Browsing by Author "Santos, MJ"

Now showing 1 - 7 of 7
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    Fanconi anemia lymphocytes
    (2001) Pincheira, J; Bravo, M; Santos, MJ; de la Torre, C; López-Sáez, JF
    The high frequency of chromosomal breaks in Fanconi anemia (FA) lymphocytes has been related to the increased oxidative damage shown by these cells,
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    G2 repair and chromosomal damage in lymphocytes from workers occupationally exposed to low-level ionizing radiation
    (1999) Pincheira, J; López, I; Sanhueza, S; Ferruz, P; Navarrete, MH; Santos, MJ; López-Sáez, JF
    The effect of the G(2) repair of chromosomal damage in lymphocytes from workers exposed to low levels of X- or gamma-rays was evaluated, Samples of peripheral blood were collected from 15 radiation workers, 20 subjects working in radiodiagnostics, and 30 healthy control donors.
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    G2 repair in Nijmegen breakage syndrome
    (1998) Pincheira, J; Bravo, M; Santos, MJ
    Lymphocytes from a patient with the Nijmegen breakage syndrome (NBS/NBS) and his parents (NBS/+) have been analyzed to identify possible disturbances in chromosomal G(2) repair. The study included the determination of G(2) duration and the analysis of the chromosomal aberration frequencies in lymphocytes with/without caffeine and cyclohexemide (CHM) treatments during G(2), under control and X-irradiated conditions. Under control conditions, NBS/NBS lymphocytes showed that the basal chromosomal damage as well as the damage detected in G(2), with caffeine treatment, and the G(2) duration were higher than cells from an age-matched control. In X-irradiated NBS/NBS lymphocytes, the basal and G(2) chromosome aberration frequencies were higher than in the controls; however, no significant differences in G(2) duration were detected between these two type of cells.
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    In vitro genotoxic evaluation of conventional bleached and biobleached softwood pulp mill effluents
    (1997) Pérez-Alzola, LP; Santos, MJ
    The effluents of pulp and paper mills contain about 300 different chemical compounds; many of them are mutagens and clastogens. Genotoxic studies have shown that chlorination stage liquors are significantly more genotoxic, in the Ames Salmonella assay, than the other process of lignin extraction, and that lyophilized effluents are genotoxic in cultured mammalian cells. Since these effluents from conventional bleaching stages are genotoxic, Chilean industries are interested in changing this process to a less toxic one, such as biobleaching using enzymes. In this study, we tested the in vitro genotoxicity of two types of effluents: an effluent obtained from a conventional radiata pine kraft-bleaching process (effluent D) and one derived from a biobleaching process with hemicellulase (effluent B). Both effluents were tested without any concentration or purification steps in the Ames Salmonella assay (TA100) and in the micronuclei (MN) and sister chromatid exchange (SCE) tests in CHO cells. The results showed that neither effluent induced base pair substitution mutations in the Ames Salmonella assay, and neither increased the micronucleus frequency in CHO cells. But, both increased the SCE frequencies in CHO cells, showing that this assay is more sensitive than the other ones, and that the two effluents contained chemical compounds in amounts enough to induce in vitro genotoxicity measured by the SCE induction. (C) 1997 Elsevier Science B.V.
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    Peroxisomal ghosts are intracellular structures distinct from lysosomal compartments in Zellweger Syndrome: A confocal laser scanning microscopy study
    (2000) Santos, MJ; Henderson, SC; Moser, AB; Moser, HW; Lazarow, PB
    Peroxisome ghosts are aberrant peroxisomal structures found in cultured skin fibroblasts from patients affected by Zellweger Syndrome (ZS), a genetic disorder of peroxisomal assembly. They contain peroxisomal integral membrane proteins (PxIMPs) and they lack most of the matrix enzymes that should be inside the organelle (Santos et al., Science 239 (1988) 1536-1538). Considerable evidence indicates that these ghosts result from genetic defects in the cellular machinery for importing newly-synthesized peroxisomal proteins into the organelle. In contrast to these observations, (Heikoop et al., Eur. J. Cell Biol. 57 (1992) 165-171) report that in Zellweger Syndrome, peroxisomal membranes are located within lysosomes and/or contain lysosomal enzymes. We have undertaken a more detailed and systematic investigation of this matter, employing confocal laser scanning microscopy (CLSM). In fibroblasts derived from ZS patients belonging to different complementation groups, peroxisomes were labeled with antibodies against PxIMPs and lysosomes were labeled with an antibody against a lysosome associated membrane protein (LAMP-2) or with LysoTracker. The results unambiguously demonstrated no appreciable colocalization of PxIMPs and LAMPs (or LysoTracker), indicating that peroxisomal ghosts are distinct subcellular structures, occupying separate subcellular locations. (C) 2000 Editions scientifiques et medicales Elsevier SAS.
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    Peroxisomal proliferation protects from β-amyloid neurodegeneration
    (2005) Santos, MJ; Quintanilla, RA; Toro, AS; Grandy, R; Dinamarca, MC; Godoy, JA; Inestrosa, NC
    Alzheimer disease is a neurodegenerative process that leads to severe cognitive impairment as a consequence of selective death of neuronal populations. The molecular pathogenesis of Alzheimer disease involves the participation of the beta-amyloid peptide (A beta) and oxidative stress. We report here that peroxisomal proliferation attenuated A beta-dependent toxicity in hippocampal neurons. Pretreatment with Wy-14.463 (Wy), a peroxisome proliferator, prevent the neuronal cell death and neuritic network loss induced by the A beta peptide. Moreover, the hippocampal neurons treated with this compound, showed an increase in the number of peroxisomes, with a concomitant increase in catalase activity. Additionally, we evaluate the Wy protective effect on beta-catenin levels, production of intracellular reactive oxygen species, cytoplasmic calcium uptake, and mitochondrial potential in hippocampal neurons exposed to H2O2 and A beta peptide. Results show that the peroxisomal proliferation prevents beta-catenin degradation, reactive oxygen species production, cytoplasmic calcium increase, and changes in mitochondrial viability. Our data suggest, for the first time, a direct link between peroxisomal proliferation and neuroprotection from A beta-induced degenerative changes.
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    Subcellular localization of catalase in sea urchin (Tetrapigus niger) gametes
    (1997) Figueroa, C; Kawada, ME; Munizaga, A; González, S; Barros, C; Koenig, C; Santos, MJ
    Peroxisomes are essential subcellular organelles that appear to be derived from pre existing organelles. To test the presence of peroxisomes in sea urchin (Tetrapigus niger) sperm and eggs, we performed biochemical and morphological experiments to evaluate the subcellular distribution of catalase as the typical peroxisomal marker. In sea urchin sperm, we found that catalase is localized in the cell cytosol. In contrast, sea urchin eggs contain sedimentable catalase, presumably contained in peroxisome-like structures detected by immunomicroscopy and by cytochemistry. Our results show, for the first time, evidence for the presence of peroxisome-like structures in sea urchin eggs and provide evidence for the peroxisome biogenesis hypothesis by division of preexisting organelles. (C) 1997 Elsevier Science Inc.