A hamster-associated epizootic of lymphocytic choriomeningitis (LCM) virus infection in medical center personnel at the University of Rochester in 1973 necessitated prompt termination of the Syrain hamster colony. Necropsies were performed on 130 hamsters, blood speciments were obtained from 60 for serotest, and viral isolation procedures were done on 47. Active virus infection, as shown by virus isolation, was associated with the presence of lymphoreticular infiltrate in liver and kidney. Intraabdominal lymphoma was seen only in groups of hamsters from which LCM virus was isolated, but LCM virus was not isolated from many of the hamsters with lymphoma. Although frequency of intraabdominal lymphoma could be markedly increased in LCM-positive hamsters treated with 7,12-dimethylbenz(a)anthracene, lymphoma was not induced in LCM-negative hamsters with this carcinogen.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1976

Chondroblastic osteosarcoma in the jejunum of a dog.

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Animals↗

PubMed1976

Food intake, body weight, and brain histopathology in mice following chronic methylmercury treatment.

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Animals↗

PubMed1975

Alkylmercurial encephalopathy in the monkey (Saimiri sciureus and Macaca arctoides): a histopathologic and autoradiographic study.

Histopathologic and autoradiographic studies were performed on monkeys of the genera Saimiri and Macaca after acute and chronic oral exposure to several dosage regimens of methylmercuric chloride (MeHg). Neuropathologic changes were primarily cortical, although subcortical lesions also were observed. Autoradiographic localization of 203-Hg was greatest within glial cells (particularly Nissl-pump astrocytes, subependymal glia and Bergmann's glia) and mast cells. High levels of label within normal appearing large neurons (particularly those within Gasserian and dorsal root ganglia) indicate a lower susceptibility of these neurons to the toxic effects of MeHg. Blood and brain levels of mercury correlated well with the degree of neuropathologic change, but individual variations in susceptibility to intoxication also existed.

Animals↗

PubMed1975

Laboratory studies of a lymphocytic choriomeningitis virus outbreak in man and laboratory animals.

Investigation of an outbreak of prolonged febrile illness in medical center personnel at the University of Rochester School of Medicine and Dentistry revealed lymphocytic choriomeningitis (LCM) virus to be the causative agent. Syrian or golden hamsters (Mesocricetus auratus) were found to be the only animals involved in maintaining the virus and were the source of human infections. Isolations of LCM virus were made from autopsy specimens of 13 of 46 (28%) golden hamsters. Virus isolations were made from 22 of 28 (79%) frozen specimens of 11 tumor lines transplanted repeatedly in golden hamster cheek pouches. No virus isolations were made from 86 autopsied laboratory mice, laboratory rats, Chinese hamsters (Cricetulus griseus), or laboratory rabbits or from 10 tumor cell lines transplanted in laboratory mice. Complement-fixation testing of 301 animal sera from the vivarium also revealed involvement primarily of golden hamsters. The probable source of virus introduction into the Rochester facilities was found to be two LCM-contaminated tumor lines sent from a biological supplier to Rochester in 1969.

Animals↗

PubMedDate not supplied

Acute and subchronic toxicity of ethylenediamine in laboratory animals.

As part of a comprehensive toxicology program on ethylenediamine (EDA), acute, short-term repeated and subchronic toxicity studies were conducted. Ethylenediamine dihydrochloride (EDA X 2HCl) was used in these studies. EDA X 2HCl was slightly to moderately toxic to laboratory rats, mice or rabbits in the following acute tests: Peroral intubation, percutaneous administration, primary skin irritation and eye injury. Following dietary inclusion of EDA X 2HCl for 7 days at up to 2.70 g/kg/day to Fischer 344 rats or B6C3F1 mice, body weight gain and some organ weights of the animals were depressed in both sexes at the highest dose level. When Fischer 344 rats were fed EDA X 2HCl at 0, 0.05, 0.25, 1.00 g/kg/day for 3 months, marked decreases in body weight gain were observed in both sexes at the highest dose level. Other dose-related effects observed in either or both sexes primarily at the highest dose level, and for some at the intermediate dose level, included organ weight changes and alterations in some clinical chemistry, hematology and urinalysis parameters. No deaths occurred during the exposure period, nor were there any significant gross lesions in any of the animals. Histologic findings indicate a dose-related increase in hepatocellular pleomorphism and mild hepatocellular degeneration.

Animals↗

PubMedDate not supplied

Practical aspects of neuropathology: a technical guide for working with the nervous system.

Toxicologic pathologists are evaluating tissues from the central and peripheral nervous systems with increasing frequency. This change is being driven by recently established regulatory guidelines and intense interest in developing pharmaceutical compounds to treat various nervous system disorders. However, morphologic evaluation of the nervous system by light or electron microscopy requires special understanding and effort. Here, we review the general concepts of fixation for the nervous system, explain perfusion procedures for optimal preservation, and provide information on handling tissues to avoid artifacts. In general, fixation with aldehydes is recommended for nervous tissue (a combination of paraformaldehyde and glutaraldehyde is preferred). Electron microscopic studies require fixatives of the highest purity possible, typically paraformaldehyde prepared fresh from powder mixed with high-grade glutaraldehyde. The final osmolality of the solution should be slightly hypertonic, in the range of 400-600 mOsmol. Slight hypertonicity is very important and will facilitate maintenance of vascular distention during whole-body perfusion, which is the best method for producing high-quality tissue preparations. Special effort is necessary for handling nervous tissue in a way that minimizes artifacts because chemical fixation is not completed immediately following the perfusion. These technical details should help toxicologic pathologists in their efforts to work with the nervous system, thereby increasing their effectiveness in supporting safety characterization of new test materials undergoing toxicologic assessments.

Animals↗

PubMedDate not supplied

Histopathology of nasal olfactory mucosa from selected inhalation toxicity studies conducted with volatile chemicals.

In recent years, histopathologic changes have been reported in the olfactory mucosa of rodents exposed, by inhalation, to a variety of volatile chemicals. In order to better characterize these lesions, a panel of experienced pathologists reviewed microscopic lesions of the olfactory epithelium of rats reported in 10 inhalation studies conducted with 8 different chemicals. The objectives were to determine if the olfactory epithelial lesions are morphologically similar or different for the chemicals of interest, to develop and recommend appropriate diagnostic criteria and nomenclature to characterize the morphology of these olfactory lesions, and to provide specific criteria for judging the degree of severity of the olfactory changes in these studies. The results indicated that the distribution and nature of the lesions were similar in all the examined studies in which olfactory changes were observed. Recommended standardized nomenclature and diagnostic criteria and a uniform method for scoring lesion severity based on the extent of distribution and severity of tissue damage are presented.

Acetates↗

PubMedDate not supplied

An evaluation of the developmental toxicity of 2,4-pentanedione in the Fischer 344 rat by vapour exposure.

The developmental toxicity of 2,4-Pentanedione (2,4-PD; CAS No. 123-54-6), a widely used industrial chemical, was investigated by vapour exposure, because of its widespread use, and potential for human exposure. Timed-pregnant Fischer 344 rats were exposed on gestational days (gd) 6 to 15 inclusive to analytically measured concentrations (as mean +/- SD) of 53 +/- 1.6, 202 +/- 4.7 and 398 +/- 5.7 ppm 2,4-PD vapour. At sacrifice (gd 21) foetuses were examined for external, visceral and skeletal variations and malformations. There was no maternal mortality, and body weight was reduced only at 398 ppm. Histological examination of maternal brains from the 398 ppm group showed no abnormalities. No treatment-related effects were seen on number of corpora lutea; total, nonviable or viable implants per litter; pre-or post-implantation losses; or foetal sex ratio. Reduced foetal body weight per litter was seen at 398 ppm (males and females and all foetuses) and 202 ppm (males and all foetuses). There was no concentration-related, or statistically significant, increase in the incidence of individual malformations, malformations by category (external, visceral or skeletal), or total malformations. Partial foetal atelectasis was increased at 398 ppm, and the increased incidence of 17 skeletal variants (out of 79 observed) indicated a consistent pattern of foetotoxicity at 398 ppm. In summary, at 398 ppm there was maternal toxicity (reduced body weight) and foetotoxicity (reduced body weight and ossification) and at 202 ppm there was foetotoxicity (reduced body weight). Embryotoxicity or teratogenicity were not seen at any concentration. The no-observable-effects concentration was 53 ppm for both maternal and developmental toxicity.

Administration, Inhalation↗