Lung burden of green nickel oxide aerosol and histopathological findings in rats after continuous inhalation

There are few inhalation studies of nickel carcinogenesis. In this study, Wistar male rats were exposed to green nickel oxide (NiO(G)) aerosols (mass median aerodynamic diameter, 0.6 μm) for 7 h/d, 5 d/wk for up to 12 mo. The average exposure concentration was controlled at 0.3 and 1.2 mg/m³ during the exposure. For histopathological examination and measurement of the nickel concentration in rat organs, the rats were sacrificed at 3, 6, and 12 mo of exposure and 8 mo clearance period following 12 mo of exposure. The nickel content in rat lungs that was observed up to 2.6 mg after 12 mo exposure, was proportional to the exposure concentration during the exposure. The clearance of the nickel from the lungs was very slow and the biological half time was determined 7.7 mo. Although the rats were exposed continuously to NiO(G), for 12 mo and kept for 8 mo clearance period, there were no malignant tumors in any of the exposed animals.     

Biological half time of deposited nickel oxide aerosol in rat lung by inhalation

Wistar male rats were exposed to nickel oxide (NiO) aerosols (mass median aerodynamic diameter, 1.2 and 4.0 μm). The average exposure concentration was controlled from a low level of 0.6 mg/m³ to a high level of 70 mg/m³ and total exposure time was 140 h. Some rats were sacrificed just after the exposure, whereas others were exposed for 1 mo and kept for 12 and 20 mo clearance periods before sacrifice. There were no differences in body weight gain between NiO exposure groups and controls. Nickel concentrations in lungs of exposure groups were much higher than those of controls and decreased with the passing of the clearance time. No apparent deposition of nickel was observed in the liver, kidney, spleen, and blood immediately after the exposure, but in the case of the high exposure groups, the nickel concentration in the liver, spleen, and blood slightly increased with the increasing time of clearance. The biological half time of NiO deposited in the lungs was estimated by the assumption that the amount of the clearance is proportional to the amount of the NiO deposited. This resulted in a biological half time of 11.5 and 21 mo for 1.2 and 4.0 μm, respectively.     

Essential trace metals and specific organ weights in diet-restricted and ad lib-fed rats

Wistar male rats were exposed to nickel oxide (NiO) aerosols (mass median aerodynamic diameter, 1.2 μm). The average exposure concentration was controlled from low level (0.6 mg/m³) to high level (8.0 mg/m³) and total exposure time ranged from 140 to 216 h. Some rats were sacrificed just after the exposure, whereas others were exposed for 1 mo and kept for a 1-yr clearance period before sacrifice. There were no differences in body weight gain between NiO exposure groups and controls. Nickel concentrations in lungs of exposure groups were much higher than those of controls. No apparent deposition of nickel was observed in liver, kidney, spleen, heart, brain, and blood, but lung burdens of up to about 2.35 mg of NiO were found. The apparent deposition fractions were 19.8 and 14.5% after the exposure to average concentrations of 1.4 and 6.5–7.0 mg/m³, respectively. The clearance rate of NiO deposited in lungs may be small.     

Comparative deposition and clearance of various nickel compounds exposed by inhalation in rats

Wistar male rats were exposed to three types of nickel compounds, NiO(G), NiO(B), and Ni₃S₂, for 6 h/d, 5 d/wk for 6 mo. The solubility of these chemicals to saline solution was 0.3 ppm for NiO(G), 3.5 ppm for NiO(B), and 310 ppm for Ni₃S₂. Controls were exposed to clean air under similar conditions. Some rats were sacrificed 24 h after the termination of the final repeated exposure, and the remaining rats were kept for a 12-mo clearance period before sacrifice. There was no significant difference in body weight between exposed rats and controls and also no significant differences in organs weights, except for lungs in the case of Ni₃S₂, between exposed rats and controls. Nickel concentration in the lungs just after the exposure to nickel compounds was the highest when compared to other organs. The apparent deposition fractions (%) in the lungs were 0.5 ± 0.1 for NiO(G), 1.0 ± 0.3 for NiO(B), and 0.5 ± 0.1 for Ni₃S₂., After the clearance period, there were no significant differences in organ weights, except for the lungs in case of Ni₃S₂, between the exposed rats and the controls. During the 12 mo of clearance, 82% of deposited NiO(G), 73% of NiO(B), and 98% of Ni₃S₂ were cleared from lungs.     

Biological half-time in rats exposed to nickel monosulfide (amorphous) aerosol by inhalation

This study reports the biological half-time of amorphous nickel monosulfide(NiS(A)) aerosol retained in rat lungs. Wistar male rats were exposed to NiS(A) aerosols (mass median aerodynamic diameter: 4.0 μm) for a single 4 h exposure, or for 7 h/d, 5 d/wk for 1 mo. The average exposure concentrations were controlled at 107 mg/m³ for the single exposure and at 8.8 mg/m³ for the repeated exposures by a dust generator consisting of a continuous fluidized bed with an overflow pipe and a screw feeder. After the exposures, the nickel contents in the rat organs, blood, and urine were measured and histopathological examinations were performed. The biological half time of NiS(A) in rat lungs was 20 h, which was extremely shorter than 21 mo of green nickel oxide (NiO(G)). There were no malignant tumors in any of the exposure groups.     

Effects of nickel oxide on the production of tumor necrosis factor by alveolar macrophages of rats

To evaluate the effect of green nickel oxide (NiO) on the production of tumor necrosis factor (TNF) by alveolar macrophages, alveolar macrophages were exposed to NiO in vitro and in vivo. For the in vitro study, rats alveolar macrophages were incubated with NiO on a microplate for 24 h. TNF activity in the culture supernatant was determined by the L929 bioassay. Rats alveolar macrophages cultured with 100 and 200 μg/mL of NiO in vitro induced the production of TNF, however, it was not statistically significant compared with the control that was free from NiO exposure. For exposure in vivo, rats were divided into two groups. Five were exposed to a daily concentration of 11.7±2.0 mg/m³ of NiO for an 8-hr/d, 5 d/wk, for 4 wk, and five rats (control) were kept in a cage and not exposed to NiO. Bronchoalveolar lavage was performed and the recovered alveolar macrophages were incubated on a microplate for 24 h. TNF production by exposed alveolar macrophages was significantly higher than that of controls.     

Electron microscopical findings with special reference to cancer in rats caused by inhalation of nickel oxide

A special exposure system was used for the inhalation of nickel oxide (NiO) aerosol by Wistar male rats. The median aerodynamic diameter and the geometric standard deviation were 1.2 μm and 2.2, respectively. A histopathological study of the rats was performed immediately, and at intervals of 12 and 20 mo after a 1-mo expsoure to NiO. Electron microscopy showed that localization of NiO particles was restricted to the lungs and that each particle had been engulfed by the alveolar macrophages. Type II pneumocytes and nonciliated bronchiolar epithelial cells (Clara cells), as well as numerous tubular myelin (surfactant) in the alveoli were prominent. In rats dissected after 12 mo, clusters of NiO particles were still present within the terminal bronchioli, alveolar walls, and lysosomes of the alveolar macrophages. Pools of tubular myelin were observed in the peribron-chial lymphatics. The Clara cells, which project into the lumen of bronchioli, showed active secretion and were filled with smooth en-doplasmic reticulum (SER) in the apical cytoplasm. In the experimental group sacrificed after 20 mo, one rat had papillary adenocarcinoma and two rats showed adenomatosis in the peripheral portion of the lung, but none in the upper respiratory tract.     

Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds.

DNA damage in cultured cells and in lungs of rats induced by nickel compounds was investigated to clarify the mechanism of nickel carcinogenesis. DNA strand breaks in cultured cells exposed to nickel compounds were measured by using a pulsed field gel electrophoresis technique. Among nickel compounds (Ni(3)S(2), NiO (black), NiO (green), and NiSO(4)), only Ni(3)S(2), which is highly carcinogenic, induced lesions of both double- and single-stranded DNA in cultured human cells (Raji and HeLa cells). Treatment of cultured HeLa cells with Ni(3)S(2) (10 microg/ml) induced a 1.5-fold increase in 8-hydroxy-2'-deoxyguanosine (8-OH-dG) compared with control, whereas NiO (black), NiO (green), and NiSO(4) did not enhance the generation of 8-OH-dG. Intratracheal instillation of Ni(3)S(2), NiO(black), and NiO(green) to Wistar rats increased 8-OH-dG in the lungs significantly. NiSO(4) induced a smaller but significant increase in 8-OH-dG. Histological studies showed that all the nickel compounds used induced inflammation in lungs of the rats. Nitric oxide (NO) generation in phagocytic cells induced by Ni(3)S(2), NiO(black), and NiO(green) was examined using macrophage cell line RAW 264.7 cells. NO generation in RAW 264.7 cells stimulated with lipopolysaccharide was enhanced by all nickel particles. Two mechanisms for nickel-induced oxidative DNA damage have been proposed as follows: all the nickel compounds used induced indirect damage through inflammation, and Ni(3)S(2) also showed direct oxidative DNA damage through H(2)O(2) formation. This double action may explain relatively high carcinogenic risk of Ni(3)S(2).     

Influence of vitamin E on polyamine metabolism in ozone-exposed rat lungs

The influence of vitamin E (E) on lung polyamine metabolism of rats exposed to ozone (O3) was examined. Rats fed diets wither E-deficient or supplemented with 1000 IU E/kg were exposed to 0.5 +/- 0.05 ppm O3 or filtered room air continuously for 5 days. They were then sacrificed and their lungs were analyzed for biochemical changes. Lung E content was strongly associated with the dietary level, and increased (36%, P less than 0.05) after O3 exposure only in E-supplemented rats. Lung polyamine metabolism was not affected in the air-control rats by E level, but increased after O3 exposure in both dietary groups. The activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase were elevated above air controls. However, the increases were significant only for E-deficient rats when compared to E-supplemented rats. After O3 exposure, putrescine increased significantly in both dietary groups; spermidine increased but was significantly higher only in the E-deficient group; and spermine remained unchanged in both dietary groups. Elevated E content of supplemented rat lungs after O3 exposure may represent its mobilization under oxidant stress. Increased polyamine metabolism of E-deficient rats suggests either a greater sensitivity to injury by O3 or a possible antioxidant function for polyamines compensating for E deficiency.     

The influence of maternal nicotine exposure on neonatal lung carbohydrate metabolism.

The influence of maternal nicotine exposure (1 mg/kg body mass/day) during pregnancy and lactation on energy metabolism of lung tissue of neonatal rats were investigated. The glucose turnover of the lung tissue of the neonatal rats exposed to nicotine via the placenta and mother's milk was 86.4% higher than that of the controls. Glycolysis was however suppressed by 22.7% (P < 0.01). The adenine nucleotide pool (ATP+ADP+AMP) was 32.8% higher for the lungs of the 3 week old neonates exposed to nicotine than that of the control rat lung. After 4 weeks of nicotine withdrawal glycolysis of those animals exposed to nicotine were still inhibited to the same extent than during exposure. The adenine nucleotide pool was 69.95% higher than that of the controls. It is proposed that the inhibition of glycolysis was due to the high ATP/ADP ratio of the lungs of the nicotine exposed rats.     

Estimation of Incremental Unit Risks for Inhaled Nickel Subsulfide and Nickel Oxide,Based on a Combination of Human and Animal Data

Both animal and human exposure–response data are used to estimate the incremental unit risks (IURs) of lung cancer for Ni₃S₂ and NiO, which are constituent compounds of nickel refinery dust. The animal experiments are used to determine relative lung cancer potencies for Ni₃S₂ and NiO, and the human epidemiological data are used as the best estimate of overall risk for refinery dust exposure. The animal data for Ni₃S₂ are fit with a linear model, while the nonlinear animal data for NiO are fit with a Weibull model. The lower 95% confidence limit at a 5% point of departure is used to calculate a tumorigenic potency ratio of Ni₃S₂ to NiO of 5.6. Analyses of actual nickel refinery dust indicate the weight% of Ni₃S₂ and NiO to be 82% and 9%, respectively. This information is used with the previously determined IUR for nickel refinery dust to calculate IUR_NiO = 5.1 × 10^?5 (μg Ni/m³)^?1 and IUR_Ni3S2 = 2.9 × 10^?4 (μg Ni/m³)^?1.     

Pulmonary histopathology and alteration in cellular pattern of bronchoalveolar lavage fluid in experimental silicosis

Pathogenesis of silicosis is still being evaluated. Cellular and histopathological changes in lung following acute and chronic exposure of quartz in rats have been investigated. Inbred wistar rats were given single intratracheal injection of quartz (10 mg in 0.05 ml saline) in groups of acute model, and inhalation of quartz (40 mg/m3 with air flow 5 l/hr in a simulation chamber, 6 hr/day) in groups of chronic model. The control groups were exposed to vehicles only. Rats were sacrificed on day 3, 5 and 7 of intratracheal injection and after 2, 4 and 8 weeks of inhalation. Total and differential cell counts (TC and DC) were performed in bronchoalveolar lavage fluid (BALF). Histopathology was done in the lungs. There was significant (P < 0.001) increase in TC and significant (P < 0.001) changes in percentage of inflammatory cell counts on DC in the BALF of silicotic rats. Histopathology showed progressive inflammatory and fibrotic response in quartz exposed lungs in both acute and chronic models. The results indicate duration dependent inflammatory changes in lungs of both the models. Changes in cell counts precede the histopathological changes and may serve as early biological marker for detection of silicosis.     

Distribution of various nickel compounds in rat organs after oral administration

In this study, eight kinds of nickel (Ni) compounds were orally administered to Wistar male rats and the distribution of each compound was investigated 24 h after the administration. The Ni compounds used in this experiment were nickel metal [Ni−M], nickel oxide (green) [NiO(G)], nickel oxide (black) [NiO(B)], nickel subsulfide [Ni₃S₂], nickel sulfide [NiS], nickel sulfate [NiSO₄], nickel chloride [NiCl₂], and nickel nitrate [Ni(NO₃)₂]. The solubilities of the nickel compounds in saline solution were in the following order; [Ni(NO₃)₂>NiCl₂>NiSO₄]≫[NiS>Ni₃S₂]>[NiO(B)>Ni−M>NiO(G)]. The Ni level in the visceral organs was higher in the rats given soluble Ni compounds; Ni(NO₃)₂, NiCl₂, NiSO₄, than that in the rats receiving other compounds. In the rats to which soluble Ni compounds were administered, 80–90% of the recovered Ni amounts in the examined organs was detected in the kidneys. On the other hand, the Ni concentration in organs administered scarcely soluble Ni compounds; NiO(B), NiO(G), and Ni−M were very low. The estimated absorbed fraction of each Ni compounds was increased with the increase of the solubility. These results suggest that the kinetic behavior of Ni compounds administered orally is closely related with the solubility of Ni compounds, and that the solubility of Ni compounds is one of the important factors for determining the health effect of Ni compounds.     

Reversibility of cold-induced hypertension after removal of rats from cold

Chronic exposure of rats to cold air induces hypertension, including elevation of blood pressure and cardiac hypertrophy. The present study was designed to assess reversibility of these changes after removal from cold. Five groups of six male rats each were exposed to cold (5 +/- 2 degrees C) for 39 days, while six control rats were maintained at 26 +/- 2 degrees C. Systolic blood pressures of the rats in one of the cold-treated groups, as well as the controls, were measured twice weekly throughout the experiment. Blood pressure of the cold-exposed rats (150 +/- 3 mmHg; 1 mmHg = 133.3 Pa) became elevated significantly above that of controls (129 +/- 3 mmHg) within 4 weeks. On day 39 of cold exposure, one group (six rats) of the cold-treated rats was sacrificed while still in the cold. The remaining four groups of cold-treated rats were than removed from cold and kept at 26 +/- 2 degrees C. One group of cold-treated rats was sacrificed weekly thereafter. During the last week, the six control rats were also sacrificed. At death, the heart, kidneys, and adrenal glands were removed and weighed. Mean heart weight of the cold-treated group (346 +/- 7 mg/100 g body weight), sacrificed prior to removal from cold, was significantly (p less than 0.01) greater than that of controls (268 +/- 5 mg/100 g body weight). The increased heart weight of the cold-treated group appeared to result mainly from an increase in left ventricular weight.(ABSTRACT TRUNCATED AT 250 WORDS)     

Airborne manganese exposure differentially affects end points of oxidative stress in an age-and sex-dependent manner

Juvenile female and male (young) and 16-mo-old male (old) rats inhaled manganese in the form of manganese sulfate (MnSO₄) at 0, 0.01, 0.1, and 0.5 mg Mn/m³ or manganese phosphate at 0.1 mg Mn/m³ in exposures of 6h/d, 5d/wk for 13 wk. We assessed biochemical end points indicative of oxidative stress in five brain regions: cerebellum, hippocampus, hypothalamus, olfactory bulb, and striatum. Glutamine synthetase (GS) protein levels, metallothionein (MT) and GS mRNA levels, and total glutathione (GSH) levels were determined for all five regions. Although most brain regions in the three groups of animals were unaffected by manganese exposure in terms of GS protein levels, there was significantly increased protein (p<0.05) in the hippocampus and decreased protein in the hypothalamus of young male rats exposed to manganese phosphate as well as in the aged rats exposed to 0.1 mg/m³ MnSO₄. Conversely, GS protein was elevated in the olfactory bulb of females exposed to the high dose of MnSO₄. Statistically significant decreases (p<0.05) in MT and GS mRNA as a result, of manganese exposure were observed in the cerebellum, olfactory bulb, and hippocampus in the young male rats, in the hypothalamus in the young female rats, and in the hippocampus in the senescent males. Total GSH levels significantly (p<0.05) decreased in the olfactory bulb of manganese exposed young male rats and increased in the olfactory bulb of female rats exposed to manganese. Both the aged and young female rats had significantly decreased (p<0.05) GSH in the striatum resulting from manganese inhalation. The old male rats also had depleted GSH levels in the cerebellum and hypothalamus as a result, of the 0.1-mg/m³ manganese phosphate exposure. These results demonstrate that age and sex are variables that must be considered whenassessing the neurotoxicity of manganese.     

Evaluation of the potential promoting effect of 60 Hz magnetic fields on N-ethyl-N-nitrosourea induced neurogenic tumors in female F344 rats

The present study investigated the possible effect of 60 Hz magnetic fields (MFs) as promoters of neurogenic tumors initiated transplacentally by a chemical carcinogen, N-ethyl-N-nitrosourea (ENU). In a preliminary study, 5 mg of ENU was shown to induce 30 to 40% neurogenic tumors in F344 rats offspring after 420 days of observation. In the present study, 400 female rats were divided into eight different groups (50 animals/group) and exposed in utero (on day 18 of gestation) to a single intravenous dose of either Saline (Group I), or ENU, 5 mg/kg (Group II to VIII). Dams in group II were given no further treatment while dams in Groups III to VII were exposed to 5 different intensities of MFs forty eight hours later. Animals in group III were sham exposed (<0.02 microT) while groups IV to VII were exposed to 2, 20, 200, and 2000 microT, respectively. Dams in Group VIII were injected intraperitoneally with 12-O-tetradecanoylphrobol-13-acetate (TPA; 10 micrograms/kg) from day 19 until delivery, and then their female offspring continued to be injected every 15 days, starting at day 14 after birth until sacrifice (positive controls). Accordingly, this study included three different types of controls: Internal controls (Groups II and III) and positive control (Group VIII). Body weight, mortality and clinical observations were evaluated in all groups of animals during in-life exposure. Necropsy was performed on all exposed and control animals that died, were found moribund or sacrificed at termination of the study. Histopathological evaluation was done for all brains, spinal cords, cranial nerves, major organs (lungs, liver, spleen, kidneys, pituitary, thyroid and adrenals) and all gross lesions observed during necropsy. All clinical observations and pathological evaluations were conducted under "blinded" conditions. The findings from this ENU/MFs promotion study clearly demonstrate that, under our defined experimental conditions, exposure to 60 Hz linear (single axis) sinusoidal, continuous wave MFs had no effect on the survival of female F344 rats or on the number of animals bearing neurogenic tumors. These results suggest that MFs have no promoting effect on neurogenic tumors in the female F344 rats exposed transplacentally to ENU.     

An integrated approach to biomonitoring exposure to styrene and styrene-(7,8)-oxide using a repeated measurements sampling design

Abstract

The aim of this work was to investigate urinary analytes and haemoglobin and albumin adducts as biomarkers of exposure to airborne styrene (Sty) and styrene-(7,8)-oxide (StyOX) and to evaluate the influence of smoking habit and genetic polymorphism of metabolic enzymes GSTM1 and GSTT1 on these biomarkers. We obtained three or four air and urine samples from each exposed worker (eight reinforced plastics workers and 13 varnish workers), one air and urine samples from 22 control workers (automobile mechanics) and one blood sample from all subjects. Median levels of exposure to Sty and StyOX, respectively, were 18.2 mg m^?3 and 133 µg m^?3 for reinforced plastics workers, 3.4 mg m^?3 and 12 µg m^?3 for varnish workers, and <0.3 mg m^?3 and <5 µg m^?3 for controls. Urinary levels of styrene, mandelic acid, phenylglyoxylic acid, phenylglycine (PHG), 4-vinylphenol (VP) and mercapturic acids (M1+M2), as well as cysteinyl adducts of serum albumin (but not those of haemoglobin) were significantly associated with exposure status (controls相似文献   

Effect of chronic fluorosis on lipid peroxidation and histology of kidney tissues in first- and second-generation rats

This experiment was designed to investigate the lipid peroxidation and histological effects of chronic fluorosis on first- and second-generation rat kidney tissues. Sixteen virgin female Wistar rats were mated with eight males (2∶1) for approx 12 h to obtain first-generation rats. Mating was confirmed by the presence of sperm in vaginal smears. Sperm in vaginal smears was observed in 10 of 16 rats (d 0). These rats were identified as pregnant and included in this experiment. Pregnant rats were divided into two experimental groups (control and fluoride-supplemented), each containing five rats. The pregnant rats in the fluoride-supplemented group were exposed to 30 mg/L sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/L NaF throughout the gestation and the lactation periods. After the lactation period, young animals (first generation [F1]) were exposed to the same amount of NaF in drinking water for 4 mo. At the end of the 4-mo experimental period, nine randomly chosen male rats (F1) were sacrificed, and the kidneys were removed for the histological and lipid peroxidation examinations. The remaining eight female rats were mated with four males (2∶1) for approx 12 h to obtain second-generation rats. Six female were identified as pregnant, and treated similarly throughout the gestation and the lactation periods. After the lactation period, the young male rats (second-generation male rats [F2]) were also treated similarly for 4 mo. At the end of the 4-mo experimental period, nine randomly chosen male rats (F2) were sacrificed, and the kidneys were removed for the histological and lipid peroxidation examinations. The rats in the control groups underwent the same procedure without NaF supplementation. It was found that the plasma fluoride and kidney TBARS levels of fluoride-supplemented F1 and F2 rats were higher than controls. Hydropic epithelial cell degenerations and moderate tubular dilatation were observed in some proximal and distal tubules. There were markedly focal mononuclear cell infiltrations and hemorrhage at some areas of the interstitium, especially at the corticomedullar junction. Mononuclear cell infiltrations were also evident in some peritubular and perivascular areas. Most of the vascular structures were congestive. Many Bowman capsules were narrowed. The severe degenerative changes in most of the shrunken glomerules and vascular congestion were also observed. It is concluded that chronic fluorosis causes a marked destruction in kidney tissues of F1 and F2 rats by causing lipid peroxidation. Department of Orthopedics, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey     

ORIGINAL ARTICLE: Evaluation of miosis,behavior and cholinesterase inhibition from low‐level,whole‐body vapor exposure to soman in African green monkeys (Chlorocebus sabeus)*

Background Relatively little is known about the effects of very low‐level exposures to nerve agents where few signs or symptoms are present. Methods African green monkeys (Chlorocebus sabeus) (n = 8) were exposed for 10 min, whole‐body, to a single concentration of soman (0.028–0.891 mg/m³). Results EC₅₀ values for miosis were determined to be 0.055 mg/m³ and 0.132 mg/m³ when defined as a 50 percent reduction in pupil area and diameter, respectively. In general, performance on a serial probe recognition task remained unchanged at lower concentrations, but responding was suppressed at the largest concentration tested. Soman produced concentration‐dependent inhibition of acetylcholinesterase activity and, to a lesser extent, butyrylcholinesterase activity. Conclusions These results characterize threshold soman exposure concentrations that produce miosis in the absence of other overt signs of toxicity and extend previous studies indicating that miosis is a valuable early indicator for the detection of soman vapor exposure.     

EFFECTS OF MICROWAVES AND ELF MAGNETIC FIELD ON THE PHAGOCYTIC ACTIVITY OF VARIOUSLY TREATED RAT MACROPHAGES

The purpose of this study was to investigate the effects of 9450-MHz microwaves and extremely low frequency magnetic fields (ELFMF) on the phagocytic activity of rat macrophages in control rats and those treated with vitamins C and E. In the microwave group, 24 albino Wistar rats were exposed to microwaves (2.65 mW/cm², specific absorption rate [SAR]: 1.80 W/kg) for 1 h/day for 21 days. Thirty-two albino Wistar rats were divided into four groups (one control, three experimental) (n = 8). The rats in the first exposure group were only exposed to microwaves for 1 h per day for 21 days. In addition to exposure with microwaves as in the first experimental group, vitamins E and C (150 mg/kg/day) were injected intraperitoneally into the rats in the second and third exposure groups, respectively. In the magnetic field exposure group, 26 albino Wistar rats were divided into two groups: the sham (n = 12) and exposed groups (n = 14). The rats in the experimental group were exposed to ELFMF (50 Hz, 0.75 mT) for 3 h/day for 3 weeks. After completing the exposure period, the rats were sacrificed under ketalar anesthesia. The viability of isolated alveolar macrophages of rats in the microwave and ELF groups was determined and compared to sham groups. The results were analyzed with the Mann–Whitney U test. In the microwave group, the phagocytic activity in the experimental groups was found to be higher than the sham groups. However, with phagocytic activity in rats treated with both microwaves and vitamins, only the vitamin C group was significant (p < 0.05). In the magnetic field group, the phagocytic activity of rats exposed to ELFMF was lower than that of the sham group, but the results were not significant (p > 0.05). Rectal temperatures of microwaveexposed groups were found to be significantly higher compared to the control group (p < 0.05).