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S Parodi

Publications and source records attributed to S Parodi.

220 records · Page 13Linked to original sources

Induction of preneoplastic nodules: quantitative predictivity of carcinogenicity.

Using data from two independent studies, the quantitative predicitivity of carcinogenicity of the liver preneoplastic nodules test was examined. It was compared with the predicitivity of two short-term parameters: the Ames test and acute toxicity. In analyzing the results of both studies, a rather high quantitative predictivity was shown for the preneoplastic nodules (r = 0.43 and r = 0.60, respectively). For one study, the predictivity was approximately of the same order as the internal consistency of the carcinogenicity data (median r = 0.69). The preneoplastic nodules were more predictive than the Ames' test as a statistical trend. The predictivity of the Ames' test has been found to be rather poor; especially in one case where r = 0.10. As expected, acute toxicity was the less predictive short-term parameter.

Animals↗

Evidence for a fast repair of apurinic sites induced by N-nitroso-dimethylamine in rat liver DNA.

Sprague Dawley male rats were treated with N-nitroso-dimethylamine and the damage induced in liver DNA was investigated using the in vivo DNA alkaline elution assay. Determination of the number of single stranded breaks after different incubation periods in alkali showed that most of them (approximately equal to 95%) were alkali-labile sites, with a half-life of about 33 min, as expected for apurinic sites. The extent of DNA methylation was calculated, by assuming depurination of N-7-methylguanine to be the rate-limiting step for breakdown of DNA. The amount of DNA fragmentation observed accounted for only one fifth of N-7-methylguanine. The calculation could be made to correspond to the extent of methylation determined experimentally, by assuming the occurrence of a fast repair in vivo of apurinic sites (t1/2 approximately equal to 18 min). Our hypothesis of a fast repair of apurinic sites is in agreement with the analysis of data of Peterson et al. (1974). Moreover, the rate of repair required by the level of spontaneous depurination of normal guanine at neutral pH and 37 degree C, agrees satisfactorily with our estimations.

Animals↗

Sensitization of human glioblastoma T98G cells to VP16 and VM26 by human tumor necrosis factor.

The effect of Tumor Necrosis Factor (TNF) on VP16 or VM26 cytotoxicity was studied in a human glioblastoma cell line T98G, which expresses TNF-receptors. Although T98G cells did not produce TNF endogenously they were resistant to the cytolytic effect of TNF. T98G cells were also moderately sensitive to the action of VP16 or VM26. TNF given at 1000 U/ml was able to increase the cell drug-sensitivity significantly. This effect was due to an increase in the VP 16-induced cleavable-complexes by TNF. These findings suggest that TNF specifically sensitizes human glioma T98G cells to the effects of VP 16 of VM26.

DNA Damage↗

Effect of granulocyte-macrophage colony-stimulating factor on growth of a xenotransplanted human ovarian cancer cell line IGROV-1 in nude mice.

The clonal growth of cell lines derived from human ovarian tumours can be stimulated by GM-CSF in vitro. Among these cell lines one of the most responsive is the IGROV-1 cell line. This report describes the influence of GM-CSF on the in vivo growth of IGROV-1 cell xenografts in nude mice. Beginning one day after transplantation of the tumour, the cytokine was administered daily for 31 consecutive days as i.m. injections distant from the tumour lesion at doses of 0.1 microgram/kg and 1 microgram/kg. GM-CSF caused no significant effects on the growth modulation of the ovarian cancer cells in vivo.

Animals↗