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Biomedical subjects

W R Richter

Publications and source records attributed to W R Richter.

At least 19 recordsLinked to original sources
PubMed2005

Decontamination assessment of Bacillus anthracis, Bacillus subtilis, and Geobacillus stearothermophilus spores on indoor surfaces using a hydrogen peroxide gas generator.

AIMS: To evaluate the decontamination of Bacillus anthracis, Bacillus subtilis, and Geobacillus stearothermophilus spores on indoor surface materials using hydrogen peroxide gas. METHODS AND RESULTS: Bacillus anthracis, B. subtilis, and G. stearothermophilus spores were dried on seven types of indoor surfaces and exposed to > or =1000 ppm hydrogen peroxide gas for 20 min. Hydrogen peroxide exposure significantly decreased viable B. anthracis, B. subtilis, and G. stearothermophilus spores on all test materials except G. stearothermophilus on industrial carpet. Significant differences were observed when comparing the reduction in viable spores of B. anthracis with both surrogates. The effectiveness of gaseous hydrogen peroxide on the growth of biological indicators and spore strips was evaluated in parallel as a qualitative assessment of decontamination. At 1 and 7 days postexposure, decontaminated biological indicators and spore strips exhibited no growth, while the nondecontaminated samples displayed growth. CONCLUSIONS: Significant differences in decontamination efficacy of hydrogen peroxide gas on porous and nonporous surfaces were observed when comparing the mean log reduction in B. anthracis spores with B. subtilis and G. stearothermophilus spores. SIGNIFICANCE AND IMPACT OF THE STUDY: These results provide comparative information for the decontamination of B. anthracis spores with surrogates on indoor surfaces using hydrogen peroxide gas.

Bacillaceae↗
PubMed1998

A dietary oncogenicity study of tributyl phosphate in the CD-1 mouse.

Tri-n-butyl phosphate (TBP), an industrial chemical, was administered in the diet at concentrations of 0, 150, 1000 or 3500 ppm to groups of 50 male and 50 female CD-1 mice for 18 months. Survival, clinical signs and hematology parameters were unaffected by treatment at any concentration. Initial weight losses and significant decreases in body weight gain occurred in males and females receiving the high dose (3500 ppm) of TBP in diet. A significant dose-related increase in absolute and relative liver weights was seen in male and female mice which received the two highest dietary concentrations of TBP (1000 and 3500 ppm). The incidence of hepatocellular adenomas was significantly increased in male mice treated with 3500 ppm TBP in diet. No other tumors were associated with TBP administration in this study. The NOEL for chronic toxicity was 150 ppm, or 28.9 mg/kg/day for females and 24.1 mg/kg/day for males. Although rats treated chronically with TBP have exhibited urinary bladder hyperplasia and urinary bladder papillomas and transitional cell carcinomas, no urinary bladder alterations attributed to TBP administration occurred in this study.

Adenoma, Liver Cell↗
PubMed1998

A dietary toxicity/oncogenicity study of tributyl phosphate in the rat.

Tri-n-butyl phosphate (TBP, CAS No. 126-73-8), an industrial chemical, was administered in the diet at concentrations of 0, 200, 700 and 3000 ppm to groups of 50 male and 50 female Sprague-Dawley rats for 2 years. Body weights and food consumption were measured weekly for the first 13 weeks and monthly thereafter. Hematology was performed at 12, 18 and 24 months; urinalyses were performed at 3 weeks and 3, 6, 12 and 18 months. All surviving animals were euthanized after 24 months of treatment. Macroscopic postmortem examinations were performed on all animals; complete histopathological evaluation was performed on control and high dose animals; target organs were examined in all dose groups. Significant decreases in body weight gain occurred in males and females receiving the 3000 ppm concentration and a slight decrease in weight gain occurred in females receiving the 700 ppm concentration. The only clinical sign attributed to TBP was an increased incidence of red discoloration of the urine in some high-dose males. Survival, hematology and urinalysis parameters were unaffected by treatment at any concentration. A dose-related increase in the incidence and severity of urinary bladder hyperplasia and the incidence of urinary bladder papillomas was evident in male and female rats receiving the 700 and 3000 ppm concentrations. Transitional cell carcinomas were present in six of 49 males and two of 50 females and a squamous cell carcinoma was present in one of 49 males in the group which received 3000 ppm. The oncogenic effects showed a clear threshold of 700 ppm in the diet. The NOEL (no observable effect level) for chronic toxicity was 200 ppm. Mean intake of TBP was 9 and 12 mg/kg/day for males and females, respectively, receiving 200 ppm; 33 and 42 mg/kg/day for males and females, respectively, receiving 700 ppm, and 143 and 182 mg/kg/day for males and females, respectively, receiving 3000 ppm. TBP was negative in genotoxicity tests, suggesting that the tumors are induced by nongenotoxic mechanisms.

Administration, Oral↗
PubMed1996

Thyroid function and thyroid tumors in toxaphene-treated rats.

Historically, a direct and irreversible genotoxic reaction of a xenobiotic with DNA has been considered to be a universal and obligatory initiating event in the etiology of neoplasia, and it was assumed therefore that (1) there was no threshold other than zero exposure for cancer initiation, and (2) like radiation, exposure was additive over a lifetime. Human exposure to xenobiotics causing neoplasia in laboratory rodents has been regulated in many countries on that basis. In the last decade evidence has accumulated indicating that some neoplasia in laboratory rodents may not be caused by a direct and irreversible interaction of xenobiotics with DNA. In addition, it has been found that some neoplasia caused in laboratory rodents by xenobiotics may not be relevant for biochemical/physiological reasons. This has raised the question whether human exposure to these xenobiotics should be regulated by the no-threshold philosophy used for direct-acting genotoxic xenobiotics or whether they can be regulated by the threshold philosophy used for classical xenobiotic-induced toxic effects. In a bioassay carried out by the National Cancer Institute and published in 1979, toxaphene was found to cause an increase in the occurrence of two spontaneously occurring tumors in laboratory rodents that since have been found to have both genotoxic and nongenotoxic etiologies in laboratory rodents. Experiments described in this paper are part of a program to help elucidate whether the increased incidence of these two neoplasms in laboratory rodents could have had a nongenotoxic origin, and thus whether toxaphene could be regulated by a threshold approach. Forty male rats were orally intubated with 100 mg/kg/day technical grade toxaphene in corn oil for 3 days. The dose was reduced to 75 mg/ kg/day on Day 4 due to toxicity. This lower dose was administered daily for 25 days. Another group of 40 male rats was orally gavaged daily with equivalent volumes of corn oil. After 0, 7, 14, and 28 doses, 10 test and 10 vehicle control animals were sacrificed for gross and histopathological examination of thyroid, parathyroid, and pituitary glands. Weights of these endocrine organs, body weights, and brain weights were determined. Prior to sacrifice, a blood sample was obtained from each animal for preparation of serum for analyses of thyroid stimulating hormone (TSH), thyroxine (T4), thyroid hormone (T3), and reverse T3 (rT3). Thyroid glands were evaluated microscopically for follicular cell hypertrophy, hyperplasia, and colloid storage. There were significant time-related increases in serum TSH in the test animals after 7, 14, and 28 doses of toxaphene. The serum levels of T3, T4, rT3, and corrected T3 (CrT3) in the test group were not significantly different from controls at each interval. Thyroid gland weights and thyroid to brain weight ratios were not significantly (p > 0.05) increased in the test group at each sacrifice interval. Pituitary weight, brain weight, and the ratios of these organ weights to body weights were similar in the test and control groups at each sacrifice interval. Thyroid follicular cell hypertrophy and intrafollicular hyperplasia increased and thyroid follicular cell colloid stores decreased with duration of treatment with toxaphene. The hormonal and histopathologic changes seen in the test group were consistent with increased excretion of T3 and/or T4 resulting from cytochrome P450 enzyme induction in the liver. This mechanism for thyroid neoplasia is not known to occur in humans.

Animals↗
PubMed1985

Toxicity study of uracil in dogs.

Uracil was administered to male and female dogs for 3 months and to male dogs for 12 months at dose levels of 0, 210, 420, 840 and 1680 mg uracil per kg body weight per day by gavage. While there were minor differences seen in food consumption, water consumption and erythroid parameters between the 3-month and the 12-month studies, it was concluded that there were no adverse effects seen on these parameters nor on body weight, EKG, clinical laboratory studies and organ weights. Pathological observations did not show treatment-related effects.

Animals↗
PubMed1981

Nephrotoxic potential of cis-diamminedichloroplatinum and four analogs in male Fischer 344 rats.

Cis-diamminedichloroplatinum [cis-DDP; NSC-119875] and four analogs (NSC-241240, NSC-271674, NSC-263158, and NSC-268252) were evaluated for their acute nephrotoxic potential in male F344 rats following iv administration. Indices of nephrotoxicity included blood urea nitrogen, serum creatinine, kidney weights, and microscopic examination. Results indicated that renal function, organ weights, and histology are important criteria for assessing the nephrotoxic potential of cis-DDP analogs, although alterations in these parameters may have been influenced by severe body weight loss. cis-DDP appeared to be the most nephrotoxic compound studied, and NSC-241240 demonstrated minimal renal damage. Ranking of compounds in order of their nephrotoxic potential (most to least) was cis-DDP, NSC-263158, NSC-268252, NSC-271674, and NSC-241240.

Animals↗
PubMed1976

Absence of pathological changes following intravenous methamphetamine and intra-arterial iothalamate meglumine.

Eleven Rhesus monkeys received injections of intravenous methamphetamine hydrochloride (Desoxyn) and/or intra-arterial 60% iothalamate meglumine (Conray) according to a schedule previously reported to produce marked radiological and pathological changes in the cerebral vasculature of the Rhesus monkey. While radiological changes consistent with impaired cerebral circulation were observed, they could not be correlated directly with the administration of intravenous methamphetamine because of the trauma and variability of the technique utilized. Moreover, significant pathological changes could not be found in animals given intravenous methamphetamine alone, intra-arterial iothalamate meglumine alone, or both drugs together. This was true for both drug naive and drug experienced monkeys. These results suggest: (1) radiological changes consistent with decreased cerebral blood flow are not necessarily pathognomonic for reported morphological lesions, and (2) further investigation is required to determine the specific factors necessary to cause the previously reported changes.

Animals↗
PubMed1975

Ultrastructure of cell surface coat (glycocalyx) in rat urinary bladder epithelium.

Earlier statements to the contrary, the present study demonstrates the presence of a cell surface coat (glycocalyx) on the luminal plasma membrane of the superficial transitional epithelial cells lining the urinary bladder of male Buffalo rats. This coat was demonstrated with ruthenium red, an electron dense stain, which revealed a surface layer, 60-80 A thick, separated from the outer leaflet of the plasma membrane by an electron lucent layer, approximately 30 A thick. The structure of the glycocalyx was not affected by 12 weeks of treatment with dibutylnitrosamine, a known bladder carcinogen.

Animals↗
PubMed1974

The Mongolian gerbil as a model for lead toxicity. I. Studies of acute poisoning.

Mongolian gerbils fed diets containing lead acetate maintained body weight comparable to gerbils fed the same diet without added lead. Intranuclear lead inclusion bodies in epithelial cells of the proximal convoluted tubules of the kidney were first observed at 4 weeks, and increased in number to about 50 per high power field at 12 weeks. At this time, a corticomedullary area of empty-appearing tubules was prominent. Transmission electron microscopy confirmed the increase in number and size of nuclear lead inclusion over the 12-week period. Cytoplasmic changes observed in proximal tubule cells containing lead inclusions were considered indicative of acute lethal injury. Distinct cytoplasmic fibrillar structures, first apparent at 8 weeks, were present in some proximal tubular lining cells and strongly resembled newly formed intranuclear lead inclusions. After 12 weeks, the total amount of lead present in the gerbil kidney was four to six times greater than that in rat kidney as determined by atomic absorption spectrophotometry. A hypothesis has been formulated that relates the more efficient nephron of the gerbil kidney to the rapid and extensive development of intranuclear inclusion bodies and the greater accumulation of total lead.

Animals↗
PubMed1973

Experimental lung injury. I. Bacterial pneumonia: ultrastructural, autoradiographic and histochemical observations.

Proteus infection in the rat produces an acute bacterial pneumonia which resolves without necrosis or significant organization within 2 weeks. Ultrastructural changes included widespread damage to type 2 cells and endothelial cells and rapid proliferation of the alveolar epithelial cells, which were the predominant site of labeling with tritiated thymidine. Histochemical staining for lysosomal enzymes showed an initial reduction in type 2 cell reactivity. The majority of proliferating epithelial cells were also unreactive until the normal pattern of staining and morphology returned at 8 to 12 days after infection. The acute inflammatory exudate was reactive, but there was only minimal to moderate staining in the subsequent clusters of alveolar macrophages. These data suggest that resolution with the preservation of the normal architecture of the peripheral airspaces may be correlated with superficial injury and limited reactivity for digestive enzymes.

Acid Phosphatase↗
PubMed1972

Histochemical distribution of carbonic anhydrase after ligation of the pancreatic duct.

The distribution of carbonic anhydrase in the exocrine pancreas of the rat has been examined during the first 3 weeks after duct ligation. The normal pattern of positive reaction in ducts, centroacinar cells and capillaries changed, by the end of the first week, to one in which all the cells in the dilated ducts showed the enzyme. This situation persisted through the third week. By electron microscopy, the enzyme was found on the apical membranes of ductular, centroacinar and acinar cells, as well as on the surface membranes of the modified cells seen at 1 week. The significance of these findings with respect to function and cell origin is discussed.

Animals↗