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Biomedical subjects

D A Creasia

Publications and source records attributed to D A Creasia.

36 records · Page 2Linked to original sources
PubMed1981

Urine cytology: early diagnosis of induced carcinoma of the rat urinary bladder.

Transitional cell carcinoma of the urinary bladder was induced in F344 rats by intragastric intubation of the animals with the known bladder carcinogen N-nitroso-N-methyl-N-dodecylamine (NMDA). Urinary cytology was used to follow the development of bladder lesions. As early as 8 weeks after the beginning of NMDA exposure, small, but distinct, differences could be detected between the morphology of exfoliated transitional cells found in the urine if animals treated with NMDA and those of control animals. Atypia was noted in the cells from some of the NMDA treated animals at about 20 weeks, and after 32 weeks definitely malignant transitional cells were identified in the urine of all NMDA treated animals. When the NMDA treated animals were killed, at 55-60 weeks after the beginning of NMDA treatment, transitional cell carcinoma of the urinary bladder was confirmed in all animals. No abnormal cells were noted in urine from any of the control animals. Urine cytology is an excellent technique for early detection of experimental urinary bladder cancer, and may be especially useful in screening industrial workers exposed to suspect bladder carcinogens.

Animals↗
PubMed1977

Stimulation of DNA synthesis in the lungs of hamsters exposed intermittently to nitrogen dioxide.

Stimulation of [3H] thymidine incorporation in the lungs of hamsters exposed singly and repeatedly to 10 ppm NO2 was studied. Within 24 hr of the first exposure to NO2, the response was characterized by a marked increase in [3H] thymidine labeling in the bronchi, bronchioles, and alveolar ducts, but not in the trachea or the peripheral alveoli. If, after the first NO2 exposure, subsequent exposures were repeated daily, no further stimulation of [3H] thymidine incorporation was observed in any part of the respiratory tract. However, if the interval between the first and subsequent exposures was 2-3 days rather than 1 day, stimulation of [3H] thymidine incorporation was observed in the bronchi, bronchioles, and alveolar ducts for up to 21 NO2 exposures. A significantly greater increase in [3H] thymidine incorporation was observed when the interval between subsequent exposures was extended to 7 days. However, no repeated exposure, whether at 2-3 or 7 day intervals, was as effective as the first NO2 exposure in stimulating incorporation of [3H] thymidine.

Animals↗
PubMed1977

Effect of respiratory infection on the elution of benzo[a]pyrene from carbon particles in the respiratory tract of mice.

The effect of respiratory infection by PR8 influenza virus on the elution of bnezo[a]pyrene (BaP) from carbon particles in the respiratory tract of mice was studied. In mice, this virus produces, among other pheneomena, a proteinaceous effusion and mixed cellular exudate in the alveolar parenchyma during the acute phase of infection. If BaP-coated carbon particles are introduced into the respiratory tract during the acute stage of infection, the rate of BaP elution from the carbon particles is increased. When BaP-coated carbon particles were instilled in the respiratory tract either 1 wk before or 2 wk after the acute stage of infection, the BaP elution rate from carbon particles were similar to that in uninfected animals.

Animals↗
PubMed1976

Elution of benzo[alpha]pyrene from carbon particles in the respiratory tract of mice.

The effect of carrier particle size on the rate of dissociation of benzo[alpha]pyrene (BaP) from carrier particles deposited in the respiratory tract of mice was studied. BaP-coated carbon particles (in two size ranges, 0.5-1.0 and 15-30 mum) plus 103Ru-tagged carbon tracer particles were intratracheally instilled in mice. The clearance of carbon particles and the simultaneous rate of elimination of BaP from the respiratory tract was measured. BaP adsorbed to 15- to 30-muM carbon particles was eliminated from the lung at essentially the same rate as the carbon particles were cleared. In contrast, BaP adsorbed to 0.5- to 1.0-muM carbon particles was eliminated from the lung approximately 4 times faster than the carbon particles were cleared. The persistence of carcinogens and their rates of elution from carrier particles are discussed in relation to the pathogenesis of lung cancer in animals treated with carcinogen-carrier particle preparations.

Animals↗
PubMed1975

Carcinogenic and cocarcinogenic effects of inhaled synthetic smog and ferric oxide particles.

The carcinogenic and cocarcinogenic activity of synthetic smog, ferric oxide (Fe2O3) dust, and a mixture of the two air contaminants was determined in a long-term inhalation study with Syrian hamsters. Inhaled Fe2O3 particles definitely enhanced diethylnitrosamine tumorigenicity in the peripheral lung. Synthetic smog did not. When tested at a concentration of 40 ppm methane equivalents or 40 mg/m3, respectively, neither air pollutant by itself appeared carcinogenic. Fe2O3 caused pulmonary fibrosis and synthetic smog caused alveolar bronchiolization in many of the exposed animals.

Air Pollutants↗
PubMedDate not supplied

Respiratory tract deposition of smoke particles using a nasal bypass device.

In order to avoid nasal absorption, an intralaryngeal cannula was tested as a device for bypassing the nose in delivering smoke into the lungs of hamsters. The intralaryngeal cannula increased lung deposition of radiolabeled smoke particles twofold to threefold over that in nose-breathing controls. Stabilization of respiration (absence of avoidance reaction), rather than prevention of nasal absorption of smoke, was demonstrated to be the cannula's major mechanism of action. Although suitable for acute exposures, the device is of limited use for chronic exposures that require daily insertion of the cannula during an extended period of time.

Animals↗
PubMedDate not supplied

A tobacco smoke inhalation exposure device for rodents.

A system which utilizes a piston pump to generate cigarette smoke under standard conditions, and expose rodents to the inhalation of diluted smoke for controlled periods of time is described. Variations of the basic system have been employed to exposure groups of ten to twenty hamsters or rats, and should allow exposures of up to forty mice. The system has been in use for approximately 24 months in routine chronic exposures of rats. Data are presented to define the operating characteristics and typical dosimetry. Animal containment peculiar to this apparatus is described.

Animals↗
PubMedDate not supplied

Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide.

Nitrogen dioxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system that also exhibits tolerance. It was found that when hamsters are preexposed daily to 10 ppm NO2, they develop tolerance for normally lethal concentrations of NO2, are protected against cytological injury from 10 ppm NO2, but are not protected from the cytotoxic effects of NO2 at concentrations greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytological injury induced by weekly exposures to 10 ppm NO2, but do develop tolerance for lethal concentrations of NO2. Thus, the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.

Animals↗
PubMedDate not supplied

Pathogenesis of nitrogen dioxide-induced respiratory lesions in reference to respiratory clearance of inhaled particulates.

The pathogenesis of NO2-induced respiratory disease and the effect of NO2 on respiratory clearance of 51Cr2O3 were studied. Young adult female mice were exposed to a 51Cr2O3 aerosol, followed by a daily exposure to either 30 ppm NO2 for 2 wk or 60 ppm NO2 for 2 wk or a single exposure to 170 ppm NO2. Exposure to 30 ppm NO2 had a minimal histopathologic effect on respiratory tract tissue. Exposure to 60 ppm NO2 produced marked histopathologic effects, which were subsequently resolved. Exposure to 170 ppm NO2 produced permanent histopathologic lesions. In mice exposed to concentrations of NO2 that produced minimal histopathologic effects, respiratory clearance of 51Cr2O3 was similar to that in unexposed mice. When mice were exposed to concentrations of NO2 that produced permanent tissue damage, prolonged impairment of respiratory clearance of 51Cr2O3 was observed, despite resolution of edema produced by inhalation of NO2. At concentrations of NO2 that produced marked edema and histopathologic effects that were resolved despite repeated NO2 exposure, there was an initial marked impairment of respiratory clearance, then an accelerated rate of clearance, and finally a clearance rate similar to that of unexposed mice. The time during which accelerated clearance occurred was well correlated with the time at which the histopathologic lesions was observed to regress.

Animals↗
PubMedDate not supplied

Toxicity, tissue distribution, and excretion of benzyl chloride in the rat.

The tissue distribution and excretion of [14C]benzyl chloride was investigated in adult male and female Fischer 344/N rats after administration of a single oral dose of [14C]benzyl chloride in corn oil at 25 mg/kg, data was correlated with histopathologic and toxicity findings elicited from a 27-37-wk repeated-dose oral toxicity study of benzyl chloride. Radioactivity was detected in all tissues selected for examination. Elimination of the isotope occurred predominantly in the urine. Female rats excreted the isotope at a faster rate than the males and also maintained slightly lower tissue concentrations (with the exception of the blood and kidneys). Isotope recovery was achieved at 90% in the urine and feces of female rats at 24 h, compared with an 80% recovery rate in males. Concentrations of radioactivity were high in the gastrointestinal tract, reflecting the route of administration; however, the squamous stomach and the small intestine consistently retained higher concentrations of isotope than the glandular stomach. Results of acute toxicity and organ histopathology studies in animals dosed with benzyl chloride for 27-37 wk are compatible with the organ distribution and excretion of [14C]benzyl chloride. Histopathologic findings included severe acute and chronic gastritis, hyperkeratosis and hyperplasia of the squamous stomach, and progressive lesions of the heart ranging from proliferation of interstitial cells to acute necrosis of myocardial fibers. Both of these studies suggest that the squamous stomach is a target organ for benzyl chloride or one of its metabolites.

Animals↗
PubMedDate not supplied

Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide.

Nitrogen idoxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system which also exhibits tolerance. It was found that when hamsters are preexposured daily to 10 ppm NO2, they develop tolerance against normally lethal concentrations of NO2; are protected against further cytological injury from 10 ppmNO2; but are not protected from the cytotoxic effects of NO2 greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytotological injury induced byweekly exposures to 10 ppm NO2, but do develop tolerance against lethal concentrations of NO2. Thus the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.

Animals↗