Donald A. Creasia

United States Army Medical Research Institute of Infectious Diseases

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Paul Nettesheim

Centre for Human Drug Research

J. D. Thurman

Corteva (United States)

David L. Bunner

United States Army Medical Research Institute of Infectious Diseases

Ronald W. Trotter

National Center for Toxicological Research

S M Naseem

University of Engineering and Technology Lahore

Harry B. Hines

Queensland Department of Environment and Science

Walden E. Dalbey

ExxonMobil (United States)

J M Ward

Frederick National Laboratory for Cancer Research

Joseph R. Beaman

Smithsonian Environmental Research Center

Winifred G. Palmer

U.S. Army Center for Health Promotion and Preventive Medicine

Cooperative Institutions

United States Army Medical Research Institute of Infectious Diseases

Oak Ridge National Laboratory

National Institutes of Health

United States Department of the Army

National Cancer Institute

Cancer Research Center

Frederick National Laboratory for Cancer Research

Harvard University

Oak Ridge Associated Universities

University of Maryland, Baltimore

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Acute Inhalation Toxicity of T-2 Mycotoxin in Mice

Toxicological Sciences (1987)

Donald A. Creasia J. D. Thurman L. J. Jones Mark Nealley Craig York

Acute Inhalation Toxicity of T-2 Mycotoxin in Mice. Creasia, D. A., THURMAN, J. D., JONES, L. J., III, NEALLEY, M. L., YORK, C. G., WANNEMACHER, R. W., Jr., and BUNNER, D. L. (1987). Fundam. Appl. Toxicol. 8, 230–235. Experiments were conducted to study the acute inhalation toxicity of T-2 mycotoxin in both young adult and mature mice. For a 10-min aerosol exposure, the 24-hr LC50 of T-2 mycotoxin in young adult mice was 0.08 ± 0.04 mg T-2/liter air and that for mature mice was 0.325 ± 0.1 mg T-2/liter air. Deaths among mice exposed to the higher aerosol concentrations used in this study (i.e., 1.5 to 2.4 mg T-2/liter air) occurred in less than 5 hr. General clinical symptoms in these animals immediately postexposure were tremors, lethargy, stilted gait, and, in some animals, prostration. In experiments separate from the concentration-response studies, total deposition of T-2 aerosol and selective retention of T-2 in the respiratory tract and nasal turbinates were determined analytically from 3H-labeled T-2. When total deposition of T-2 was quantitated, there was excellent agreement between that amount of T-2 deposited and that amount of T-2 predicted from calculations based on aerosol size and animal minute volume. Based on the aerosol deposition data, the LD50 values of T-2 mycotoxins was 0.24 mg/kg for young adult mice and 0.94 mg/kg for mature mice. For mice, inhalation of T-2 mycotoxin is at least 10 times more toxic than systemic administration (LD50 ∼ 4.5 mg/kg) and at least 20 times more toxic than dermal administration (LD50 > 10 mg/kg).

Inhalation exposure

Liter

Respiratory tract

Lethargy

10.1093/toxsci/8.2.230

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Citations (8)

Comparative binding and toxicity of saxitoxin and saxitoxinol in mice and in cultured cells

IUBMB Life (1997)

Syed M. Naseem Donald A. Creasia

The binding characteristics of saxitoxin (STX), a known voltage-gated sodium channel blocker, and its analog saxitoxinol (STXOL), were studied in neuroblastoma, peritoneal macrophage, hepatocytes and PC-12 cell lines. 3H-STXOL bound to the cell-surface sites which appear to be the same as those occupied by 3H-STX and which can, therefore, be identified as STX receptors. The relative agreement of respective Kd obtained by saturation, competition, association and dissociation kinetics for STX and STXOL suggest the absence of any artifact in binding measurements. Unlike STX, STXOL was non-toxic to mice by intratracheal instillation. The major advantage of using 3H-STXOL is that the tritium label is not exchangeable. Data from this study suggest that 3H-STXOL can be used to identify STX receptors at 37 degrees C.

Saxitoxin

10.1080/15216549700201391

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Citations (1)

Carcinogenesis (1983)

J M Ward James Mahmud Rice Donald A. Creasia Peter Lynch Charles W. Riggs

Journal Article Dissimilar patterns of promotion by di(2-ethylhexyl)phthalate and phenobarbital of hepatocellular neoplasia initiated by diethylnitrosamine in B6C3F1 mice Get access J.M. Ward, J.M. Ward Laboratory of Comparative Carcinogenesis, Division of Cancer Cause and Prevention, and Frederick Cancer Research Facility, National Cancer InstituteFrederick, MD 21701, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar J.M. Rice, J.M. Rice Laboratory of Comparative Carcinogenesis, Division of Cancer Cause and Prevention, and Frederick Cancer Research Facility, National Cancer InstituteFrederick, MD 21701, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar D. Creasia, D. Creasia Laboratory of Comparative Carcinogenesis, Division of Cancer Cause and Prevention, and Frederick Cancer Research Facility, National Cancer InstituteFrederick, MD 21701, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar P. Lynch, P. Lynch Laboratory of Comparative Carcinogenesis, Division of Cancer Cause and Prevention, and Frederick Cancer Research Facility, National Cancer InstituteFrederick, MD 21701, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar C. Riggs C. Riggs Laboratory of Comparative Carcinogenesis, Division of Cancer Cause and Prevention, and Frederick Cancer Research Facility, National Cancer InstituteFrederick, MD 21701, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Carcinogenesis, Volume 4, Issue 8, August 1983, Pages 1021–1029, https://doi.org/10.1093/carcin/4.8.1021 Published: 01 August 1983 Article history Received: 21 March 1983 Accepted: 12 May 1983 Published: 01 August 1983

Phenobarbital

Weanling

Hepatocellular adenoma

Tumor promotion

10.1093/carcin/4.8.1021

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Citations (143)

Sequential changes in phospholipid composition and synthesis in lungs exposed to nitrogen dioxide.

PubMed (1978)

Merle L. Blank Walden E. Dalbey Paul Nettesheim Janet E. Price Donald A. Creasia

Studies were performed to investigate the time course of biochemical and histologic changes in the lungs of rats after exposure to various concentrations of nitrogen dioxide. Special attention was given to identify lipid classes and the molecular species preferentially affected. Increased incorporation of thymidine, labeled with tritium, into deoxyribonucleic acid was first detected 12 hours after a 5-hour exposure to 40 ppm of nitrogen dioxide and reached a peak after 24 to 36 hours. The first histologic signs of a hyperplastic response in the alveolar ducts and alveoli became recognizable at 24 hours. In contrast, increased incorporation of palmitic acid, labeled with carbon-14, into phosphatidylcholine and the accumulation of this lipid class in the lungs could be detected as early as 6 hours after exposure to nitrogen dioxide. Lung wet weights and lung protein were also increased at this time. These findings suggest that the increase in phosphatidylcholine in the lungs exposed to nitrogen dioxide occu...

Nitrogen dioxide

10.1164/arrd.1978.117.2.273

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Citations (32)

Acute Inhalation Toxicity of T-2 Mycotoxin in Mice and Guinea Pigs

Donald A. Creasia J. D. Thurman Robert W. Wannemacher David L. Bunner

Abstract : In this study a concentration-response was determined for rats and guinea pigs systematically exposed to an aerosol of T-2 toxin. The LC50 for a 10 min exposure to T-2 toxin aerosol was 0.020 mg T-2/liter air for rats and 0.21 mg T-2/liter air for guinea pigs. Data from total T-2 deposition in rats and guinea pigs exposed to their respective LC50 aerosol concentration gave an LD50 of 0.046 mg T-2/kg body weight for the rat and 0.50 mg T-2/kg body weight for the guinea pig. These data show that inhaled T-2 toxin is at least 10 times more toxic to the rat (0.046 mg T-2/kg body weight inhaled vs 1.0 mg T-2/kg body weight systemic) and twice as toxic to the guinea pig (0.5 mg T-2/kg body weight inhaled vs. 1-2 mg T-2 kg body weight systemic) than systemically administered T-2 toxin. Guinea pigs exposed to T-2 aerosols with varied times and aerosol concentration showed that when given the same received dose over a shorter interval of time, T-2 was more toxic, Histopathology of major organs in both the rat and guinea pig after respiratory exposure to T-2 toxin was similar to that after systemic administration of T-2 toxin. Histopathology of the respiratory tract after T-2 aerosol exposure was minimal and could not account for the increased toxicity of inhaled T-2 toxin. Keywords: Phytotoxins.

Histopathology

Respiratory tract

Source

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Citations (0)

Pathogenesis of nitrogen dioxide‐induced respiratory lesions in reference to respiratory clearance of inhaled participates

Journal of Toxicology and Environmental Health (1981)

Donald A. Creasia

The pathogenesis of NO 2 ‐induced respiratory disease and the effect of NO 2 on respiratory clearance of s1Cr 2 O i were studied. Young adult female mice were exposed to a 51Cr 2 O 3 aerosol, followed by a daily exposure to either 30 ppm NO 2 for 2 wk or 60 ppm NO 2 for 2 wk or a single exposure to 170 ppm NO 2 . Exposure to 30 ppm NO 2 had a minimal histopathologic effect on respiratory tract tissue. Exposure to 60 ppm NO 2 produced marked histopathologic effects, which were subsequently resolved. Exposure to 170 ppm NO 2 produced permanent histopathologic lesions. In mice exposed to concentrations of NO 2 that produced minimal histopathologic effects, respiratory clearance of 51 Cr 2 O 3 was similar to that in unexposed mice. When mice were exposed to concentrations of NO 2 that produced permanent tissue damage, prolonged impairment of respiratory clearance of 51 Cr 2 O 3 was observed, despite resolution of edema produced by inhalation of NO 2 . At concentrations of NO 2 that produced marked edema and histopathologic effects that were resolved despite repeated N0 2 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 lesion was observed to regress.

Respiratory tract

Pathogenesis

Clearance rate

Inhalation exposure

Respiratory Rate

Histopathology

10.1080/15287398109530121

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Citations (10)

Acute inhalation toxicity of T-2 mycotoxin in mice*1

Fundamental and Applied Toxicology (1987)

Donald A. Creasia

Liter

Inhalation exposure

Lethargy

Respiratory tract

10.1016/0272-0590(87)90121-7

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Citations (79)

Enhancement of Two-Stage Skin Carcinogenesis by Exposure of Distant Skin to UV Radiation<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref><xref ref-type="fn" rid="FN4">4</xref>

JNCI Journal of the National Cancer Institute (1985)

Paul T. Strickland Donald A. Creasia Margaret L. Kripke

Exposure of C3H/HeN mice to UV 280-320 nm (UVB) radiation induces a systemic, immunologic alteration that interferes with the rejection of highly antigenic UVB radiation-induced skin cancers. The effect of this systemic alteration, induced by ventral UVB irradiation of mice, was tested on the induction of dorsal skin tumors resulting from initiation with UVB radiation and promotion with 12-O-tetradecanoylphorbol 13-acetate (TPA). The systemic effect of UVB radiation markedly potentiated carcinogenesis at the distant site. More important, mice treated with TPA alone on the dorsal skin developed a significant number of dorsal tumors if the mice also had been exposed ventrally to UVB radiation. Treatment of dorsal skin with UVB radiation alone did not result in the development of cancers, regardless of whether the mice received ventral irradiation. These results suggest that the systemic effect of UVB radiation is exerted during the promotion phase of two-stage carcinogenesis. Furthermore, they imply that a systemic effect of UVB radiation interferes with a natural host control mechanism that ordinarily holds skin cancers in check.

10.1093/jnci/74.5.1129

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Citations (43)

Respiratory response of guinea pigs to low levels of sulfuric acid

Environmental Research (1978)

Mary O. Amdur Marc Dubriel Donald A. Creasia

10.1016/0013-9351(78)90122-6

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Citations (63)

A Sequential Study of Methapyrilene Hydrochloride-Induced Liver Carcinogenesis in Male F344 Rats2

JNCI Journal of the National Cancer Institute (1984)

Masahiro Ohshima J M Ward L M Brennan Donald A. Creasia

Methapyrilene hydrochloride [2-((2-(dimethylamino)-ethyl)-2-thenylamino)pyridine monohydrochloride (CAS: 135-23-9)]-induced hepatocarcinogenesis was studied in male F344/NCr rats by sequential histologic, histochemical, and biologic methods. Methapyrilene hydrochloride was administered in the feed to rats at a concentration of 1,000 ppm for periods up to 89 weeks. Groups of rats were killed after 5, 10, 15, 29, 40, or 73 weeks of ingesting the carcinogen. Another group was allowed to live out their life-span. Hepatocellular eosinophilic foci and adenomas were seen after 10 and 15 weeks, respectively. Basophilic foci and adenomas were found after 29 and 40 weeks, respectively. Hepatocellular carcinomas developed in 5 of 10 rats at week 40, in 3 of 5 rats at week 73, and in 19 of 19 rats that lived out their life-span. Carcinomas arose within adenomas or as small in situ carcinomas. The histologic types included trabecular, adenocarcinoma, mixed, and solid poorly differentiated hepatocellular carcinomas. Eleven of the mixed and solid poorly differentiated carcinomas metastasized to the lung. Solid poorly differentiated heptocellular carcinomas grew upon transplantation to the mammary fat pad of weanling F344 rats. Cholangiocarcinomas were found in 7 of 19 rats only in the life-span group. Mucous cholangiofibrosis was seen in all rats after 15 weeks. With the use of Regaud's mitochondrial stain, an increased cellular density of mitochondria was seen in some hepatocytes of peripheral and central lobular areas and in some hepatocellular carcinoma cells, but not in cells in many of the adenomas and foci. Cellular a-fetoprotein was found by immunoperoxidase staining in portions of hepatocellular carcinomas, but not in foci, adenomas, and nonneoplastic areas. The majority of hepatocytes in foci, adenomas, and hepatocellular carcinomas contained γ-glutamyl transpeptidase. The findings suggest that multiple pathways may be followed in the development of methyapyrilene-induced liver cancer that are similar to those found in rats exposed to many other hepatic carcinogens.

Basophilic

Weanling

10.1093/jnci/72.3.759

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Citations (28)