David N. Erwin

Influence of radiofrequency radiation on chromosome aberrations in CHO cells and its interaction with DNA-damaging agents.

A limited number of contradictory reports have appeared in the literature about the ability of radiofrequency (rf) radiation to induce chromosome aberrations in different biological systems. The technical documentation associated with such reports is often absent or deficient. In addition, no information is available as to whether any additional genotoxic hazard would result from a simultaneous exposure of mammalian cells to rf radiation and a chemical which (by itself) induces chromosome aberrations. In the work described, we have therefore tested two hypotheses. The first is that rf radiation by itself, at power densities and exposure conditions which are higher than is consistent with accepted safety guidelines, can induce chromosome aberrations in mammalian cells. The second is that, during a simultaneous exposure to a chemical known to be genotoxic, rf radiation can affect molecules, biochemical processes, or cellular organelles, and thus result in an increase or decrease in chromosome aberrations. Mitomycin C (MMC) and Adriamycin (ADR) were selected because they act by different mechanisms, and because they might put normal cells at risk during combined-modality rf radiation (hyperthermia)-chemotherapy treatment of cancer. The studies were performed with suitable 37 degrees C and equivalent convection heating-temperature controls in a manner designed to discriminate between any thermal and possible nonthermal action. Radiofrequency exposures were conducted for 2 h under conditions resulting in measurable heating (a maximum increase of 3.2 degrees C), with pulsed-wave rf radiation at a frequency of 2450 MHz and an average net forward power of 600 W, resulting in an SAR of 33.8 W/kg. Treatments with MMC or ADR were for a total of 2.5 h and encompassed the 2-h rf radiation exposure period. The CHO cells from each of the conditions were subsequently analyzed for chromosome aberrations. In cells exposed to rf radiation alone, and where a maximum temperature of approximately 40 degrees C was achieved in the tissue culture medium, no alteration in the frequency from 37 degrees C control levels was observed. Relative to the chemical treatment with MMC alone at 37 degrees C, for two different concentrations, no alteration was observed in the extent of chromosome aberrations induced by either simultaneous rf radiation exposure or convection heating to equivalent temperatures. At the ADR concentration that was used, most of the indices of chromosome aberrations which were scored indicated a similar result.(ABSTRACT TRUNCATED AT 400 WORDS)

Radiofrequency (Microwave) Radiation Exposure of Mammalian Cells during UV-Induced DNA Repair Synthesis

The effect of continuous-wave (CW) and pulsed-wave (PW) radiofrequency radiation (RFR) in the microwave range on UV-induced DNA repair has been investigated in MRC-5 normal human diploid fibroblasts. RFR exposure at power densities of 1 (or 5) and 10 mW/cm2 gave a maximum specific absorption rate (SAR) (at 10 mW/cm2) of 0.39 +/- 0.15 W/kg for 350 MHz RFR, 4.5 +/- 3.0 W/kg for 850 MHz RFR, and 2.7 +/- 1.6 W/kg for 1.2 GHz RFR. RFR exposures for 1 to 3 h at 37 degrees C, in either continuous-wave or pulsed-wave modes, had no effect on the rate of repair replication label incorporated into preexisting UV-damaged DNA. RFR exposures (PW), with a constant medium temperature of 39 degrees C at 350 and 850 MHz during the repair period after UV damage, also had no effect. Assay for induction of repair synthesis by RFR exposure alone in non-UV irradiated cells was negative for the 350-, 850-, and 1200-MHz CW and PW RFR at 37 degrees C and the 350- and 850-MHz PW RFR at 39 degrees C. RFR does not induce DNA repair under these exposure conditions. In preliminary experiments--with the tissue culture medium maintained at 39 degrees C and RFR exposures (PW) at the frequencies of 350, 850, and 1200 MHz--no effect on incorporation of [3H]thymidine into DNA undergoing semiconservative synthesis was observed.

Diazoluminomelanin: A Synthetic Electron and Nonradiative Transfer Biopolymer

The green hemoprotein (GHP) of erythrocytes is a type-b cytochrome with no known function except for the incidental finding of its ferroactivation of phosphoenolpyruvate carboxykinase which is not present in erythrocytes (Chee and Lardy, 1981). We have previously postulated that GHP can transfer superoxide to methemoglobin, converting it to oxyhemoglobin (Kiel et al., 1988). Although no artificial substrate has been available for measuring the electron transfers mediated by GHP, previous data has indicated that the peroxidations putatively mediated by GHP and hemoglobin in erythrocytes can be inhibited by 3-amino-L-tyrosine (Kiel and Erwin., 1986; Kiel et al., 1988). This derivatized tyrosine is an inhibitor of peroxidases (Kiel, 1988) and inhibits the oxidative burst (superoxide and hydrogen peroxide production) of mouse peritoneal macrophages (Lefkowitz et al., 1988). The latter is associated with an electron transport chain containing a type-b cytochrome (Rossi et al., 1986). Furthermore, when lactoperoxidase is reduced by thiol, its binding of tyrosine derivatives becomes significantly enhanced (Pommier and Cahnmann, 1979). Therefore, a potential existed for the development of a tyrosihe-derived substrate that specifically bound to GHP.