The effect of repeated microwave irradiation on the frequency of sex-linked recessive lethal mutations in Drosophila melanogaster

The effect of repeated microwave irradiation (2375 MHz, CW) on mutagenic changes in Drosophila melanogaster was investigated. Oregon-R males were exposed to sublethal doses of microwaves (15 W/cm2 for 60 min, 20 W/cm2 for 10 min, and 25 W/cm2 for 5 min) for 5 days. The Muller-5 cross was used to detect sex-linked recessive lethal mutations. 4 lethals were found in treated groups but their frequency was not significantly different from that of the control group. No cumulative effect of repeated exposures on the mortality of the treated males was observed; on the contrary, their mortality decreased with the number of exposures. Irradiation did not affect the sex ratio of the F1. A significant decrease in the number of F1 offspring was noted in the group exposed to the power density of 15 W/cm2. A negative thermal effect of microwaves on male germ cells was probably manifested by this long exposure.     

Thermoregulatory adjustments in squirrel monkeys exposed to microwaves at high power densities

The present study was undertaken to investigate the thermal adjustments of squirrel monkeys exposed in a cold environment to relatively high energy levels of microwave fields. The animals (Saimiri sciureus) were equilibrated for 90 min to a cool environment (Ta = 20 degrees C) to elevate metabolic heat production (M). They were then exposed for brief (10-min) or long (30-min) periods to 2,450-MHz continuous-wave microwaves. Power densities (MPD) were 10, 14, 19, and 25 mW/cm2 during brief exposures and 30, 35, 40, and 45 mW/cm2 during long exposures (rate of energy absorption: SAR = 0.15 [W/kg]/[mW/cm2]). Individual exposures were separated by enough time to allow physiological variables to return to baseline levels. The results confirm that each microwave exposure induced a rapid decrease in M. In a 20 degree C environment, the power density of a 10-min exposure required to lower M to approximate the resting level was 35 mW/cm2 (SAR = 5.3 W/kg). During the long exposures, 20 min was needed to decrease M to its lowest level. Cessation of irradiation was associated with persistence of low levels of M for periods that depended on the power density of the preceding microwave exposure. Vasodilation, as indexed by changes in local skin temperature, occurred at a high rate of energy absorption (SAR = 4.5 W/kg) and was sufficient to prevent a dramatic increase in storage of thermal energy by the body; vasoconstriction was reinstated after termination of irradiation. Patterns of thermophysiological responses confirm the influence both of peripheral and of internal inputs to thermoregulation in squirrel monkeys exposed to microwaves in a cool environment.     

The relationship of decreased serum thyrotropin and increased colonic temperature in rats exposed to microwaves

Although decreased serum thyrotropin (TSH) concentration has been found to be part of the endocrine response pattern in rats exposed to microwaves and other stimuli, the response of individual endocrine organs was not activated simultaneously by a given irradiance. Therefore, analytical evaluation of the function of endocrine organs individually as well as collectively is required to characterize the extent of biological involvement in microwave exposure. We have studied the changes in TSH concentration in unanesthetized rats exposed to 2.45 GHz amplitude modulated (120 Hz) microwaves in the far field for 2 and 4 h, between 0 and 55 mW/cm2, and from 1 to 10 times to demonstrate any possible cumulation, acclimation, or sensitization process. Ether inhalation was administered to test the responsiveness of TSH in groups of rats that failed to respond to microwave exposure by lowering TSH concentration. In addition, groups of rats were sampled 24 h after microwave exposure to test the persistency of the microwave effect on serum TSH concentration. Results showed that TSH concentration decreased in rats after microwave exposure. Influence of microwave exposure on serum TSH concentration was independent of the number of exposures indicating absence of cumulation, acclimation, or sensitization. The microwave effect on serum TSH could be dependent on duration of exposure. Decreased TSH concentration was usually accompanied by increased colonic temperature. For 4-h exposure, the lowest irradiance was 20 mW/cm2 or a 0.3 degree C increase in colonic temperature independent of the number of exposures. For 2-h exposure, the lowest irradiance was 30 mW/cm2 or a 1.1 degree C increase in colonic temperature regardless of the number of exposures. All the rats exposed at 10 mW/cm2 for 2 h had a lower TSH concentration than those of sham-exposed rats. Occasionally, significant reduction in TSH concentration could not be found in rats exposed to 20 or 25 mW/cm2 for 2 h. None of the rats exposed at an irradiance lower than 10 mW/cm2 had any change in TSH concentration. Failure of change in TSH concentration in response to microwave exposure was not a reflection of a deficiency since these rats responded to ether inhalation by lowering their TSH concentration. The effect of microwave exposure on TSH concentration was not persistent after exposure. The relation between TSH concentration and colonic temperature was curvilinear (exponential). From these results, two mechanisms and their implications for man were discussed.(ABSTRACT TRUNCATED AT 400 WORDS)     

Naltrexone pretreatment blocks microwave-induced changes in central cholinergic receptors

Repeated exposure of rats to pulsed, circularly polarized microwaves (2,450-MHz, 2-microseconds pulses at 500 pps, power density 1 mW/cm2, at an averaged, whole-body SAR of 0.6 W/kg) induced biphasic changes in the concentration of muscarinic cholinergic receptors in the central nervous system. An increase in receptor concentration occurred in the hippocampus of rats subjected to ten 45-min sessions of microwave exposure, whereas a decrease in concentration was observed in the frontal cortex and hippocampus of rats exposed to ten 20-min sessions. These findings, which confirm earlier work in the authors' laboratory, were extended to include pretreatment of rats with the narcotic antagonist naltrexone (1 mg/kg, IP) before each session of exposure. The drug treatment blocked the microwave-induced changes in cholinergic receptors in the brain. These data further support the authors' hypothesis that endogenous opioids play a role in the effects of microwaves on central cholinergic systems.     

Absence of corneal endothelium injury in non‐human primates treated with and without ophthalmologic drugs and exposed to 2.8 GHz pulsed microwaves

Microwave‐induced corneal endothelial damage was reported to have a low threshold (2.6 W/kg), and vasoactive ophthalmologic medications lowered the threshold by a factor of 10–0.26 W/kg. In an attempt to confirm these observations, four adult male Rhesus monkeys (Macaca mulatta) under propofol anesthesia were exposed to pulsed microwaves in the far field of a 2.8 GHz signal (1.43 ± 0.06 µs pulse width, 34 Hz pulse repetition frequency, 13.0 mW/cm² spatial and temporal average, and 464 W/cm² spatial and temporal peak (291 W/cm² square wave equivalent) power densities). Corneal‐specific absorption rate was 5.07 W/kg (0.39 W/kg/mW/cm²). The exposure resulted in a 1.0–1.2 °C increase in eyelid temperature. In Experiment I, exposures were 4 h/day, 3 days/week for 3 weeks (nine exposures and 36 h total). In Experiment II, these subjects were pretreated with 0.5% Timolol maleate and 0.005% Xalatan® followed by 3 or 7 4‐h pulsed microwave exposures. Under ketamine–xylazine anesthesia, a non‐contact specular microscope was used to obtain corneal endothelium images, corneal endothelial cell density, and pachymetry at the center and four peripheral areas of the cornea. Ophthalmologic measurements were done before and 7, 30, 90, and 180 days after exposures. Pulsed microwave exposure did not cause alterations in corneal endothelial cell density and corneal thickness with or without ophthalmologic drugs. Therefore, previously reported changes in the cornea exposed to pulsed microwaves were not confirmed at exposure levels that are more than an order of magnitude higher. Bioelectromagnetics 31:324–333, 2010. Published 2010 Wiley‐Liss, Inc.     

Thermal and metabolic responsiveness of Japanese quail embryos following periodic exposure to 2,450 MHz microwaves

Two studies were performed to determine if repeated exposure of the avian egg to microwaves can alter metabolism, temperature, and growth rate of embryos. Another aim was to supplement conventional heating with microwave heating and provide an optimal temperature for growth. Japanese quail (Coturnix coturnix japonica) eggs were exposed from day 1 through 15 of incubation (8 h/day) to sham or microwave (2,450 MHz) irradiation. Microwave exposures were at two power densities, 5 or 20 mW/cm2, and at three ambient temperatures (Tas), 30.0, 33.1, or 35.4 degrees C. Specific absorption rates for unincubated and 15-day-old incubated eggs were, respectively, 0.76 and 0.66 W kg-1 mW-1 cm-2 (i.e., 3.8 and 3.3 W/kg at 5 mW/cm2 and 15.2 and 13.2 W/kg at 20 mW/cm2). Eggs were concurrently sham exposed at each of five Tas, ranging from 27.9 to 37.5 degrees C. Tests were conducted during the 16th day of incubation (i.e., 1 day post-treatment), in the absence of microwaves, to determine metabolic rate of embryos and internal and external egg temperatures at different Tas. Repeated exposures to microwaves at 5 and 20 mW/cm2 at the same Ta (30 degrees C) increased wet-embryo mass on the 16th day by an average, respectively, of 9% and 61% when compared with predicted masses for embryos exposed at the same Ta in the absence of microwave radiation. There was no reliable indication, from post-treatment tests and comparisons with control embryos of similar mass, that repeated exposure to microwave radiation resulted in abnormal physiological development. Microwave radiation can be used to increase egg temperature and embryonic growth rate at Tas below normal incubation level without altering basic metabolic and thermal characteristics of the developing bird.     

Serum-thyroxine levels in microwave-exposed rats

The nature of the response of the thyroid gland in animals exposed to microwave irradiation is controversial. An enlarged thyroid and an increase of radioiodine uptake in microwave workers have been reported. Absence of thyroid disorders has also been reported in other exposed populations. Animal experimentation has contributed to the controversy because both increased and decreased thyroid functions have been reported. The thyroxine concentration in rats as representative of thyroid function in animals exposed to 2.45-GHz, 120-Hz amplitude-modulated microwaves has been studied. Comparison was made between thyroxine concentrations in microwave- and sham-exposed rats by Student's t test. After a 1-hr exposure, an increased thyroxine concentration was found in rats exposed at 40 and 70 mW/cm2, but not at 1, 5, 10, 20, 50, or 60 mW/cm2. After a 2-hr exposure, increased thyroxine concentration was noted in rats exposed at 25, 30, and 40 mW/cm2, but not at 1, 5, 10, and 20 mW/cm2. After a 4-hr exposure, thyroxine concentration increased in rats exposed at 1 mW/cm2 and decreased in rats exposed at 20 mW/cm2; but changes were not noted at 5 or 10 mW/cm2. Other experiments included animals that were exposed once for 4 hr (0.1, 1, 10, 25, and 40 mW/cm2), sampled 24 hr after a 4-hr exposure (0.1, 1, 10, 25, and 40 mW/cm2), or exposed for 4 hr 3 times (1, 10, 20, 30, 40, and 55 mW/cm2) and 10 times (1, 10, 20, 25, 30, and 40 mW/cm2), to evaluate the consistency of the thyroxine response. None of the rats in these experiments displayed any alteration of thyroxine concentration, except that decreased thyroxine was noted in rats exposed at 40 mW/cm2 for the third time. These studies covered a long time span; rats from two commercial sources (BS and CR) were used and subjected to different numbers of exposures, and therefore these data were evaluated for their stability. Two factors could influence the result significantly, i.e., source of animal and number of sham exposures. Rats used in the 2-hr exposures were from two different commercial sources; rats from CR had a higher (but normal) thyroxine concentration than did rats from BS. Therefore the data of these animals were separated by commercial source for reevaluation. Instead of increased thyroxine concentration in rats exposed at 25, 30, and 40 mW/cm2, changes were not noted in any microwave-exposed rats. The influence of sham exposure revealed that appropriate concurrent control and specification of animal source are needed in longitudinal studies.(ABSTRACT TRUNCATED AT 400 WORDS)     

Induction of neoplastic transformation in C3H/10T1/2 cells by 2.45-GHz microwaves and phorbol ester

C3H/10T1/2 cells were exposed to 2.45-GHz microwaves for 24 h and/or 1.5 Gy of 238-kVp X rays at 3.75 Gy/min. Transformation frequency and cell survival were measured with or without postirradiation addition of the tumor promoter tetradecanoyl-phorbol-13-acetate (TPA) at 0.1 microgram/ml. We previously reported (Carcinogenesis 6,859-864, 1985) an enhancement of transformation frequency when 10T1/2 cells exposed to a special sequence of microwaves and X rays were subsequently cultured in TPA. The same sequence of microwaves and X rays without promotion resulted in a transformation response similar to that induced by X rays alone. We now report statistically significant (at P greater than 0.999) enhancement of transformation response by TPA in cells exposed to 2.45-GHz microwaves (SAR = 4.4 W/kg). Microwaves alone had no effect on transformation. Plating efficiency and cell survival were not affected by TPA or microwave treatments.     

Influence of anesthesia on ocular effects and temperature in rabbit eyes exposed to microwaves

To investigate the effect of systemic anesthesia on ocular effects and temperature in rabbit eyes exposed to microwaves, one eye each of 43 male pigmented rabbits (Dutch, 1.8-2.2 kg) was exposed at 2.45 GHz for 60-20 min (300 mW/cm2; 108 W/kg), either under anesthesia (ketamine hydrochloride (5 mg/kg) + xylazine (0.23 mg/kg)) or without anesthesia. Changes in the anterior segment were evaluated by image analysis utilizing a Scheimpflug camera, specular microscopy, and a laser flare cell meter. Temperatures within the eye were measured during microwave exposure by a Fluoroptic thermometer. The exposed eyes showed miosis, conjunctival congestion, corneal edema, and an increase in the light scattering of the anterior shallow cortex in the pupillary area of the lens. The group under systemic anesthesia showed much stronger symptoms than those treated without anesthesia. All of the anterior ocular changes disappeared within a week. The highest temperature during exposure was in the vitreous, followed by the anterior chamber, and the retrobulbar cavity of the orbit. The ocular temperatures of the rabbits under systemic anesthesia were 2-9 degrees C higher than those without anesthesia. Body temperature showed an increase of 1 degrees C during the exposure. Acute high intensity microwave exposure temporarily induced anterior segments inflammation and lens changes. The more pronounced ocular effects in the anesthetized rabbits were associated with the significantly higher ocular temperatures in the anesthetized animals. The influence of systemic anesthesia on ocular changes should be considered.     

Thermoregulatory responses of the immature rat following repeated postnatal exposures to 2,450-MHz microwaves

This study was designed to determine the changes that occur in the thermoregulatory ability of the immature rat repeatedly exposed to low-level microwave radiation. Beginning at 6-7 days of age, previously untreated rats were exposed to 2,450-MHz continuous-wave microwaves at a power density of 5 mW/cm2 for 10 days (4 h/day). Microwave and sham (control) exposures were conducted at ambient temperatures (Ta) which represent different levels of cold stress for the immature rat (ie, "exposure" Ta = 20 and 30 degrees C). Physiological tests were conducted at 5-6 and 16-17 days of age, in the absence of microwaves, to determine pre- and postexposure responses, respectively. Measurements of metabolic rate, colonic temperature, and tail skin temperature were made at "test" Ta = 25.0, 30.0, 32.5, and 35.0 degrees C. Mean growth rates were lower for rats exposed to Ta = 20 degrees C than for those exposed to Ta = 30 degrees C, but microwave exposure exerted no effect at either exposure Ta. Metabolic rates and body temperatures of all exposure groups were similar to values for untreated animals at test Ta of 32.5 degrees C and 35.0 degrees C. Colonic temperatures of rats repeatedly exposed to sham or microwave conditions at exposure Ta = 20 degrees C or to sham conditions at exposure Ta = 30 degrees C were approximately 1 degrees C below the level for untreated animals at test Ta of 25.0 degrees C and 30.0 degrees C. However, when the exposure Ta was warmer, rats exhibited a higher colonic temperature at these cold test Ta, indicating that the effectiveness of low-level microwave treatment to alter thermoregulatory responses depends on the magnitude of the cold stress.     

Physiological changes in rats after exposure to low levels of microwaves

The effects of exposure to sublethal levels of microwaves were studied. Young albino rats of both sexes were exposed for 60 days to 7.5-GHz microwaves (1.0-KHz square wave modulation, average power 0.6 mW/cm2) for 3 h daily. During and after microwave exposure several physiological parameters were measured in both control and exposed animals. It was found that the animals exposed to microwaves tended to eat and drink less and thus showed a smaller gain in body weight. Some of the hematological parameters and organ weights were also significantly different. It is proposed that a nonspecific stress response due to microwave exposure and mediated through the central nervous system is responsible for the observed physiological changes.     

Evaluation of genotoxic effects in male Wistar rats following microwave exposure

Wistar rats (70 days old) were exposed for 2 h a day for 45 days continuously at 10 GHz [power density 0.214 mW/cm2, specific absorption rate (SAR) 0.014 W/kg] and 50 GHz (power density 0.86 microW/cm2, SAR 8.0 x10(-4) W/kg). Micronuclei (MN), reactive oxygen species (ROS), and antioxidant enzymes activity were estimated in the blood cells and serum. These radiations induce micronuclei formation and significant increase in ROS production. Significant changes in the level of serum glutathione peroxidase, superoxide dismutase and catalase were observed in exposed group as compared with control group. It is concluded that microwave exposure can be affective at genetic level. This may be an indication of tumor promotion, which comes through the overproduction of reactive oxygen species.     

Effects of microwaves on the adrenal cortex

Six-hundred-and-one male Long-Evans rats were used to study the effect of microwaves on adrenocortical secretion. Power density ranged from 0.1 to 55 mW/cm2 (SAR 0.02 to 11 W/kg). The microwave signal was 2.45 GHz amplitude modulated at 120 Hz. Serum corticosterone (CS) concentration was used as an index of adrenocortical function. Ten different exposure protocols were used to identify confounding factors influencing the sensitivity of adrenal cortex to microwave exposure. Increases in CS concentration were proportional to power density or colonic temperature and inversely proportional to the baseline CS. Increased CS concentration was never observed without increased colonic temperature and was not persistent 24 h after exposure. Acclimation (reduction in magnitude of response) could be noted after the tenth exposure. Facilitated heat loss attenuated the magnitude of CS increases by limiting the degree of hyperthermia. Ethanol enhanced the hyperthermic response and desensitized the adrenal response to microwave hyperthermia by increased baseline CS. Ether stimulated adrenal secretion irrespective of previous microwave exposure or adrenal stimulation induced by microwaves. Minor inhibition was also noted occasionally as decreased CS concentration at lower intensity (less than 20 mW/cm2) and decreased postexposure urinary CS excretion at 40 mW/cm2. Adrenal stimulation required minimally a 20 mW/cm2 (4 W/kg) or 0.7 degrees C increase in colonic temperature. An SAR lower than 4 W/kg may stimulate adrenal secretion by potentiating the hyperthermic effect if the ambient temperature is well above 24 degrees C.     

Effects of 460 MHz microwave radiation on Drosophila embryos under raised temperature

Combined effect of 460-MHz microwave irradiation and increased (up to 40 degrees C) temperature on Drosophila embryos of definite age was studied. It was demonstrated that the effect of 5-min exposures to non-modulated microwaves with 6 W/kg SAR accompanied with heating is only a little stronger than at normal temperature (24.5 degrees C). Irradiation with pulse-modulated microwaves with pulse repetition rates of 6, 10, 16, and 22 p.p.s. with average SAR of 0.12 W/kg (pulsed SAR 3 W/kg) combined with increased temperature caused some changes in PID dependent on the pulse rate. At 6 and 22 p.p.s, the increase in PID was close to that observed at normal temperature while at 10 and 16 p.p.s. the microwave irradiation did not produce any noticeable effect on development of the Drosophilas.     

Low-Level Microwave Irradiations Affect Central Cholinergic Activity in the Rat

Sodium-dependent high-affinity choline uptake was measured in various regions of the brains of rats irradiated for 45 min with either pulsed or continuous-wave low-level microwaves (2,450 MHz; power density, 1 mW/cm2; average whole-body specific absorption rate, 0.6 W/kg). Pulsed microwave irradiation (2-microseconds pulses, 500 pulses/s) decreased choline uptake in the hippocampus and frontal cortex but had no significant effect on the hypothalamus, striatum, and inferior colliculus. Pretreatment with a narcotic antagonist (naloxone or naltrexone; 1 mg/kg i.p.) blocked the effect of pulsed microwaves on hippocampal choline uptake but did not significantly alter the effect on the frontal cortex. Irradiation with continuous-wave microwaves did not significantly affect choline uptake in the hippocampus, striatum, and hypothalamus but decreased the uptake in the frontal cortex. The effect on the frontal cortex was not altered by pretreatment with narcotic antagonist. These data suggest that exposure to low-level pulsed or continuous-wave microwaves leads to changes in cholinergic functions in the brain.     

Japanese encephalitis virus (JEV): potentiation of lethality in mice by microwave radiation.

The expression of Japanese Encephalitis Virus (JEV) lethality in mice requires entry of the virus into the central nervous system. This entry is presumably through the capillary endothelial cells (CEC), because entry between CECs is inhibited by bands of circumferential tight-junctions. A viremic stage occurs during the first 4 to 5 days after JEV administration in mice, and both microwave radiation (2.45-GHz, continuous wave, 10-min exposure) and hypercarbia were employed to increase CEC permeability to JEV. Exposure to microwaves at power densities of 10-50 mW/cm2 resulted in a dose-dependent increase in JEV-induced lethality. Mice did not become tolerant or sensitized to microwave potentiation of JEV-induced mortality because 4 daily exposures at 10 or 50 mW/cm2 (SARS, approximately 24-98 W/kg) did not alter the lethality pattern to subsequent microwave radiation of JEV-exposed animals. Similarly, hypercarbia (5, 10, and 20% CO2) was observed to produce a dose-dependent increase in JEV-induced lethality. Both microwave radiation and hypercarbia are thought to promote pinocytosis in CNS capillary endothelial cells. This may be one mechanism by which they enhance JEV-induced lethality in adult Swiss-Cox mice.     

Increased sensitivity of the non-human primate eye to microwave radiation following ophthalmic drug pretreatment.

Previous studies in our laboratory have established that pulsed microwaves at 2.45 GHz and 10 mW/cm2 are associated with production of corneal endothelial lesions and with disruption of the blood-aqueous barrier in the non-human primate eye. In the study reported here we examined ocular damage in monkeys (M. mulatta and M. fascicularis) following topical treatment with one of two ophthalmic drugs (timolol maleate and pilocarpine) that preceded exposure to pulsed microwaves. Anesthetized monkeys were sham exposed or exposed to pulsed, 2.45 GHz microwaves (10 microseconds, 100 pps) at average power densities of 0.2, 1, 5, 10, or 15 mW/cm2 4 h a day for 3 consecutive days (respective SARs were 0.052, 0.26, 1.3, 2.6, and 3.9 W/kg). Immediately before microwave exposure, one or both eyes were treated topically with one drop of 0.5% timolol maleate or of 2% pilocarpine. Following administration of a drug, we observed a significant reduction in the power-density threshold (from 10 to 1 mW/cm2) for induction of corneal endothelial lesions and for increased vascular permeability of the iris. Diagnostic procedures (in vivo specular microscopy and fluorescein iris angiography) were performed following each exposure protocol. In addition, increased vascular permeability was confirmed with horseradish peroxidase tracer techniques. Although we did not measure intraocular temperatures in experimental animals, the results suggest that a mechanism other than significant heating of the eye is involved. Our data indicate that pulsed microwaves at an average SAR of 0.26 W/kg, if administered after pretreatment with ophthalmic drugs, can produce significant ocular effects in the anesthetized primate.     

Microwave irradiation of rats at 2.45 GHz activates pinocytotic-like uptake of tracer by capillary endothelial cells of cerebral cortex

Far-field exposures of male albino rats to 2.45-GHz microwaves (10-microseconds pulses, 100 pps) at a low average power density (10 mW/cm2; SAR approximately 2 W/kg) and short durations (30-120 min) resulted in increased uptakes of tracer through the blood-brain barrier (BBB). The uptake of systemically administered rhodamine-ferritin complex by capillary endothelial cells (CECs) of the cerebral cortex was dependent on power density and on duration of exposure. At 5 mW/cm2, for example, a 15-min exposure had no effect. Near-complete blockade of uptake resulted when rats were treated before exposure to microwaves with a single dose of colchicine, which inhibits microtubular function. A pinocytotic-like mechanism is presumed responsible for the microwave-induced increase in BBB permeability.     

Increased serum enzyme activity in microwave-exposed rats

Heat stable serum enzymes were studied in rats exposed to microwaves (2.45 GHz, 120 Hz amplitude modulated) 24 hr after a single 4-hr exposure or immediately after 3 and 10 exposures to 0.1 to 55 mW/cm2. In addition, stable colonic temperature at 41.5 degrees C for 30 min was maintained by microwave exposure in a group of five rats under barbiturate anesthesia. Alkaline phosphatase and lactic dehydrogenase did not increase as a result of microwave exposure. Increased serum glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) were noted in the 41.5 degrees C group 24 hr after exposure. A threshold body temperature for acute cellular injury after microwave exposure was demonstrated. The acute cellular injury could be in the liver. These mild elevations in the serum enzyme levels (mean +/- SE, GOT = 167 +/- 40 U/liter: GPT = 74 +/- 26 U/liter) indicated that the injuries were not accompanied by any significant sequelae in the rat. From this threshold and colonic temperature (41.5 degrees C for 30 min) in barbiturate-anesthetized, microwave-exposed rats, we derived a tentative threshold for the whole-body average absorption rate at 14 W/kg (70 mW/cm2 at 2.45 GHz for adult rats) for 4 hr. This tentative threshold is subject to changes by duration of exposure and by compounding variables influencing maintenance of body temperature.     

Low intensity microwave radiation effects on the ultrastructure of Chang liver cells

Chang liver cells (CCL-13 ATCC) exposed to 2450 MHz microwaves of field intensities ranging from 5 to 20 mW/cm2 for different periods up to 2 h show distinct alterations in the cytomembrane ultrastructure. A 30-min exposure of 10 mW/cm2 produces well-defined cytoplasmic lesions which appear as clear areas of degenerated rough endoplasmic reticulum (RER). Extensive degeneration of RER along with fragmentation and vacuolation, disorganization of mitochondrial membranes and matrix, increased lysosomal activity, and in some cases disruptions of nuclear membrane are seen in longer exposures. Radiation at 20 mW/cm2 produces significant damage to cell membranes in short exposures and treatments of 30 min and longer exposures lead to total disruption of organized cell ultrastructure. The identity of many organelles is lost as the cells become highly heteropycnotic with numerous cytoplasmic projections. Short exposures of 5 mW/cm2 produce very few noticeable differences in ultrastructure. These results confirm earlier observations that membranes may be the primary targets of microwave radiation in cells.