ID Number		1130
Study Type		In Vivo
Model		8-18 GHz (radar), 474 THz (632 nm visible) exposure to mice and cells in culture and analysis of immune response, signaling and stress.
Details		NMRI mice (males) were immunized against bovine carboangydrase protein and exposed to 8.15-18 GHz (PW) radar pulses for 1.5 hours/day for 30 days at a power density of 0.3 uW/cm2. Exposure was reported to increase TNF, but not IL-3, synthesis. In addition, exposure increased the number of peritoneal macrophages by 7 fold and the number of spleenic T-cells by 1.5 fold. In tumor bearing animals, increase in TNF production due to RF exposure was also observed, and suggested by the authors to possibly be tumor suppressive. In acute studies, mice were exposed as above at a power density of 1 mW/cm2 for 5 hours also had increased TNF in peritoneal macrophages and splenic T cells, as well as increased and immune response in T lymphocytes after 3 days. The effect was synergized with a diet of lipid-soluble nutrients (beta-carotene, alpha-tocopherol and ubiquinone Q9). The authors suggest this demonstrates that MW exposure stimulates the immune potential of macrophages and T cells, and the antioxidant treatment enhances the effect. In a related using exposures as above, exposure increased TNF in peritoneal macrophages and spleenic T-cells of hibernating Arctic squirrels in certain months, although the effect did appear to be seasonal. In a short summary presented at Rhodes Greece, the authors report MW exposures decreased (in contrast to the above reports) TNF production and increased hsp70 expression in mice. In a 2009 study, the authors report exposure of isolated spleen cells (pre-incubated with geldanamycin to inhibit HSP90 expression) to at either 8-18 GHz (1 W/cm2) or 474 THz (632 nm visible light) resulted in activation (phosphorylation) of members of the SAPK/JNK signaling pathway, suggesting a stress response. AUTHORS' ABSTRACT: Glushkova et al. 2015 (IEEE #5822): Purpose: To investigate the role of the toll-like receptor 4 (TLR4), nuclear factor ºB (NF-ºB), and stress activated protein kinases/Jun N-terminal kinase (SAPK/JNK) signalling pathways in the responses of RAW 264.7 macrophages to low-intensity microwaves (MW). Materials and methods: Three inhibitors of TLR4, SAPK/JNK, and NF-ºB signalling, namely CLI-095, SP600125, and IKK Inhibitor XII, respectively, were added to cultured RAW 264.7 macrophages before MW treatment. Results: MW exposure resulted in stimulation of RAW 264.7 cell activity manifested by increases in cytokine production and the stimulation of cell signalling. The blocking of a key kinase of the NF-ºB pathway by IKK Inhibitor XII resulted in decreased MW-induced TLR4 expression and increased SAPK/JNK and NF-ºB phosphorylation in irradiated cells. In addition, IKK Inhibitor XII significantly decreased tumor necrosis factor-± (TNF-±), interferon-³ (IFN-³), interleukin 1± (IL-1±), interleukin 6 (IL-6), and interleukin 10 (IL-10) production in both exposed and unexposed RAW 264.7 macrophages. Inhibitor SP6000125 did not prevent an MW effect on signal proteins with the exception of decreased SAPK/JNK phosphorylation in RAW 264.7 cells. Cytokine production was markedly decreased in MW-exposed cells cultured with SP6000125. The inhibitor of TLR4, CLI-095, did not affect signal proteins and cytokine production changes in MW-exposed cells. Conclusions: The results suggest that low-intensity MW promotes macrophage activity via mechanisms involving cellular signalling, particularly the NF-ºB pathway. AUTHORS' ABSTRACT: Novoselova et al. 2016 (IEEE #6617): Purpose: To clarify whether extremely low-level microwaves alone or in combination with p38 inhibitor affect immune cell responses to inhalation exposure of mice to low-level toluene. Materials and methods: The cytokine profile, heat shock proteins expression, and the activity of several signal cascades, namely, NF-ºB, SAPK/JNK, IRF-3, p38 MAPK, and TLR4 were measured in in spleen lymphocytes of mice treated to air deliveredtoluene (0.6 mg/m3) or extremely low-level microwaves (8.15-18 GHz, 1¼W/cm2, 1 Hz swinging frequency) or combined action of these two factors. Results: A single exposure to air delivered low-level toluene induced activation of NF-ºB, SAPK/JNK, IFR-3, p38 MAPK and TLR4 pathways. Furthermore, air toluene induced the expression of Hsp72 and enhanced IL-1, IL-6, and TNF-± in blood plasma, which is indicative of a pro-inflammatory response. Exposure to MW alone also resulted in the enhancement of the plasma cytokine values (e.g., IL-6, TNF-±, and IFN-³) and activation of the NF-ºB, MAPK p38, and especially the TLR4 pathways in splenic lymphocytes. Paradoxically, pre-exposure to MW partially recovered or normalized the lymphocyte parameters in the toluene-exposed mice, while the p38 inhibitor XI additionally increased protective activity of microwaves by down regulating MAPKs (JNK and p38), IKK, as well as expression of TLR4 and Hsp90-±. Conclusions: The results suggest that exposure to low-intensity MW at specific conditions may recover immune parameters in mice undergo inhalation exposure to low-level toluene via mechanisms involving cellular signaling.
Findings		Effects
Status		Completed With Publication
Principal Investigator		Russian Acad Sci, Moscow Russia
Funding Agency		Nat'l Res Prog, Russia
Country		RUSSIAN FEDERATION
References		Cherenkov, DA et al. Biofizika, (2009) 54:256-259 Fesenko, EE et al. Bioelectrochem. Bioenerg., (1999) 49:29-35 Novoselova, EG et al. Bioelectrochem Bioenerg, (1999) 49:37-41 Gapayev, AB et al. Biophysics, (1997) 42:1149-1158 Glushkova, OV et al. International Journal of Radiation Biology., (2015) 91:321-328 Novoselova, EG et al. International Journal of Radiation Biology., (2017) 93:5 :535-543 Novoselova, EG et al. Biofizika., (2008) 53:457-461
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