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T Chavarría

Publications and source records attributed to T Chavarría.

3 recordsLinked to original sources

Homocysteine inhibits the proliferation and invasive potential of HT-1080 human fibrosarcoma cells.

The impairment of homocysteine metabolism has been related to several disorders and diseases. Recently, homocysteine has been shown to inhibit key steps of angiogenesis, including endothelial cell proliferation, invasion, and remodeling of the extracellular matrix. Since these are also key steps in tumor invasion and metastasis, it can be hypothesized that homocysteine can also interfere in these processes. Therefore, we studied the effects of homocysteine on tumor proliferation and invasion, as well as on urokinase, a key extracellular matrix-degrading protease, using a model human tumor cell line. This study demonstrates that, in fact, homocysteine inhibits HT-1080 proliferation and invasion, and is a potent inhibitor of tumor cell urokinase expression.

Cell Division↗

Histamine prevents polyamine accumulation in mouse C57.1 mast cell cultures.

The effects of histamine on polyamine uptake and metabolism was studied in a mouse mast cell line (C57.1), as a cell model in which both biogenic amines are important for maintaining cell function and viability. Results obtained after incubations with exogenous histamine indicated that histamine prevents polyamine accumulation by affecting polyamine uptake. A plasma membrane transport system for polyamines has been also studied in mast cells. It seems to be a Na(+)-dependent uptake with high affinity for both spermine and spermidine and lower affinity for putrescine and agmatine. Polyamine uptake was reduced in both cells treated with exogenous histamine and histamine-preloaded cells. However, ornithine decarboxylase activity and cell proliferation were not affected by histamine. Incubation with histamine enhanced the spermidine/spermine acetyl transferase induction caused by N(1)-ethyl-N(11)-[(cyclopropyl)methyl]-4,8-diazaundecane, suggesting that polyamine acetylation could be another mechanism by which histamine prevents polyamine accumulation in C57.1 mast cells.

Acetyltransferases↗

DNA-chlorpheniramine interaction studied by spectroscopic techniques.

It was previously studied that the antihistaminic chlorpheniramine elicits a biphasic response on cell growth and regulates polyamine metabolism, as described for polyamines. In part, polyamine effects on macromolecular synthesis and cell growth are attributed to nucleic acid:polyamine interactions. In this work, we have tested the hypothesis of a DNA:chlorpheniramine interaction, using fluorometry, FTIR and Raman spectroscopic techniques. The results indicate that DNA:chlorpheniramine interaction occurs inducing conformational changes in the macromolecule by affecting both phosphodiester bonds and bases. Results open new perspectives for characterization of action mechanisms of natural or synthetic diamines with pharmacological or physiological importance.

Chlorpheniramine↗