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Biomedical subjects

H J Klimisch

Publications and source records attributed to H J Klimisch.

47 records · Page 3Linked to original sources
PubMed1976

[Experimental studies on the rumorigenic activity of cigarette smoke condensate on mouse skin. VI. Fractionation of cigarette smoke condensate (author's transl)].

This experiment has been performed to clarify the question to which extent fractions containing polycyclic aromatic hydrocarbons (PAH) or other carcinogenic compounds are responsible for the biological activity of cigarette smoke condensate. With chromatographic procedures using organic gels it was possible to separate quantitatively polar compounds from the PAH-fraction and to obtain fraction IX representing 0.4% of the whole condensate. In this fraction the PAH were enriched 250fold. Significant losses of tumorigenic effects by this fractionation method could not be observed. This PAH-containing fraction showed 50% of activity compared with the overall activity of whole smoke condensate of a reference cigarette. A so-called PAH-free fraction showed with 7% of the overall activity of the whole smoke condensate a weak carcinogenic effect. The importance of PAH for the tumorigenic effect of cigarette smoke is emphasized by these results.

Animals↗
PubMed1975

[Gaschromatographic determination of carbon monoxide and carbon dioxide. Investigations from the gas phase of cigarette smoke].

A gaschromatographic method for the quantitative determination of CO and CO2 is described. The method is suitable in a wide sensitivity range from ppm to % content of these gases. CO, CH4 and CO2 are separated under isothermic working conditions by the use of a column filled with carbon molecular sieve CMS. The column should be regenerated only after more than 1000 analyses. The quantitative determination of CO and CO2 in cigarette smoke is reported. With a total retention time of less than one min. this system enables the analysis of the carbon oxides to be performed puff by puff. The CO and CO2 contents of the vapour phase of various test cigarettes are discussed.

Carbon Dioxide↗
PubMed1975

Uptake of carbon monoxide in blood of miniture pigs and other mammals.

Different affinities of blood for CO were observed in in vivo and in vitro experiments. Hamsters showed the greatest relative affinity (1.0), the corresponding value for rats was 0.8, for pigs 0.74 and for rabbits 0.58. The upward shift of the saturation curves was dependent on the rate of respiratory exchange per unit of body weight, e.g. the curves were less steep for pigs than for rabbits. After increased motor activity the equilibrium saturation of CO in blood is reached more rapidly. From the results of in vitro experiments the following affinity constants for the blood of different species could be calculated: pig K = 130, hamster K = 181, rat I = 141, rabbit K = 109. For equal atmospheric CO concentrations the saturation values were lower (37-40%) in experiments in vitro than in vivo. Similar saturation values were obtained with light excluded, when O2 concentration was decreased to the level of alveolar oxygen concentration. With regard to the affinity of blood for CO, the blood of domestic pigs did not differ from that of minature pigs in in vitro experiments.

Animals↗
PubMedDate not supplied

n-Butyl acrylate: prenatal inhalation toxicity in the rat.

n-Butyl acrylate was examined for its prenatal toxicity in Sprague-Dawley rats. Inseminated rats were exposed to concentrations of 0, 25, 135 and 250 ppm for a duration of 6 hours per day from the 6th to 15th day post coitum. Subsequently the animals were held to the 20th day post coitum. During the inhalation period concentrations of 135 and 250 ppm n-butyl acrylate led to maternal toxicity (delayed body weight gain depending on the concentration, clinical signs of irritation). At the end of the exposure period the signs subsided. The same concentrations induced embryolethality (increased number of dead implantations depending on the concentration). 25 ppm of n-butyl acrylate did not lead to maternal toxicity or embryolethality. Under the conditions chosen, a teratogenic effect of the test substance was not detected at any concentration.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

n-Butyl acrylate: cytogenetic investigations in the bone marrow of Chinese hamsters and rats after 4-day inhalation.

Chinese hamsters and rats were exposed to an average concentration of 817 ppm and 820 ppm n-butyl acrylate (acrylic acid n-butyl ester), respectively for 4 days. In both animal species, the exposure led to distinct signs of toxicity; four of ten male Chinese hamsters died during the exposure period. The chromosome analysis carried out in the bone marrow of the animals after the 4-day inhalation did not indicate any chromosome-damaging effect of n-butyl acrylate. Under the experimental conditions chosen the percentage of metaphases damaged was always in the same range as that of the controls for both Chinese hamsters and rats.

Acrylates↗
PubMedDate not supplied

Long-term inhalation toxicity of N-vinylpyrrolidone-2 vapours. Studies in rats.

In previous subchronic studies inhaled N-vinylpyrrolidone-2 (NVP) was haemotoxic, hepatotoxic and irritant to the nose. In the first of two long-term studies, study A, Sprague-Dawley rats were exposed by inhalation to 0, 5, 10 or 20 ppm NVP (6 hr/day, 5 days/wk) for 24 months. Satellite groups were killed after 3, 12 or 24 months. In study B, female Sprague-Dawley rats were exposed to 0 or 45 ppm NVP for 3 months and killed at 3 or 12 and 24 months post-exposure. In study A, survival was unaffected, but reduced body weight gain, haemotoxicity, effects on clinical chemistry parameters indicative of hepatotoxicity, increased liver weight, hepatocellular carcinomas, necrosis, reparative hyperplasia, adenomas and adenocarcinomas of the nasal cavity, and squamous cell carcinomas of the larynx were seen. Increased tumour incidence was seen only in the liver and upper respiratory tract. In study B, the effect of NVP on body weight evident at 3 months disappeared before 1 yr, but effects on liver pathology persisted throughout the subsequent 21-month exposure-free period, and a few liver tumours were seen at 2 yr. As NVP gave negative results in a battery of in vitro and in vivo genotoxicity tests, it appears that the tumours that arose were manifestations of a non-genotoxic mechanism.

Adenoma↗
PubMedDate not supplied

Subchronic inhalation and oral toxicity of N-vinylpyrrolidone-2. Studies in rodents.

N-Vinylpyrrolidone-2 (NVP) is a monomeric compound used as an industrial intermediate. Nine of 11 studies previously reported involved exposure of rats (two different strains), mice or hamsters to NVP by the inhalation route at concentrations of up to 120 ppm (6 hr/day, 5 days/wk) over a period of 1 wk to 12 months. The remaining two studies involved exposure of rats to NVP through the drinking water or by gavage at dose levels of up to 100 mg/kg body weight/day. Reduced body weight gain was seen in rats exposed by inhalation to 5 ppm or more for 3 months and in mice and hamsters exposed to 45 ppm for only 1 day. Effects were seen on haematological (reduced haemoglobin, erythrocyte count, haematocrit) and clinical chemistry parameters (specially raised gamma-glutamyltransferase activity and decreases in plasma protein), liver weight increase and liver lesions (centrilobular single-cell necrosis and foci of hepatocellular alteration) in rats and mice but not hamsters. Rats exposed to 40 mg/kg body weight/day NVP or more for 3 months by gavage developed similar liver changes. Atrophy of olfactory epithelium and hyperplasia of nasal respiratory epithelium was seen in rats exposed by inhalation to 5 ppm NVP for 7 wk but not in response to 1 ppm for 13 wk (no observed-adverse-effect level, NOAEL). These studies indicated that the upper respiratory tract and the liver are the main targets for NVP toxicity.

Administration, Inhalation↗