The comparative study of the effects of 5.8 mW/cm(2) Millimeter Waves (MMW) and near Infrared (IR) irradiation on thermal properties, specific adsorption rate (SAR), specific electrical conductivity (SEC) and hydrogen peroxide (H(2)O(2)) content of distilled water (DW), and physiological solutions (PS) was performed. The thermal effect of MMW irradiation appeared only after the first minute of irradiation, while the IR heating started from the first minute of irradiation. The heat fusion of frozen MMW-treated DW and PS was significantly less than sham and IR-treated DW and PS. MMW irradiation had time-dependent elevation effect on water SEC and SAR, which was accompanied by the increase of H(2)O(2) formation in it. We suggest that the MMW-induced vibration of water dipole molecules caused the non thermal changes of physicochemical properties of DW and PS, which promote the formation of H(2)O(2) in water.

The effect of magnetized physiological solution (MPS) on isolated, perfused snail heart muscle contractility, (45)Ca uptake and intracellular level of cAMP, and cGMP was studied. The existence of the relaxing effect of MPS on heart muscle at room temperature (22 degrees C) and its absence in cold medium (4 degrees C) was shown. The MPS had a depressing effect on (45)Ca uptake by muscles and intracellular cAMP content and an elevating effect on intracellular cGMP level. It is suggested that the relaxing effect of MPS on heart muscle is due to the decrease of intracellular Ca ions as the result of activation of cGMP-dependent Ca efflux. The MPS induced decrease of intracellular cAMP content can be considered as a consequence of intracellular Ca loss, leading to the Na + K-ATPase reactivation, and causing the decrease of the intracellular level of ATP, serving as a substrate and positive modulator of cyclase activity.

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The dual effect of magnetized physiological solution (MPS) on snail heart muscle contractility (muscle relaxation and stimulation of heartbeat) was shown previously. The MPS-induced relaxation of the heart muscle has been explained by activation of cGMP-dependent Ca(2+) effluxes from the muscle; however, the mechanism of the stimulating effect of MPS on heartbeat remains unclear. As in the presence of paramagnetic oxygen molecules, magnetic fields could generate the exogenous reactive oxygen species such as hydrogen peroxide (H(2)O(2)), we hypothesize that H(2)O(2) may play a role as the possible messengers through which the activation effect of MPS on heartbeat is realized. To test this hypothesis, the dose-dependent effects of exogenous H(2)O(2) on heart muscle contractility and (45)Ca uptake were studied. Here we compared the obtained data with the previous results of the effects of MPS on heart muscle contractility and (45)Ca uptake. We found that exogenous H(2)O(2) and MPS have similar effects on Na(+)-K(+) pump-induced transient inhibition of muscle contractility and (45)Ca uptake. The Na(+)-K(+) pump-induced depression of H(2)O(2)-sensitivity of muscle contractility is determined by activation of Ca(2+) efflux from the cell. On the basis of these data we suggest the exogenous H(2)O(2) as a possible messenger through which the stimulation effect of MPS on heart muscle is realized.

Daily intraperitoneal injection of cyclophosphamide (CPA) (50 mg·kg -1 of body weight) for 5 days resulted in reduced levels of marrow and blood cellularity, which was most pronounced in 18 days post-treatment (pt). On day 18 after CPA treatment the enhanced levels of nitric oxide (NO) precursors and metabolites (L-arginine, L-citrulline, reactive nitrogen species (RNS)) of marrow and blood cells (platelet, neutrophil, lymphocyte and monocyte) resulted from upregulation of Ca(II)/calmodulin(CaM)-independent "inducible" NO synthase (iNOS), with a lesser contribution of Ca(II)/CaM-dependent "constitutive" cNOS isoforms to systemic NO. Biphasic response to CPA of marrow nitrergic system, i.e. both iNOS and cNOS showed significantly depressed activities, as well as diminished levels of NO metabolites on day 9 pt, suggested that signals in addition to NO might be involved in CPA-induced inhibition of hematopoesis, while a gradual increase of neutrophil and platelet NOS activity appeared to be contributed to a CPA-induced development of granulopenia, thrombocytopenia and hemorrhage.