The role of nitric oxide in the mechanisms of stress-protective action of low-intensity extremely high-frequency electromagnetic radiation in acute and chronic stress

BACKGROUND: The study of stress mechanisms is an area of current interest in physiology and medicine. Understanding the role of nitric oxide (NO) in the mechanism of stress-protective action of low-intensity extremely high-frequency electromagnetic radiation (EHF EMR) requires investigating the main components of the stress response.

AIM: To determine the role of NO in the development of the anti-stress effect of low-intensity EHF EMR.

MATERIALS AND METHODS: 140 male Wistar rats weighing 200–220 g were divided into the following seven groups of 20 animals each: intact animals; AS, animals after a single exposure to acute stress; EHF-AS, animals irradiated with EHF EMR for 10 days and exposed to acute stress on day 10; L-NAME-EHF-AS, animals who were administered the NOS inhibitor L-NAME (10 mg/kg, intraperitoneally) for 10 days and irradiated with EHF EMR after 1 hour; HK, animals exposed to chronic hypokinetic stress for 10 days; EHF-HK, animals exposed to EHF EMR and hypokinetic stress for 10 days; L-NAME-EHF-HK, animals who were administered the NOS inhibitor L-NAME (10 mg/kg, intraperitoneally) for 10 days, irradiated with EHF EMR after 1 hour, and exposed to hypokinetic stress after another 1 hour. The levels of middle-weight molecules (MWM), circulating immune complexes (CIC), and malondialdehyde (MDA) were determined in the blood serum.

RESULTS: Acute stress increased the level of malondialdehyde, activating lipid peroxidation processes; in the EHF-AS group, this effect disappeared. NO blockade in the L-NAME-EHF-AS group activated endotoxication processes, the stress cascade, and physiologically active regulatory peptides (increase in the MWM level at 280 nm), oxidative metabolism of proteins and lipids (increase in the CIC and MDA levels), and inhibited immunogenesis. Hypokinetic stress suppressed the stress inhibiting system of the body and physiologically active regulatory peptides (decrease in the MWM level at 280 nm), suppressed immunogenesis, and increased oxidative metabolism of proteins and lipids (increase in the CIC and MDA levels). The stress-protective effect of EHF EMR was observed in the EHF-HK group. NO blockade in the L-NAME-EHF-HK group activated endotoxication processes, stress cascade and stress inhibiting systems of the body, physiologically active regulatory peptides (increase in the MWM level at 254 and 280 nm), oxidative metabolism of proteins and lipids (increase in the CIC and MDA levels), and inhibited immunogenesis.

CONCLUSIONS: NO blockade with L-NAME amplifies the effects of acute and hypokinetic stress under the exposure to low-intensity EHF EMR. Normal NO levels are necessary for the stress-protective effect of EHF EMR to develop during acute and hypokinetic stress.