consequently.

Effects of power frequency electric field exposure on kidney.

With the rapid development of ultra high voltage alternating current (UHV AC) transmission, the intensity of environmental power frequency electric field (PFEF) near UHV AC transmission lines increased continuously, which has attracted considerable public attention on the potential health effects of PFEF. In this study, the effect of PFEF exposure on the kidney was explored. Institute of Cancer Research (ICR) mice were exposed to 35 kV/m PFEF (50 Hz). Two indicators relating to renal function (urea nitrogen and creatinine) were tested after the exposure of 7d, 14d, 21d, 35d and 49d. The pathological morphology and cellular ultrastructure of kidney were observed respectively by light microscopy and electron microscopy after the exposure of 25d and 52d. Results showed that compared with that of the control group, the concentration of urea nitrogen of 35 kV/m PFEF exposure group significantly increased on the 21st and 35th days, and the concentration of creatinine significantly increased on the 14th, 21st and 35th days. However, the concentrations of creatinine and urea nitrogen both returned to normal levels on the 49th day. Furthermore, an enlarged Bowman's space, the vacuolation of renal tubular epithelial cells and the foot process effacement of podocyte were found after 25d exposure, but no abnormality was observed after 52d exposure. Obviously, a short-term (35d) exposure of 35 kV/m PFEF could cause kidney injury, which could be recovered after a longer-term (52d) exposure. Based on this study and relevant literatures, one explanation for this two-way effect is as follows. Kidney injury was caused by the disequilibrium of mitochondrial dynamics under 35 kV/m PFEF exposure. PFEF could also activate Wnt/ß-catenin signal to promote the recovery of renal tubular epithelial cells and glomerular podocytes, so kidney injury could be repaired.