Comparison between the antiproliferative effect and intracellular glutathione depletion induced by Casiopeína IIgly and cisplatin in murine melanoma B16 cells

Alemón-Medina, Radamés; Bravo-Gómez, María Elena; Gracia-Mora, María Isabel; Ruíz-Azuara, Lena

doi:10.1016/j.tiv.2011.02.007

Cited by 32 publications

(20 citation statements)

References 43 publications

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“…Furthermore, the proportion of cells in S‐phase was significantly increased in HEMA‐exposed cells, but not in BSO‐treated cells. The role of glutathione in cell proliferation is reported to be of importance to the control of tumour growth, and glutathione depletion is a desired effect of several anticancer drugs . However, the different pattern of cell growth and cell death after exposure to HEMA and BSO argues that glutathione depletion alone is the cause of these HEMA‐induced changes.…”

Section: Discussionmentioning

confidence: 99%

Cell toxicity of 2‐hydroxyethyl methacrylate (HEMA): the role of oxidative stress

Morisbak

Ansteinsson

Samuelsen

2015

European J Oral Sciences

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2-Hydroxyethyl methacrylate (HEMA) is a methacrylate monomer used in polymer-based dental-restorative materials. In this study, the viability of human lung epithelial cells, BEAS-2B, was investigated after exposure to this monomer. Exposure to HEMA reduced the viability of the BEAS-2B cells as a result of increased apoptosis, interruption of the cell cycle, and decreased cell proliferation. Depletion of cellular glutathione and increased levels of reactive oxygen species (ROS) were seen after exposure of BEAS-2B cells to HEMA. The glutathione synthase inhibitor, L-buthioninesulfoximine (BSO), was used to study whether the reduced viability was caused by glutathione depletion and increased levels of ROS. Similarly to incubation with HEMA, incubation with BSO resulted in glutathione depletion and increased ROS levels, without increasing cell death or inhibiting cell growth. The results indicate that HEMA-induced cell damage is not caused exclusively by these mechanisms. Mechanisms other than glutathione depletion and ROS formation seem to be of importance for the toxic effect of HEMA on lung epithelial cells.

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Section: Discussionmentioning

confidence: 99%

Cell toxicity of 2‐hydroxyethyl methacrylate (HEMA): the role of oxidative stress

Morisbak

Ansteinsson

Samuelsen

2015

European J Oral Sciences

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“…atom whose reduction from Cu (II) to Cu (I) generates multiple reactive oxygen species including hydroxyl and superoxide (Trejo-Solís et al 2005). These radicals are probably the main factors leading to apoptosis in the cells exposed to antitumoral molecules (De Vizcaya-Ruiz et al 2000;Carvallo-Chaigneau et al 2008;Alemón-Medina et al 2011). Nevertheless, the precise mechanism(s) of action for each Cas is still poorly understood and a detailed description of the events that lead to cell death remains unexplained.…”

Section: Electronic Supplementary Materialsmentioning

confidence: 99%

The metal-coordinated Casiopeína IIIEa induces the petite-like phenotype in Saccharomyces cerevisiae

López-Rodríguez

Cárabez-Trejo²,

Rosas-Sanchez³

et al. 2011

Biometals

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The Casiopeínas® are mixed chelate copper (II) complexes and promising antineoplastics agents against cancer cells and tumors in vitro and in vivo. However, the action mode of these compounds is poorly characterized. In this work the effect of the antineoplastic Casiopeína IIIEa on the metabolism and ultrastructure of the yeast Saccharomyces cerevisiae was investigated. Exposure of cells growing in rich or in low-iron medium to 5 μM of the compound decreased duplication time and reduced oxygen consumption. Those cells formed smaller colonies when growing in a non-fermentable carbon source and low-iron medium, and under the light microscope, multiple folds were observed along the plasma membrane accompanied with a reduction in the diameter of the yeast. These observations were confirmed under the electron microscope, which also revealed a slight reduction of the mitochondrial size. A correlation was found with smaller colonies exhibiting lower rates of oxygen consumption, and yeast labelled with fluorescent MitoTracker(TM) consistently exhibited reduced mitochondrial activity. It appears that Casiopeína IIIEa gives rise to smaller yeast and petite-like colonies by reducing the mitochondrial respiratory activity without significantly affecting the mitochondrial structure.

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“…Nevertheless, apoptosis might be the result of several processes acting alone or in concomitance. The evidence supports three main targets: a) generation of reactive oxygen species (ROS) [16,23,24] with DNA oxidation and degradation [16,25], plus depletion of antioxidant defenses like GSH as consequence [24,26,27], b) mitochondrial toxicity [28,29] or c) DNA damage through direct interaction with complex by an intercalative or non intercalative mechanism [23,[30][31][32]. The mechanism of action is not fully understood and more work will be performed in this area in order to identify the main signals; however, it is important to highlight that several mechanism are possible and they are not mutually exclusive.…”

Section: Introductionmentioning

confidence: 99%

Antineoplastic Evaluation of Two Mixed Chelate Copper Complexes (Casiopeínas®) in HCT-15 Xenograft Model

Paz

Gracia-Mora

2017

J. Mex. Chem. Soc.

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Casiopeínas® is a family of copper complexes with the general formulae [Cu(N-N)(N-O)]NO3 and [Cu(N-N)(O-O)]NO3; where N-N = substituted aromatic diimine (2,2’-bipyridine (bipy) or 1,10-phenanthroline (phen)); N-O = α-aminoacidate or a peptide; and O-O = acetylacetonate (acac) or salicylaldehydate. These compounds have shown antiproliferative activity in vitro and antitumor activity in several mouse models with promissory results. Efforts have been done in order to understand the role played by ligands in the biological activity. With the aim of finding out the effect of secondary ligand (N-O or O-O), two of the most active complexes in vitro assays were selected to perform in vivo study on HCT-15 colon adenocarcinoma xenograft model. Both complexes, [Cu(3,4,7,8-tetramethyl-1,10-phen anthroline)(glycinato)]NO3 (1) and [Cu(3,4,7,8-tetramethyl-1,10-phenanthroline)(acetylacetonato)]NO3 (2) share the same diimine ligand and the secondary ligand changes from glycinate (gly) to acac. Results show that 2 is effective to reduce tumor size but 1 does not achieve the values required according to protocols, revealing an important difference between compounds attributable to change of ligand from gly to acac.

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Comparison between the antiproliferative effect and intracellular glutathione depletion induced by Casiopeína IIgly and cisplatin in murine melanoma B16 cells

Cited by 32 publications

References 43 publications

Cell toxicity of 2‐hydroxyethyl methacrylate (HEMA): the role of oxidative stress

Cell toxicity of 2‐hydroxyethyl methacrylate (HEMA): the role of oxidative stress

The metal-coordinated Casiopeína IIIEa induces the petite-like phenotype in Saccharomyces cerevisiae

Antineoplastic Evaluation of Two Mixed Chelate Copper Complexes (Casiopeínas®) in HCT-15 Xenograft Model

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