Behavioral Abnormality along with NMDAR-related CREB Suppression in Rat Hippocampus after Shortwave Exposure

Objective To estimate the detrimental effects of shortwave exposure on rat hippocampal structure and function and explore the underlying mechanisms. Methods One hundred Wistar rats were randomly divided into four groups(25 rats per group) and exposed to 27 MHz continuous shortwave at a power density of 5, 10, or 30 m W/cm^2 for 6 min once only or underwent sham exposure for the control. The spatial learning and memory, electroencephalogram(EEG), hippocampal structure and Nissl bodies were analysed. Furthermore, the expressions of N-methyl-D-aspartate receptor(NMDAR) subunits(NR1, NR2 A, and NR2 B), c AMP responsive element-binding protein(CREB) and phosphorylated CREB(p-CREB) in hippocampal tissue were analysed on 1, 7, and 14 days after exposure. Results The rats in the 10 and 30 m W/cm^2 groups had poor learning and memory, disrupted EEG oscillations, and injured hippocampal structures, including hippocampal neurons degeneration, mitochondria cavitation and blood capillaries swelling. The Nissl body content was also reduced in the exposure groups. Moreover, the hippocampal tissue in the 30 m W/cm^2 group had increased expressions of NR2 A and NR2 B and decreased levels of CREB and p-CREB. Conclusion Shortwave exposure(27 MHz, with an average power density of 10 and 30 m W/cm^2) impaired rats' spatial learning and memory and caused a series of dose-dependent pathophysiological changes. Moreover, NMDAR-related CREB pathway suppression might be involved in shortwave-induced structural and functional impairments in the rat hippocampus.

Effects of Electromagnetic Radiation on Autophagy and its Regulation

With the ever increasing application of electronic technology, our exposure to artificial electromagnetic energy is also rapidly increasing. Electromagnetic radiation （EMR） is the fourth largest source of pollution, after air, water, and noise.

Inhibition of Micro RNA 219 Expression Protects Synaptic Plasticity via Activating NMDAR1, Ca MKIIγ,and p-CREB after Microwave Radiation

In recent decades,the potential health hazards of microwave exposure have been attracting increasing attention.Our previous studies have demonstrated that microwave exposure impaired learning and memory in experimental animal models[1,2].

Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling

Objective To investigate microwave-induced morphological and functional injury of natural killer（NK） cells and uncover their mechanisms. Methods NK-92 cells were exposed to 10, 30, and 50 m W/cm^2 microwaves for 5 min. Ultrastructural changes, cellular apoptosis and cell cycle regulation were detected at 1 h and 24 h after exposure. Cytotoxic activity was assayed at 1 h after exposure, while perforin and NKG2 D expression were detected at 1 h, 6 h, and 12 h after exposure. To clarify the mechanisms, phosphorylated ERK（p-ERK） was detected at 1 h after exposure. Moreover, microwave-induced cellular apoptosis and cell cycle regulation were analyzed after blockade of ERK signaling by using U0126. Results Microwave-induced morphological and ultrastructural injury, dose-dependent apoptosis（P 〈 0.001） and cell cycle arrest（P 〈 0.001） were detected at 1 h after microwave exposure. Moreover, significant apoptosis was still detected at 24 h after 50 m W/cm^2 microwave exposure（P 〈 0.01）. In the 30 m W/cm^2 microwave exposure model, microwaves impaired the cytotoxic activity of NK-92 cells at 1 h and down regulated perforin protein both at 1 h and 6 h after exposure（P 〈 0.05）. Furthermore, p-ERK was down regulated at 1 h after exposure（P 〈 0.05）, while ERK blockade significantly promoted microwave-induced apoptosis（P 〈 0.05） and downregulation of perforin（P 〈 0.01）. Conclusion Microwave dose-dependently induced morphological and functional injury in NK-92 cells, possibly through ERK-mediated regulation of apoptosis and perforin expression.

Dose-dependent Cardiac Dysfunction and Structural Damage in Rats after Shortwave Radiation

Objective To detect the effects of shortwave radiation on dose-dependent cardiac structure and function in rats after radiation and to elucidate the mechanism of shortwave radiation induced cardiac injury to identify sensitive indicators and prophylactic treatment.Methods One hundred Wistar rats were either exposed to 27 MHz continuous shortwave at a power density of 5,10,and 30 mW/cm^2 for 6 min or undergone sham exposure for the control(the rats had to be placed in the exposure system with the same schedules as the exposed animals,but with an inactive antenna).The Ca^2+,glutamic oxaloacetic transaminase(AST),creatine kinase(CK)and lactate dehydrogenase(LDH)content in the peripheral serum of the rats were detected by an automatic blood biochemical analyser.The electrocardiogram(ECG)of standard lead II was recorded by a multi-channel physiological recording and analysis system.The cardiac structure of rats was observed by light and electron microscopy.Results The results showed that the 5,10,and 30 mW/cm^2 shortwave radiation caused a significant increased in the levels of Ca2+,AST,CK,and LDH in the peripheral serum of rats.The cardiac structure was damaged by radiation and showed a disordered arrangement of myocardial fibres,the cavitation and swelling of myocardial mitochondria.These injuries were most significant 7 d after radiation and were not restored until 28 d after radiation.Conclusion Shortwave radiation of 5,10,and 30 mW/cm^2 can damage rat cardiac function,including damage to the tissue structure and ultrastructure,especially at the level of the myocardial fibres and mitochondria.Shortwave radiation at 5,10,and 30 mW/cm^2 induced damage to rat heart function and structure with a dose-effect relationship,i.e.,the greater the radiation dose was,the more significant the damage was.