Stimulation of nuclear protein kinase activity in rat liver induced by the administration of 3,5,3'-triiodo-L-thyronine (T3).
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Biomedical subjects
Publications and source records attributed to E Fugassa.
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The induction of DNA damage on 1.5- and 24-h cultured hepatocytes was tested after a 3-h exposure to 5 and 50 microM mono-, di-, and trinitrochlorobenzene (100-00-5; 97-00-7; 88-88-0). DNA-repair synthesis, elicited by nitrochlorobenzene treatment, was also estimated 24 and 48 h after the withdrawal of the nitro-aryl halides. DNA damage and repair were evaluated by determining the DNA elution rate in alkali. A dose-related rate of DNA damage was obtained by exposure of 1.5-h-cultured hepatocytes to 5 and 50 microM nitrochlorobenzenes . DNA of 24-h-cultured cells was not affected by nitrochlorobenzene treatment. The data obtained by exposure to 5 microM methyl methanesulfonate (66-27-3) and nitrosodimethylamine (62-75-9), direct and indirect methylating agents, suggest that 24-h-cultured liver cells are still able to transform nitrosodimethylamine but not nitrochlorobenzenes . Isolated hepatocytes maintain their capability of repairing the induced DNA damage when cultured for 24 and 48 h in fresh medium. The system offers an interesting model to investigate the perturbations related to the metabolism of xenobiotics.
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The rat uterus has been shown to be a site of production of insulin-like growth factor-I (IGF-I) and multiple IGF-binding proteins (IGFBP-2, -3, -4, -5, -6) which are involved in estrogen-induced uterine proliferation. The presence of T3-receptors in rat uterus suggests a role of thyroid hormone in the regulation of uterus responses to estradiol. In this study IGF-I and IGFBP-4 mRNAs in uterus, oviduct and cervix from euthyroid, hypothyroid and T3-treated rats were quantified by Northern blot analysis. Our results demonstrate: i) a marked decrease in IGF-I and IGFBP-4 mRNA levels in the uterus but an increase in the oviduct of hypothyroid rats; ii) a marked increase in IGF-I and IGFBP-4 mRNA levels in the uterus but a net decrease in the cervix of T3-treated rats. The uterine changes in IGF-I and IGFBP-4 mRNA levels associated with hypothyroid status were in agreement with those observed in liver.
In order to better understand the role of thyroid hormones in testis development, the influence of tri-iodothyronine on protein metabolism of immature pig Sertoli cells has been investigated. Sertoli cells were isolated enzymatically from 2- to 3-week-old piglet testes and cultured in the presence or absence of tri-iodothyronine. Protein labelling was evaluated in Sertoli cell monolayers incubated in medium containing a tracer dose of [3H]leucine. The results demonstrate that thyroid hormone can directly stimulate the process of protein synthesis in immature porcine Sertoli cells, without significantly affecting the protein degradation rate; moreover thyroid hormone exposure results in a significant decrease of intracellular ATP level. The evidence that tri-iodothyronine can increase Sertoli cell protein synthesis, supplies additional evidence about the fundamental role of thyroid hormone in the regulation of growth and differentiation of the mammalian testis through a direct action on the Sertoli cells.