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E Bomhard

Publications and source records attributed to E Bomhard.

29 records · Page 2Linked to original sources
PubMed1988

Induction of light hydrocarbon nephropathy by p-dichlorobenzene.

In order to clarify the etiology of a dose-related increase in the incidence of tubular cell adenocarcinomas of the kidney in male rats, the nephrotoxicity of p-dichlorobenzene (p-DCB) was investigated in a subchronic study. Groups of ten male and ten female Fischer 344 rats were dosed by gavage with 0 (controls), 75, 150, 300 or 600 mg p-DCB/kg/day in corn oil. Half of the animals were sacrificed after 4 weeks and the remainder after 13 weeks. Increased urinary LDH and epithelial cell excretion and exacerbation of hyaline droplet accumulation in the cytoplasm of renal cortical cells were observed in male rats over the entire dose range investigated. Tubular single cell necrosis, dilated tubules with granular cast formation in the outer zone of the medulla, were evident in male rats after 4 and 13 weeks of treatment with doses of 150-600 mg/kg/day. In female rats there was no indication of a nephrotoxic action of p-DCB. The effects on the kidney, both in their morphological characteristics and the fact that they occur exclusively in male animals, correspond to the light hydrocarbon nephropathy observed as a result of short-term treatment with a number of aliphatic and cyclic hydrocarbons. The development of cortical renal tumors seems to be associated with this kind of kidney damage which is unique to male rats. The literature on this subject generally regards these renal effects as not predictive for man.

Acetylglucosaminidase↗
PubMed1987

Chronic effects on single and multiple oral and subcutaneous cadmium administrations on the testes of Wistar rats.

Thirty mature male Wistar rats were administered cadmium as CdCl2 X 1H2O in single doses of 50 mg/kg p.o. or 2.5 mg/kg i.p. or 10 weekly doses of 5 mg/kg p.o. or 0.25 mg/kg i.p., respectively. Ten males, each treated correspondingly with the vehicle, served as control groups. Some of the animals were necropsied after 12 and 18 months, respectively, the remainder were kept for up to 30 months. In a supplementary study 25 males were each treated once with 200 mg/kg p.o. or 2 mg/kg s.c. and 35 males with 100 mg/kg p.o. This experiment was terminated after 6 months. Animals having received 1 X 100 or 1 X 200 mg/kg p.o. or 1 X 2.0 or 1 X 2.5 mg/kg s.c. showed severe lesions of the whole testicular parenchyma with massive calcification of the necrotic tubuli and pronounced fibrosis of the interstitium. All animals receiving 2.5 mg/kg s.c. had a Leydig cell tumor in at least one of the testes. In 5 out of 15 animals surviving 18 months these tumors were classified as malignant (mean time of induction: 858 +/- 77 days). All the other tumors detected were not regarded as causally related to treatment. The results of the supplementary study indicate that with very high oral cadmium dosages Leydig cell tumors may be induceable. Since the massive lesion of the testes appears to be the prerequisite for the occurrence of induced Leydig cell tumors, a non-genetic mechanism is to be assumed in respect to the formation of these tumors.

Administration, Oral↗
PubMed1987

Test guideline. Behavioral toxicity testing in animal experiments according to section 9, para. 1, No. 2 of the Chemicals Act (Chemikaliengesetz) of the Federal Republic of Germany.

The German Chemicals Act requires that chemicals are tested for behavioral toxicity at stage 2 of the testing procedure, i.e. if more than 1000 annual tons are produced. For this purpose a guideline was developed according to which data on behavioral toxicity are to be collected, which are based on cageside observations during longterm exposure. The protocol covers outer appearance, as well as motor, sensory, autonomic and central nervous system functions. Data are to be reported in tabular form and should be evaluated by taking all aspects of the toxicological profile into account.

Animals↗
PubMed1982

Subchronic oral toxicity and analytical studies on nickel rutile yellow and chrome rutile yellow with rats.

The inorganic pigments nickel rutile yellow and chrome rutile yellow were fed to groups of 15 male and 15 female rats each for 3 months at dietary levels of 0, 10, 100, 1000 and 10000 ppm, respectively. On an additional 5 animals each, levels of nickel and antimony or chromium and antimony in liver and kidneys, respectively, were measured after 1 and 2 months. Appearance, behaviour, food consumption, growth, mortality, haematological and clinical chemical data, organ weights, and gross and micromorphology of organs were not affected in any dose group. In livers and kidneys antimony median levels below 30 ppb were detectable only in the group of rats fed the highest level of 10000 ppm of the two pigments.

Animals↗
PubMedDate not supplied

Urinary antigens as markers of papillary toxicity. II: Application of monoclonal antibodies for the determination of papillary antigens in rat urine.

We have previously reported the preparation of monoclonal antibodies specific for antigens localized in the rat renal papilla. Three of the monoclonal antibodies reacting with antigens localized in papillary and cortical collecting duct epithelia were selected for the development of enzyme-linked immunosorbent assay (ELISA)-type assays. The papillary antigens ('PapA') determined in these tests were designated PapAl (applying the monoclonal antibody PapX 5C10), PapA2 (applying the monoclonal antibody PapX 12F6), and PapA3 (applying the monoclonal antibody PapXI 3C7). Using these assays antigen excretion was determined in the urine of rats. Depending on the test compound used. the application route, and the dose, the observed antigen release patterns differed. Whereas after a single intraperitoneal application of 2-bromoethanamine or of propyleneimine an increased release of PapA1 but not of the two other antigens was observed oral application of bromoethanamine had minor effects. In contrast, both a single intraperitoneal application or repeated oral applications of indomethacin resulted in an increased release of all the three antigens. Daily application of ipsapirone in the diet or in drinking water resulted in significantly elevated urinary release of PapAl which increased incrementally for the duration of the application. Release of PapA2 and PapA3 was not affected and remained in the normal range. These results show that with the tests developed changes in the rat renal papilla caused by xenobiotics can be detected early by urinary analysis and monitored during follow-up studies. Moreover. the different antigen release patterns obtained after application of the different compounds suggest a possible differing mode of action.

Animals↗
PubMedDate not supplied

Comparative investigations on the effects of acute intraperitoneal cadmium, chromium, and mercury exposure on the kidney.

Urinary excretion of lactate dehydrogenase (LDH), glutathione-S-transferase (GST), leucine arylamidase (LAS), gamma-glutamyltransferase (GGT), beta-galactosidase (GAL), beta-N-acetyl-D-glucosaminidase (NAG), sodium, and glucose were determined in female Sprague-Dawley rats the subsequent three days after intraperitoneal treatment with single doses of 4.5 mg CdCl2 X 1H2O/kg, 20 mg Na2CrO4/kg, and 0.75 mg HgCl2/kg body weight. Although the pathological effects were localized within the same part of the nephron (i.e., the proximal tubule), there were marked differences with regard to the extent and time course of the parameters affected. Treatment with cadmium resulted essentially in a marked decline in sodium and glucose excretion. The administration of chromate led to a slightly to moderately elevated excretion of the enzyme activities measured with the cytosolic LDH as the most increased enzyme (ca. 500% of controls on Day 3 postadministration). Median glucose excretion was unaffected whereas sodium excretion was transiently reduced. The maximum of enzyme excretion after HgCl2 was essentially the same on the first day postadministration and the amount of enzyme activity in urine up to 20 times higher compared to that after chromium. Sodium excretion was below that of controls on Days 2 and 3, whereas glucose excretion was markedly elevated (up to 8000% of controls). The results indicate that it is possible to discriminate with the use of selected urinary enzymes, substrates, and electrolytes various kinds of nephrotoxic actions not only in different but also within the same part of the nephron.

Acetylglucosaminidase↗
PubMedDate not supplied

Spontaneous tumors of 2000 Wistar TNO/W.70 rats in two-year carcinogenicity studies.

Eleven two-year toxicity/carcinogenicity experiments in control Wistar TNO/W.70 rats were started between 1973 and 1976. Tumors occurring were compiled on the basis of histopathological reports. Of the 1,000 male and 1,000 female rats at the beginning of the studies, 962 males and 968 females were evaluated. The remaining animals were unavailable due to autolysis or early death (before day 400). The histopathologic diagnosis for the eleven reports were performed by five different pathologists or groups of pathologists. A total of 827 tumors (375 in males and 452 in females) was seen in 686 rats (303 males, 383 females). 183 tumors (67 in males, 116 in females) were classified as malignant. 719 (86.9%) of all tumors and 120 (65.6%) of all malignant tumors were located in endocrine organs (pituitary, thyroid, adrenal, pancreatic islets) or in genital organs (testes, epididymides, seminal vesicles, ovaries, uterus, mammary gland). Average incidences of primary tumors found in the following organs were: pituitary 20.0%, thyroid 9.6%, uterus 9.2%, adrenals 4.1%, mamma 3.2%, testes 2.9%, ovaries 1.8%, skin 1.4% and 17 other organs each with a tumor frequency below 1%. This wide spectrum of spontaneous tumors with a mostly low incidence makes the Wistar rat a preferred strain for carcinogenicity studies. Despite nearly identical husbandry conditions, a marked variability was observed among experiments regarding the general incidence of benign and/or malignant tumors, particular tumors, and number of tumor-bearing animals. Differences in mortality among experiments had no pronounced effect on the variability of tumor incidences. Different evaluation criteria used by different pathologists did not appear to be a major cause of the observed variability with the probable exception of lesions in endocrine organs. The major cause would seem to be the biological variability of the animal material. The observed marked variability of tumor incidences between experiments would indicate that a considerable natural variability may also occur between groups of one carcinogenicity study. Therefore, information on historical control tumor data from the same rat strain kept under similar conditions is needed to interpret the incidences of tumors in carcinogenicity experiments.

Adrenal Gland Neoplasms↗