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Tumour cell death can be evaluated in the living mouse by externally measuring the rate of loss of tumour-bound DNA tracer. By sequentially labelling the tumour-bearing animals with ¹²⁵IUdR and ¹³¹IUdR 50 h apart, the average tumour cells at the time of the second injection are labelled by ¹²⁵IUdR and the euoxic tumour cells are specifically labelled with ¹³¹IUdR. Tumour treatment at this stage of labelling permits the observation of the reaction of euoxic cells and average tumour cells and finally yields data on hypoxic cells and thus on the oxygen enhancement ratio. This information adds to results from tumour control and growth delay.
With this technique effects were analysed of 60-Co γ-rays, cyclotron neutrons (E = 6 MeV), misonidazole (500 mg/kg body wt) and hyperthermia (42°C water-bath), or combinations of these.
Misonidazole (15 min before irradiation) altered the oxygen enhancement ratio by a factor of 1·5 for γ-rays and of 1·1 for neutrons; when evaluated from tumour-growth delay and TCD-50 misonidazole gave a dose modifying factor of 1·47 for γ-rays and of 1·2-1·3 for neutrons.
Based on percentage tumour regression 100 days after treatment, the enhancement ratio from hyperthermia (after irradiation) was 2·75 for γ-rays (at 10 Gray) and 2·2 for neutrons (at 3·2 Gray). For neutrons combined with misonidazole and hyperthermia the ratio was 2·4.
These results demonstrate that effects of neutron irradiation may be modified by electron-affinic substances and/or hyperthermia.
Dexamethasone (DEX) is a potent and widely used anti-inflammatory and immunosuppressant glucocorticoid. It can bind and activate the pregnane X receptor (PXR), which plays a critical role as xenobiotic sensor in mammals to induce the expression of many enzymes, including cytochromes P450 in the CYP3A family. This induction results in its own metabolism. We have used a series of transgenic mouse lines, including a novel, improved humanized PXR line, to compare the induction profile of PXR-regulated drug-metabolizing enzymes after DEX administration, as well as looking at hepatic responses to rifampicin (RIF). The new humanized PXR model has uncovered further intriguing differences between the human and mouse receptors in that RIF only induced Cyp2b10 in the new humanized model. DEX was found to be a much more potent inducer of Cyp3a proteins in wild-type mice than in mice humanized for PXR. To assess whether PXR is involved in the detoxification of DEX in the liver, we analyzed the consequences of high doses of the glucocorticoid on hepatotoxicity on different PXR genetic backgrounds. We also studied these effects in an additional mouse model in which functional mouse Cyp3a genes have been deleted. These strains exhibited different sensitivities to DEX, indicating a protective role of the PXR and CYP3A proteins against the hepatotoxicity of this compound.
In-beam study of ¹⁴³ Eu
(1988)
In-beam study of ¹⁴⁴ Gd
(1978)
In-beam study of ¹⁴⁴ Gd
(1977)