![]() |
|
|
Genotoxicity of anticancer drugs in eukaryotic cells The effect of chemical mutagens (bleomycin, streptonigrin and streptozotocin) on human and animal chromosomes as well as the mechanisms involved in the production of chromosome damage by these agents are the main research lines currently under study in this Laboratory. Related projects are: > Analysis of incomplete chromosome elements and excess acentric fragments induced by chemical mutagens in mammalian cells using a telomeric PNA probe : Fluorescence in situ hybridization (FISH) with a telomeric peptide nucleic acid (PNA) probe is employed to analyze the induction of incomplete chromosome elements (ICE, i.e., unjoined or "open" chromosome elements with telomeric signal at only one end) and excess acentric fragments (i.e., excess of fragments resulting from the formation of dicentric and ring chromosomes) by the chemical mutagens bleomycin, streptonigrin and streptozotocin in mammalian cells. > Analysis of spontaneous and mutagen-induced chromosome damage in flight personnel of Argentina . > Effect of thiol compounds on the DNA and chromosome damage induced by bleomycin in human cells : The aim of this project is to determine whether thiol compounds of different electric charge and size modulate genetic damage induced by the antitumor antibiotic bleomycin (BLM). BLM is a radiomimetic agent acting through oxygen free radical formation; hence, thiol compounds from the cellular antioxidant defensive system may be involved in the modulation of such damage. > Possible mechanisms of resistance to cisplatin (CDDP) mediated by thiol compounds : CDDP is an anticarcinogenic agent which produces cytotoxicity by forming DNA adducts. Some cancer patients show natural or acquired resistance to this drug. An increase in the cellular concentration of some thiol compounds may determine part of such resistance. The main objective of this project is to determine whether the increase in concentration of cellular thiol compounds as glutathione produces the increase of cell survival and decrease in the adduct frequency by cisplatin in human lymphoblastoid cells.
Staff BOLZÁN, Alejandro Daniel, Investigador Independiente CONICET - Jefe de Laboratorio |
|