Biomedical subjects

A G Stead

Publications and source records attributed to A G Stead.

At least 19 recordsLinked to original sources

PubMed1995

Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

BACKGROUND AND PURPOSE: Serum lipoprotein(a) [Lp(a)] levels are genetically determined and considered to be an independent risk factor for atherosclerosis. The aim of this study was to provide a complete analysis of Lp(a) serum levels, apolipoprotein(a) phenotypes, and other lipid parameters for different forms of severity of symptomatic ischemic cerebrovascular disorders as well as for different stages of carotid atherosclerosis. METHODS: Lp(a) concentration, apolipoprotein(a) phenotype, triglyceride, low-density lipoprotein, high-density lipoprotein, and total cholesterol levels of blind-coded specimens as well as degree of carotid artery stenosis were assessed in a consecutive series of patients with ischemic cerebrovascular disease. We evaluated 265 male (34%) and female (66%) patients (mean age, 51 +/- 7.4 years) with transient ischemic attack (55.8%), prolonged reversible ischemic neurological deficits (28.3%), and cerebral infarction (15.9%) as well as 288 male (30%) and female (70%) control subjects (mean age, 51 +/- 7.1 years). All subjects were white. RESULTS: Lp(a), total, and low-density lipoprotein cholesterol were statistically significantly elevated in all patients compared with control subjects. Lp(a) correlated with the severity of symptomatic cerebrovascular disease and the degree of carotid stenosis. Logistic regression analysis revealed Lp(a) as the best single marker for the presence of cerebrovascular disease (P < .001) followed by high-density lipoprotein cholesterol (P = .003) and triglycerides (P = .049). With a cutoff of 20 mg/dL of Lp(a), the odds ratio for a subject to have had ischemic stroke with elevated Lp(a) was 20.3 and 23.7 depending on the method of the Lp(a) estimation, whereas the odds ratio when the sonography score was > 0 was 15.4. The investigation of the distribution of the apo(a) phenotypes revealed that 16.73% of the control subjects had major isoforms < or = 580 kD molecular weight (B, F, S1, S2) versus 42.65% of the patients' group (P < .001). These isoforms were also present in 14.71% of all individuals with a sonography score of 0 but in 52.30% of all individuals with a sonography score > 0 (P < .001). CONCLUSIONS: This case-control study shows that an elevated Lp(a) level is the primary factor associated with the presence of ischemic cerebrovascular disease and that the increased portion of the smaller-molecular-weight apo(a) isoforms in patients and individuals with a sonography score > 0 points toward an inherited predisposition for this disease.

Adult↗

PubMed1990

Morphometric analysis of osteosclerotic bone resulting from hexachlorobenzene exposure.

Hexachlorobenzene (HCB) exposure has been shown to induce hyperparathyroidism and osteosclerosis in rats. Experiments were undertaken to investigate the effects of HCB-induced hyperparathyroidism and osteosclerosis on femur morphometry as well as femur breaking strength. Fischer 344 rats were dosed 5 d/wk for 15 wk with 0, 0.1, 1, 10, or 25 mg HCB/kg body weight. Hyperparathyroidism was produced in the two higher dose groups as reported previously (Andrews et al., 1989). Femur weight was significantly increased in the rats receiving 0.1, 1, and 25 mg HCB/kg body weight, whereas density was increased significantly at 1, 10, and 25 mg HCB/kg dose levels. Bone strength was also significantly increased at the three higher dose levels. Cross-sectional area of the midpoint of the femur was significantly increased at the 1 mg/kg HCB dose level. Cortical area and the proportion of the total area of the bone that the cortex occupied were significantly increased at the three higher dose levels. Medullary cavity area was significantly increased at the 0.1 mg/kg dose level but significantly decreased at the 2 higher dose levels of HCB. The right femur was significantly predominant to the left femur in weight, volume, and density through all dosing regimens. HCB exposure significantly altered bone morphometry and strength characteristics in the Fischer 344 rat.

Alkaline Phosphatase↗

PubMed1990

Pulmonary effects due to subchronic exposure to oil fog.

Male and in some cases female rats were exposed to an oil fog generated by flash vaporization and subsequent condensation of light-weight lubricating oil. Exposures were for 3.5 h/d, 4d/wk for 13 wk. Males were exposed at concentrations of 1.5, 0.5, 0.2 or 0.0 mg/l (1500, 500, 200, and 0 mg/m3) and a particle size of approximately 1 micron (mass median aerodynamic diameter). A number of biologic endpoints were assessed the day after the last exposure and, in some cases, after a 4 wk recovery period. Effects of 1.5 mg/l on male and female rats were compared. Diffuse accumulation of macrophages in the alveoli was observed in all oil fog exposed groups. The degree of severity was concentration dependent. Histopathologic changes were more prominent in males than in females and represented the most notable gender-related differences. Histologic effects observed one day and 4 wk post exposure were similar. Minimal histopathologic changes and minimal increase in lavage fluid protein were the only effects observed at the 0.2 mg/l exposure level. There was a significant increase in lavage fluid protein, percent lavagable polymorphonuclear leukocytes and lung wet and dry weight following exposure to both 0.5 and 1.5 mg/l. At the highest exposure concentration effects on lung weights were still evident 4 wk post exposure. Pulmonary function endpoints including total lung capacity, vital capacity, residual volume, diffusing capacity to CO, compliance, and end expiratory volume (EEV) were unaffected by oil fog exposure with the exception of EEV in males exposed at the 1.5 mg/l level. All of the changes observed following oil fog exposure were consistent with a mild inflammatory edema.

Aerosols↗

PubMed1989

Effect of ampicillin-induced alterations in murine intestinal microbiota on the survival and competition of environmentally released pseudomonads.

The environmental release of genetically altered microorganisms has prompted the investigation of their potential health effects by the employment of other-than-human models. Although direct health effects are addressed, this investigation examines primarily some potential indirect health effects associated with environmentally released microorganisms. Indirect effects examined include colonization of the gastrointestinal tract, competition with the resident microbiota, and translocation of the dosed microorganisms to other organs. Pseudomonads used in this study were isolated from a commercial product marketed for environmental PCB degradation. When mice were dosed by gavage with approximately 10(9) ampicillin-resistant pseudomonads, an increase in recovery from the intestinal tract, as compared to untreated animals, was observed 48 hr after dosing. Intestinal survival of Pseudomonas aeruginosa strain BC16 was enhanced 1000-fold and that of P. maltophilia strain BC6, 10-fold. Strains BC17 and BC18 were unaffected. Ampicillin treatment had a significant effect on the relative number of microbiota in the intestine, by selecting primarily for the facultative species. The lactose-fermenting enterobacteria, obligately anaerobic predominantly Gram-negative rods, and total aerobic and anaerobic populations were monitored in the presence and absence of the PCB-degrading pseudomonad. P. aeruginosa strain BC17 and P. maltophilia strain BC6 had a dose effect (p less than 0.05) on the total aerobic and anaerobic populations as well as the lactose-fermenting enterobacteria. These results are similar to those for the mouse isolate control, strain PAMG. P. aeruginosa strain BC18 had a dose effect (p less than 0.05) on the total anaerobic population, including the obligately anaerobic Gram-negative bacilli. No translocation of the dosed strains to the liver, spleen, or lung was observed 48 hr after dosing.

Ampicillin↗

PubMed1989

Temperature regulation following nickel intoxication in the mouse: effect of ambient temperature.

1. The purpose of this study was to examine the interaction between ambient temperature (Ta) and the effects of nickel chloride on the thermoregulatory system of the mouse. 2. Male mice of the BALB/c strain were injected with nickel chloride at dosages of 0, 0.1, 1.0, 2.5, 5.0 and 10.0 mg/kg intraperitoneally and placed in an environmental chamber set at a Ta of either 10, 20, 30 or 35 degrees C for 60 min. Colonic temperature was then measured after one hour of exposure at a given Ta. 3. The thermoregulatory effects of nickel chloride were highly dependent on Ta. Nickel chloride had no effect on body temperature at Ta's of 30 and 35 degrees C. 4. 10 mg/kg dosage of nickel chloride caused a significant reduction in colonic temperature at a Ta of 20 degrees C. At a Ta of 10 degrees C the 5 and 10 mg/kg dosages of nickel chloride caused a significant lowering of body temperature. 5. Using segmented linear regression techniques it was shown that the threshold dose of nickel chloride for causing hypothermia was 9.6 and 3.3 mg/kg at Ta's of 20 and 10 degrees C, respectively. 6. This study has shown that two stressors, low Ta and nickel chloride intoxication, when applied independently have no effect on body temperature; however, when applied simultaneously, they have a significant toxic effect on thermoregulation.

Animals↗

PubMed1989

Polychlorinated biphenyl-degrading pseudomonads: survival in mouse intestines and competition with normal flora.

Although naturally occurring and mutant organisms, historically, have been released into the environment for various purposes, health concerns associated with the release of microorganisms have recently resurfaced. Federal agencies have been given the task of reassuring society that any released organisms are not likely to produce adverse health effects. Methods, therefore, for evaluating the potential health effects due to environmental release of mutant and genetically engineered microorganisms are under investigation. A mouse model was developed that examines morbidity, mortality, and more indirect effects such as colonization potential of the intestinal tract, as well as competition with and alteration of the intestinal microbiota populations. The Pseudomonas spp. used in this study were isolated from a commercial product and used for degrading polychlorinated biphenyls. Mice were dosed individually with 10(3), 10(6), and 10(9) colony-forming units of each microorganism. At specific time intervals the intestines were removed and examined for the presence of the dosed microorganism. At the two higher doses, 10(6) and 10(9) colony-forming units, P. maltophilia strain BC6 and two P. aeruginosa strains, BC16 and BC18, were recoverable 48 h after dosing. The naturally occurring P. aeruginosa strain, PAMG, isolated from a mouse intestinal homogenate produced a similar response. Statistical analysis indicated that in some of the dosed animals, an alteration in the distribution of normal intestinal microflora occurred. Pseudomonas maltophilia strain BC6 and P. aeruginosa strains BC16 and BC17 caused a change in the obligately anaerobic predominantly gram-negative rod counts, and P. aeruginosa strain BC17 produced a dose effect on the total anaerobic count at the 10% confidence level. The total aerobic count was unaffected by the presence of the dosed pseudomonads.

Animals↗

PubMed1989

Hexachlorobenzene-induced hyperparathyroidism and osteosclerosis in rats.

Hexachlorobenzene (HCB) exposure has been shown to alter the normal concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D3 in rats and to result in osteoporosis in humans. Experiments were undertaken to investigate the effects of HCB on the homeostatic mechanism of calcium metabolism and to determine its effect on bone in rats. Fischer 344 rats were dosed 5 days/week for 5, 10, or 15 weeks with 0, 0.1, 10.0, or 25.0 mg HCB/kg body wt. Body weight was not affected by any of the exposure conditions. Liver weight was significantly elevated above control values at the two higher dose levels at all three time periods. Kidney weight and kidney-to-body weight ratio were significantly elevated at the highest dose level after 10 weeks and at the two higher dose levels after 15 weeks of exposure. Serum alkaline phosphatase was significantly decreased at the two higher dose levels after both 10 and 15 weeks of exposure. 1,25-Dihydroxyvitamin D3 was measured in the 5-week exposure group only and was significantly elevated in the three higher dose levels. After 5 and 15 weeks of HCB exposure, parathyroid hormone concentration was significantly elevated at the two higher dose levels at both time periods. Wet femur density was significantly increased at the two higher dose levels of HCB after 10 weeks of exposure and the three higher dose levels after 15 weeks of exposure. Dry femur density was also increased in the cases where wet femur density was increased. However, femur weight was not affected at any dose level. The results from this study indicate that HCB induces hyperparathyroidism in rats, as demonstrated by increased serum parathyroid hormone levels and osteosclerosis of the femur.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Effect of ethyl alcohol on thermoregulation in mice following the induction of hypothermia or hyperthermia.

This study was designed to assess the effects of ethyl alcohol (ethanol) administration on behavioral and autonomic thermoregulation in mice subjected to severe hypothermia or hyperthermia. Male mice of the BALB/c strain were injected intraperitoneally with ethanol at dosages of 0, 0.3, 1.0, or 3.0 g/kg and then placed within a hot environmental chamber to raise their body temperature to 41 degrees C or, alternatively, within a cold chamber to lower it to 28 degrees C. Once the desired hypothermic or hyperthermic state was achieved, the mice were removed from the chamber and placed in either a temperature gradient to monitor behavioral thermoregulatory responses or in an environmental chamber thermostabilized at an ambient temperature (Ta) of 28 degrees C to monitor metabolic rate. The 3.0 g/kg dosage significantly affected behavioral thermoregulatory responses of the hyperthermic mice when initially placed in the temperature gradient. The ability to increase metabolic rate following hypothermia was significantly suppressed at 3.0 g/kg. Dosages of 1.0 and 3.0 g/kg inhibited metabolic rate of hyperthermic mice. Both hypothermic and hyperthermic mice given 3.0 g/kg of ethanol had colonic temperatures significantly below normal after placement in the temperature gradient and metabolic chamber. In conclusion, relatively large dosages of ethanol impair behavioral and autonomic thermoregulation and may lower the set-point for the control of body temperature in mice.

Animals↗

PubMed1988

Evaluation of effects of ozone exposure on influenza infection in mice using several indicators of susceptibility.

Mice were exposed to 1 ppm O3, 3 hr/day, for 5 consecutive days. Separate groups of mice were infected with influenza following each of the individual exposures. A twofold increase in the incidence of mortality and a 3-day decrease in mean survival time were observed in mice infected after the second exposure. There were no effects on percentage mortality or mean survival time due to exposure to 1 ppm O3 in mice infected after the first, third, fourth, or fifth exposure. When the exposure concentration was lowered to 0.5 ppm, there were no effects on mortality in mice infected after the second exposure. Five, daily, 3-hr exposures to 1 ppm O3 had no effect on virus titers in the lungs of mice infected after either the second or fifth exposure. In contrast, wet lung weights were significantly enhanced over infected air controls in mice infected after the second O3 exposure at both 1 and 0.5 ppm but not at 0.25 ppm exposure concentrations. This effect on lung wet weight was observed in mice infected with a dose of virus which produced 7-33% mortality in controls as well as in mice infected with a sublethal dose of virus. Histopathologic changes due to sublethal influenza infection, including nonsuppurative pneumonitis and necrosis, squamous metaplasia and hyperplasia of the epithelium lining the bronchi and bronchioles, were more severe in mice infected after the second of five, 1 ppm O3 exposure than in comparable air controls. Sublethal infection caused a loss of lung volume with secondary reduction in diffusing capability and homogenity of ventilation distribution. These latter two effects were also exacerbated in mice infected after the second of five, 1 ppm O3 exposures as compared to air controls. When mice were infected after the fifth, 1 ppm O3 exposure, there was no effect due to ozone on either lung wet weight or histopathology. The data indicate that O3 has little if any effect on antiviral defense mechanisms since virus titers in the lungs were not affected by O3 exposure. However, mortality and morbidity, as indicated by lung wet weights, histopathology, and pulmonary function changes, were enhanced by O3 exposure in mice infected after the second of five exposures suggesting that symptoms due to infection can be enhanced in the absence of enhanced virus replication, possibly due to synergistic effects of O3 and virus in production of lung pathology.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Behavioral thermoregulation in the rat following the oral administration of ethanol.

To assess if ethyl alcohol (ethanol) causes a reduction in the set-point for control of body temperature, behavioral thermoregulatory responses in the Fischer rat were measured following a single oral administration of ethanol. In a preliminary study, five rats were given 3.0 g/kg ethanol dissolved in saline (20%; v/v) by gavage and placed in a longitudinal temperature gradient for 2 hr. The temperature gradient permitted the rats to behaviorally thermoregulate (i.e. select a thermal preferendum). The selected ambient temperature (Ta) in the temperature gradient was notably lower during the initial and final stages of the test period when compared to the response of rats administered similar volumes of saline. Colonic temperature upon removal from the gradient was approximately 1.0 degree C below that of the saline-treated animals. In a follow-up study, rats were placed in the temperature gradient for 1 hr for accommodation purposes. The rats were then gavaged with 0, 1.0 or 3.0 g/kg ethanol and placed back in the gradient for another 2 hr. Selected Ta was significantly reduced in the 3.0 g/kg group during the second hour post-ethanol exposure. The 1.0 g/kg dosage had little effect on selected Ta. As in the preliminary study, the colonic temperature of the rats in the follow up study given 3.0 g/kg was 1.0 degree C below that of the control at 2 hr post-injection. Because the 3.0 g/kg treated animals were significantly hypothermic and selected cooler Tas in the temperature gradient, it was concluded that ethanol exerted a lowering of the set-point for control of body temperature.

Adaptation, Physiological↗

PubMed1987

Saturation of lindane metabolism in chronically treated (YS x VY) F1 hybrid mice.

The organochlorine insecticide lindane (gamma-hexachlorocyclohexane) induces hepatomas in select strains of mice including two of three phenotypic classes of (YS X VY) F1 hybrid mice. In contrast, lindane does not induce hepatomas in rats and other strains of mice. It has been suggested that variations in the biotransformation of lindane may play a role in the different susceptibility of rodents to lindane-induced hepatomas. This study reports the effect of chronic treatment with 160 ppm dietary lindane on the comparative metabolism and disposition of this insecticide in obese yellow Avy/a, lean pseudoagouti Avy/a, and lean black a/a phenotypes of (YS X VY) F1 hybrid female mice at 17, 30, 56, and 86 wk of age. At 24 h prior to necropsy, all mice were dosed po with 18 mg lindane (containing 55 muCi [U-14C]lindane)/kg. Urine, feces, and expired air were sampled for analysis. Data indicated that metabolism of lindane and excretion of its metabolites by these mice differ significantly from those of rats that are resistant to lindane-induced hepatomas. Treatment of the mice with 160 ppm lindane in the diet appeared to saturate the elimination pathways and resulted in an increased tissue burden of the insecticide and its metabolites in the older animals. Results indicate that differences in lindane metabolism and disposition observed in the (YS X VY) F1 hybrid mice were associated with chronic lindane treatment, aging, and obesity but not with genotype.

Animals↗

PubMed1987

Pulmonary effects due to short-term exposure to oil fog.

Rats were exposed to an oil fog generated by flash vaporation and subsequent condensation of lightweight lubricating oil. Exposures were for 3.5 h/d, 4 d/wk, for 4 wk, at concentrations of 1.5, 0.5, or 0.0 mg/l and a particle size of approximately 1 micron. Samples of respiratory tissues were taken for histopathologic analyses, lavage fluid samples were collected, and pulmonary function measurements were made the day after the last exposure. An accumulation of macrophages within the alveolar lumen, an increase in lavage fluid protein content, and an increase in total cell content in lavage fluid due to an influx of polymorphonuclear leukocytes was noted in rats exposed at the 1.5-mg level. Also, for this exposure group there was an increase in lung wet and dry weight and an increase in end-expiratory volume, and pneumonitis was observed histopathologically in 4 of 10 male rats exposed. Pneumonitis was not observed among six female rats examined. Oil fog had no effect on total lung capacity, residual volume, vital capacity, lung compliance, or the distribution of ventilated air within the lung. Effects following exposure to 0.5 mg/l were limited to slight accumulation of macrophages in the alveolar lumen and an increase in the total cells in lavage fluid, which could not be attributed to an increase in any particular cell type.

Air Pollutants↗

PubMed1986

Sister chromatid exchange and chromosome aberration analyses in mice after in vivo exposure to acrylonitrile, styrene, or butadiene monoxide.

The use of polymers in plastic and rubber products has generated concern that monomers potentially active in biological systems may be eluted from these substances. We have evaluated two such monomers, acrylonitrile and styrene, for the induction of chromosome damage in mice. Butadiene monoxide, a presumed metabolite of a third important monomer, 1,3-butadiene, was also tested. These chemicals were administered as a single intraperitoneal injection; sister chromatid exchanges and chromosome aberrations were analyzed in bone marrow cells. Acrylonitrile and styrene were largely negative for these endpoints when tested at doses ranging to 60 mg/kg and 1,000 mg/kg, respectively. Butadiene monoxide, which previously has not been tested in a mammalian system, was determined to be a very effective inducer of sister chromatid exchanges and chromosome aberrations. Both endpoints showed a clear dose response and a greater than ten-fold increase over control levels at high doses. These studies represent an initial step in our efforts to evaluate genetic risk associated with exposure to common polymeric chemicals.

Acrylonitrile↗

PubMed1986

Nitrogen dioxide exposure and lung antioxidants in ascorbic acid-deficient guinea pigs.

We have previously found that ascorbic acid (AA) deficiency in guinea pigs enhances the pulmonary toxicity of nitrogen dioxide (NO2). The present study showed that exposure to NO2 (4.8 ppm, 3 hr) significantly increased lung lavage fluid protein (a sensitive indicator of pulmonary edema) only in guinea pigs fed rabbit chow (a diet not supplemented with vitamin C) for at least 7 days, at which time lung AA was about 50% of normal. The rabbit chow diet did not cause reduced body weight as did commercial synthetic scorbutic diets, even when they were supplemented with AA. After 14 days of feeding rabbit chow, lung AA was reduced to 15% of control. At this time, alpha-tocopherol (AT) in the same lungs was reduced to 85% of control, and lung nonprotein sulfhydryls (NPSH) were increased to 114% of control. Exposure of the guinea pigs to NO2 (4.5 ppm, 16 hr) increased wet lung weight and further altered the antioxidants in deficient (but not normally fed) animals in the following manner: NPSH content was increased to 130% of control, AT was decreased to 74% of control, and AA was increased from 15 to 50% of control. These findings suggest that depletion of AA in guinea pigs removes an important defense against NO2. The lung appears to be able to partially compensate for the dietary lack of antioxidant by accumulating AA from other tissues and by increasing NPSH concentrations. However, sufficient exposure to NO2 leads to oxidation of AT and pulmonary edema. Conditions in which NO2 produced edema were accompanied by only a slight consumption of AT, and no detectable oxidation of lung AA or NPSH.

Animal Feed↗

PubMed1986

Species comparison of acute inhalation toxicity of ozone and phosgene.

A comparison of the concentration-response effects of inhaled ozone (O3) and phosgene (COCl2) in different species of laboratory animals was made in order to better understand the influence of the choice of species in inhalation toxicity studies. The effect of 4-h exposures to ozone at concentrations of 0.2, 0.5, 1.0, and 2.0 ppm, and to COCl2 and 0.1, 0.2, 0.5, and 1.0 ppm was determined in rabbits, guinea pigs, rats, hamsters, and mice. Lavage fluid protein (LFP) accumulation 18-20 h after exposure was used as the indicator of O3- and COCl2-induced pulmonary edema. All species had similar basal levels of LFP (250-350 mg/ml) when a volume of saline that approximated the total lung capacity was used to lavage the collapsed lungs. Ozone effects were most marked in guinea pigs, which showed significant effects at 0.2 ppm and above. Mice, hamsters, and rats showed effects at 1.0 ppm O3 and above, while rabbits responded only at 2.0 ppm O3. Phosgene similarly affected mice, hamsters, and rats at 0.2 ppm and above, while guinea pigs and rabbits were affected at 0.5 ppm and above. Percent recovery of lavage fluid varied significantly between species, guinea pigs having lower recovery than other species with both gases. Lavage fluid recovery was lower following exposure to higher levels of O3 but not COCl2. Results of this study indicate that significant species differences are seen in the response to low levels of O3 and COCl2. These differences do not appear to be related in a simple manner to body weight.

Animals↗

PubMed1986

Temperature regulation in the mouse and hamster exposed to microwaves in hot environments.

Colonic temperature was measured in naive BALB/c mice and golden hamsters immediately following 90-min exposures to 2450-MHz radiofrequency (RF) radiation at an ambient temperature (Ta) of 32.2 or 35 degrees C (dry air). Exposures were performed in a temperature-controlled waveguide which permitted continuous monitoring of the specific absorption rate (SAR) of RF energy. At a Ta of 32.2 degrees C the threshold SAR for elevating colonic temperature and the SAR resulting in a 0.5 degree C elevation in colonic temperature were, respectively, 4.3 and 6.5 W/kg for the mouse and 0.68 and 1.1 W/kg for the hamster. At a Ta of 35 degrees C these values were 0.12 and 0.63 W/kg for the mouse and 0.46 and 0.8 W/kg for the hamster. The SARs required to elevate body temperature in the mouse and hamster at these relatively warm Ta's are considerably lower than those required at cooler Ta's of 20 to 30 degrees C. Overall, the hamster became hyperthermic at lower SARs than the mouse. Ta's of 35 degrees C and greater are frequently encountered during heat waves in the summer months. Under such stressful environmental conditions where heat loss is impaired, absorption of RF radiation at relatively low SARs may lead to significant hyperthermia which would otherwise be readily dissipated at lower Ta's.

Animals↗

PubMed1986

Tumorigenesis and genotoxicity of ethyl carbamate and vinyl carbamate in rodent cells.

Vinyl carbamate (VC) is a suspect metabolic intermediate in ethyl carbamate (EC) carcinogenesis. In the present studies, EC and VC were evaluated for their relative abilities to induce adenomas and sister chromatid exchanges (SCEs) in lung cells of A/J, C3HeB/FeJ, and C57BL/6J strain mice. For both end points, animals were administered a single i.p. injection of the test chemical. Percentage of mice with adenomas and number of adenomas per mouse were compared among the three strains 24 weeks following exposure to EC or VC. Although the relative order of strain sensitivity was the same for both chemicals: A/J greater than C57BL/6J greater than C3HeB/FeJ, VC was much more potent than EC. For SCE analysis of primary lung cells cultured from treated animals, EC and VC showed potency differences similar to those observed for tumorigenesis. All three mouse strains revealed significant dose-dependent increases in SCE frequency. However, there was no strain specificity for this effect. SCE persistence over time was also compared in treated A/J and C57BL/6J mice. Although EC- and VC-induced SCE frequencies declined over a 2-week observation period, again, there was no strain specificity for this effect. VC was also tested for enhancement of SA7 virus transformation of Syrian hamster embryo cells. Significant concentration-dependent increases in cell transformation frequency were observed.

Animals↗

PubMed1986

Effect of nickel and cadmium chloride on autonomic and behavioral thermoregulation in mice.

Male BALB/c mice were injected intraperitoneally (i.p.) with nickel chloride (0, 5, 10, and 15 mg/kg) or cadmium chloride (0, 2, 4, and 6 mg/kg) and preferred ambient temperature (Ta) and activity were measured. Both metals caused marked reductions in preferred Ta and activity within 30 min postinjection. Preferred Ta and activity were depressed for up to 90 min. In a second experiment, body temperature was measured 60 min following the injection of nickel or cadmium chloride at a Ta of 20, 30, or 35 degrees C. Nickel and cadmium caused large reductions in body temperature when injected at a Ta of 20 and 30 degrees C but produced either no effect or only a slight elevation in body temperature at a Ta of 35 degrees C. In a third experiment, metabolic rate was measured continuously for 60 min following an i.p. injection of a relatively large dose of nickel (15 mg/kg) or cadmium chloride (6 mg/kg) at a Ta of 20, 30, and 35 degrees C. Both metals caused significant reductions in metabolic rate at TaS of 20 and 30 degrees C. At a Ta of 35 degrees C, cadmium caused a slight inhibition in metabolic rate while nickel had insignificant effects. These data indicate that nickel and cadmium chloride injected i.p. produce hypothermia by reducing metabolic rate and the preferred Ta.

Animals↗