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Biomedical subjects

H Witschi

Publications and source records attributed to H Witschi.

At least 127 records · Page 7Linked to original sources
PubMed1973

Qualitative and quantitative aspects of the biosynthesis of ribonucleic acid and of protein in the liver and the lung of the Syrian golden hamster.

1. The incorporation of orotic acid and of uridine into total RNA was measured in vivo in liver and lung of the Syrian golden hamster. Specific activities of total acid-soluble UMP were measured in both organs. An estimation of the rate of RNA biosynthesis showed that hamster lung synthesizes RNA at about one-half of the rate of that of hamster liver. 2. The apparent K(m) and V(max.) values of a few enzymes involved in pyrimidine biosynthesis were measured in the 100000g supernatants of liver and lung. The apparent K(m) values were very similar in both organs. From the estimated V(max.,) it was concluded that hamster lung cells have less capacity to metabolize orotic acid than have liver cells. 3. A time-response and a dose-response study showed that actinomycin D inhibits pulmonary RNA synthesis as efficiently as hepatic RNA synthesis. 4. Protein synthesis, measured as the incorporation of leucine, was inhibited in both organs 30min after a dose of 2mg of cycloheximide/kg. The dose-response patterns were similar in both liver and lung 3h after cycloheximide. 5. It is concluded that RNA and protein synthesis in vivo in hamster lung are very similar to the corresponding reactions in liver. Alterations of RNA and protein synthesis by toxic agents can therefore be evaluated in lung with a similar approach to that used to study the pathological biochemistry of liver.

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PubMed1973

The effects of diethylnitrosamine on ribonucleic acid and protein synthesis in the liver and lung of the Syrian golden hamster.

1. Syrian golden hamsters were treated with a single subcutaneous dose of 200mg of diethylnitrosamine/kg. In the liver the treatment produced a significant and early inhibition of the incorporation of orotic acid into RNA and of leucine into protein. Diethylnitrosamine also lowered basal and 20-methylcholanthrene-stimulated activities of hepatic aryl hydrocarbon hydroxylase. 2. RNA synthesis, protein synthesis and aryl hydrocarbon hydroxylase activity were also evaluated in the lungs of the same animals. In this organ only protein synthesis was affected by diethylnitrosamine, but not RNA synthesis or aryl hydrocarbon hydroxylase activity. 3. The incorporation of thymidine into DNA was inhibited in both organs early after diethylnitrosamine treatment and increased 2-3 days later. 4. Although diethylnitrosamine, injected subcutaneously, accumulates in liver and lung in toxicologically active amounts, the acute biochemical responses of the two organs are not identical.

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PubMedDate not supplied

Effect of lung, liver, and kidney toxicants on respiratory rate in the mouse.

The intraperitoneal administration of either butylated hydroxytoluene (BHT) +/- thoracic X-irradiation, or cyclophosphamide, and intravenous injection of oleic acid, resulted in lung injury and repair in BALB/c mice which could be assessed in unanesthetized animals by changes in respiratory rate (RR) using a total body plethysmograph. Studies with BHT +/- X-rays, and cyclophosphamide found that the RR right before sacrifice (2 weeks after BHT and 3 weeks after cyclophosphamide) correlated well (r = 0.19) with the degree of pulmonary fibrosis as measured by changes in hydroxyproline content. However, prior to this timepoint, there was a peak and trough in respiratory rate response that could not be correlated with the time course of fibrosis development in the BHT-X-ray model. In an effort to determine the influence of pulmonary edema and lung cell proliferation on respiratory rate changes, an agent (oleic acid) capable of producing lung injury followed by a high level of cellular proliferation with only minimal development of fibrosis was studied. These studies showed that good correlations were found on day 3 following injection (day of peak increase in respiratory rate) between respiratory rate and either lung wet weight (r = 0.81) or the degree of cellular proliferation as measured by the incorporation of thymidine into pulmonary DNA (r = 0.80). Liver (carbon tetrachloride) and kidney (mercuric chloride) toxicants, and starvation produced decreases or no change in RR.

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PubMedDate not supplied

Nicotine- or epinephrine-induced uteroplacental vasoconstriction and fetal growth in the rat.

We examined the relationship between nicotine-induced vasoconstriction in pregnant rat dams and fetal growth during the third trimester of pregnancy. Pregnant rats were continuously treated between days 13 and 19 of gestation with either nicotine (9.6, 4.8 or 2.4 mg/kg/day), epinephrine (0.72 microgram/kg/day), or saline via continuous infusion from a subcutaneously implanted osmotic minipump. Placental weights in rats treated with high dose nicotine and dams' body weights were severely reduced. However, fetal weights were not affected. Blood flows in uterus and placenta were quantified by measurement of tissue content of 85Sr-labelled microspheres injected via a carotid artery catheter. Both nicotine and epinephrine caused a significant reduction (> 40%) in uterine and placental blood flow. We conclude that vasoconstriction alone as a result of nicotine or epinephrine administration during the last trimester of gestation does not necessarily reduce nutrient supply to the fetus and does not affect fetal growth in rats.

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PubMedDate not supplied

Effects of oxygen and ozone on mouse lung tumorigenesis.

Oxygen and ozone both have been found to enhance or to inhibit the development of tumors in mouse lung. As a general rule, preexposure to the oxidant, before administration of a carcinogen, or exposure to high levels for a comparatively short time immediately following carcinogen administration favors development of tumors. On the other hand, prolonged exposure begun after a certain time following carcinogen exposure inhibits tumor development. The paradoxical effects of the two oxidants depend on experimental design; results can be tentatively explained in terms of oxidant-induced cell proliferation or by oxidant-mediated cytotoxicity. Besides being capable of modifying chemically induced lung tumorigenesis, ozone and oxygen also appear to induce tumors in mouse lung on their own. The conclusions drawn from the study of mouse lung tumors have recently been reinforced in experiments with hamsters, where hyperoxia has clear tumor-modulating effects.

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