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Biomedical subjects

D Steinhoff

Publications and source records attributed to D Steinhoff.

At least 19 recordsLinked to original sources
PubMed1993

[A Q fever epidemic in Berlin. The epidemiological and clinical aspects].

An epidemic of Q fever in Berlin affected at least 80 patients (45 females, 35 males; age range 1-75 years). Sheep were identified as the focus of infection: they had been brought to a veterinary clinic because of nonspecific symptoms. The peak incidence of the infection was in April and May, 1992. Most of the patients were staff or students at the veterinary clinic. This is the most northern and, at the same time largest, Q fever epidemic recorded in Germany over the last 28 years. The complement fixation reaction (CFR) was not helpful diagnostically in the acute stage of the disease as it remained negative in the first 14 days (CFR < or = 1:5). Most of the patients had sudden fever to over 40 degrees C, severe headache and dry cough. Pulmonary infiltrates were seen in the chest radiograph of 8 of the 10 patients presented in this contribution. Auscultation was largely negative. Two patients had signs of hepatic involvement (GPT as high as 71 U/l). The drug of choice was doxycycline at a dosage of 200 mg twice daily for 14 days.

Adolescent↗
PubMed1991

On the question of a carcinogenic action of cobalt-containing compounds.

After subcutaneous injections of doses of 5 x 2 and 1 x 10 mg cobalt (II) oxide/kg/week (total dose 1,000 mg/kg), respectively 5 out of 10 and 4 out of 10 rats in a lifetime study developed local malignant tumours (controls 0/10). After intraperitoneal injections of 3 x 200 mg cobalt (II) oxide/kg 14 out of 20 rats developed malignant intraperitoneal tumours (controls 1/20). With a Co/Al/Cr spinel the same treatment produced malignant intraperitoneal tumours in only 2 out of 20 rats. After intratracheal instillation of cobalt (II) oxide in single doses of 2 mg/kg (total dose 78 mg/kg) and 10 mg/kg (total dose 390 mg/kg) there were 2 benign pulmonary tumours among 100 rats in the low-dose group and 2 benign and 4 malignant pulmonary tumours among 100 rats in among 100 rats in the high-dose group. The Co/Al/Cr spinel was tested intratracheally only in the high dose (total dose 390 mg/kg); among the 100 rats this produced 3 malignant pulmonary tumours. Alternating intratracheal instillation of cobalt (II) oxide (total dose 470 mg/kg) and benzo[a]pyrene (total dose 200 mg/kg) led to 9 malignant pulmonary tumours in 20 rats, whereas benzo[a]pyrene alone caused only 1 malignant pulmonary tumour in 20 rats. The results suggest that cobalt (II) oxide (76.7% Co) has a weakly carcinogenic effect. The Co/Al/Cr spinel investigated is still less active, and even in very sensitive tests (i.p. and i.t. administration) shows no statistically significant carcinogenic effect. This smaller effect may possibly be explained by its lower cobalt content (24.0%) or its much lower solubility (only less than 10% of the solubility of CoO in 0.1 n HCl).

Animals↗
PubMed1991

Carcinogenesis studies with iron oxides.

Seven different types of iron oxide were examined for carcinogenic properties in intratracheal instillation and intraperitoneal injection tests on rats, which represent particularly sensitive methods for local carcinogenic effects. The total doses lay in the range of maximum tolerance (390/1,530 mg/kg i.t. or 600 mg/kg i.p.). With one exception, at least 50 male and 50 female Sprague-Dawley rats were used per test group, control group and route of administration. Two iron oxides were additionally instilled intratracheally in combination with benzo[a]pyrene. No carcinogenic effect could be demonstrated for the test iron oxides RBW 07105/SV2 (fibrous, magnetic, surface doped with 1.85% cobalt), development product Bayferrox AC 5100 M (fibrous, magnetic, bulk doped with 2.1% cobalt), Bayferrox 1352 (fibrous alpha-Fe2O3), Bayferrox 920 (fibrous alpha-FeOOH), Bayferrox 130 (cubic alpha-Fe2O3), Bayferrox 306 (cubic Fe3O4), or Brazilian iron ore AC 5031 N (alpha-Fe2O3).

Animals↗
PubMed1990

On the question of the carcinogenic action of hydrazine--evaluation on the basis of new experimental results.

Hydrazine has not previously been shown to have any carcinogenic action in man. After the administration of probably clearly toxic doses (the data in earlier publications are very fragmentary) or doses severely irritating to the sensitive nasal epithelium of the rodent over a large part of its life, hydrazine was shown in the majority of the studies described in the literature to be carcinogenic in rodents. Even under these severe experimental conditions, however, the carcinogenic action was not very pronounced or was even very weak. In the study in mice described below, which was carried out according to modern guidelines, no carcinogenic action was detected for hydrazine even after the administration of toxic doses over the entire lifespan of the animals. Administration of a still higher dose would have conflicted with all current recommendations. On the basis of the results available in the literature, indirect alkylation of DNA was assumed to be the mechanism of the carcinogenic action of hydrazine. According to the current level of knowledge, this effect, like the mutagenic and the carcinogenic action of the substance, is closely linked with the toxic activity of hydrazine. Overall, hydrazine should be regarded as a substance having a probably indirect weakly carcinogenic action after toxic doses administered over the entire lifespan.

Animals↗
PubMed1988

The question of carcinogenic effects of hydrazine.

In a number of older studies by various authors, hydrazine showed carcinogenic effects after toxic or subtoxic doses. Our own preliminary studies with maximum tolerable doses (rats, s.c. or i.t.), however, yielded negative results, as did the administration of maximum tolerable hydrazine doses simultaneously with benzo(a)pyrene treatment (rat i.t. and mouse i.p.). These preliminary experiments were therefore followed by a carcinogenicity study in rats, in which hydrazine was administered with the drinking water in concentrations of 0 mg/l (= control), 2, 10, and 50 mg/l. Each group comprised 50 male and 50 female Wistar rats. The investigation was continued until the spontaneous death of all the rats. The concentration of 2 mg/l was tolerated with hardly any damage; 10 mg/l proved to be the maximum tolerable dose, and 50 mg/l was clearly toxic although the survival times were not affected appreciably. Only under the toxicity of the highest concentration could a weak carcinogenic effect of hydrazine be detected, namely in the very late occurrence of small, usually benign liver cell tumours (overall 11.5%). A similar study carried out in mice revealed no macroscopic evidence of a carcinogenic effect of hydrazine (histology currently in preparation). According to these results, hydrazine is only weakly carcinogenic even after lifelong ingestion of unequivocally toxic doses. The classification of hydrazine as a "carcinogen" should therefore be re-evaluated.

Adenoma, Bile Duct↗
PubMed1986

Carcinogenicity study with sodium dichromate in rats.

Solutions of sodium dichromate were administered to Sprague Dawley rats by intratracheal instillations over a period of 30 months. Dosage was 0.01, 0.05 or 0.25 mg/kg, five times a week, or 0.05, 0.25 or 1.25 mg/kg once a week. Each group consisted of 40 male and 40 female rats. Groups left untreated or given saline served as negative controls. The highest chromate dose proved to be within the range of the maximum tolerable amount. The main determinant of effect was the concentration of chromate instilled, not the total dose per week. Non-neoplastic pulmonary lesions, which occurred predominantly in the highest dose group, were fibrotic regions containing residual distorted bronchiolar lumens or cellular inflammatory foci containing alveolar macrophages, proliferated epithelium and chronic inflammatory thickening of alveolar septa. Fourteen rats given 1.25 mg/kg sodium dichromate had a total of 20 lung tumours (12 benign, 8 malignant). One rat given 0.25 mg/kg once a week had a malignant tumour. Tumours were generally small and were non-fatal. A comparable solution of calcium chromate, which was tested at the two highest dose levels, had virtually the same effect. The positive controls, benzo(a)pyrene and dimethylcarbamyl chloride, induced a high rate of fatal malignant tumours in the respiratory tract.

Adenocarcinoma↗
PubMed1983

Evaluation of amitrole (aminotriazole) for potential carcinogenicity in orally dosed rats, mice, and golden hamsters.

Amitrole was evaluated for carcinogenic potential in lifespan studies on Wistar rats, NMRI mice, and golden hamsters. At the start of the studies the animals were 6 weeks old. Amitrole was administered, mixed with pulverized chow, at dietary concentrations of 0, 1, 10, and 100 micrograms/g (ppm). Each treated group and control group consisted of 75 male and 75 female rats and mice and of 76 male and 76 female golden hamsters. Additional animals were used to evaluate the functional state of the thyroid. Somewhat lower body weights, slightly reduced survival times, and transient effects on thyroid function were observed in golden hamsters at 100 ppm. In mice, a slight increase in pituitary gland hyperemias was seen at 100 ppm; also an effect on thyroid function usually occurred at the same concentration. In rats, a very large number of cystic dilatations of follicles in the thyroid at 100 ppm and a dose-unrelated increase in hemorrhages and hyperemias in the pituitary gland were indicative of an effect of amitrole on these organs. The strongest effect of amitrole on thyroid function, as compared to golden hamsters and mice, was seen in rats at 100 ppm. At this concentration a highly increased number of thyroid and pituitary gland tumors was observed in rats. In golden hamsters and mice, no tumor induction was seen.

Amitrole↗
PubMed1981

Possible methods of carcinogenicity testing for substances used at the place of work.

Even in the early stages of the development of new chemical substances the chemist should know as much as possible about their eventual carcinogenic properties. In most cases extensive carcinogenicity testing cannot be performed. In that situation, a sensitive and relatively inexpensive approach to carcinogen testing is proposed. Subcutaneous, intratracheal, or intraperitoneal applications to rodents give reliable results even with regard to the necessary quantification of potency. In such tests the unknown substances (unknown with regard to carcinogenicity) can be handled more safely than in other tests. Examples of the implementation of the methods are given and comparisons are made with classical methods of testing.

Animals↗
PubMed1975

Effect of diethylnitrosamine on the livers of rats after high oral doses administered at intervals varying between three and twenty-four days.

When 200 mg of diethylnitrosamine per kg of body weight was administered with a stomach tube once a week to female Wistar W.64 rats, all of them died within three weeks from severe hepatocellular injuries and haemorrhages of the liver, lungs and small intestine. Weekly administrations of 100 mg per kg of body weight consistently caused the rats to die after seven to fifteen weeks from severe hepatic cirrhoses characterized by large tubercles. Weekly doses of 50 mg per kg of body weight caused much less severe hepatic cirrhosis. Under these conditions death occurred after 17 to 23 weeks, all the rats having contracted multiple hepatocellular carcinomas and in most cases pronounced hepatic cirrhosis. When this amount of diethylnitrosamine was administered for twelve weeks only the hepatic cirrhosis was less apparent, but a substantial influence on the tumor development was not observed. After a reduction of the dose to 25 mg per kg of body weight once a week all the rats in the relevant group died after 26 to 35 weeks, likewise from multiple hepatocellular carcinomas. Hepatic cirrhosis were then relatively inconspicuous. Similar results were obtained when, not the dose, but the interval between doses (100 mg/kg each) was varied. This clearly differential effect of diethylnitrosamine in the rat thus makes it a simple matter to induce hepatic cirrhosis or cancers that are suitable for a variety of tests and also, for example, as models for therapy trials.

Animals↗