Literature DB >> 23653222

Generation of hydrogen peroxide-resistant murine neuroblastoma cells: a target discovery platform for novel neuroprotective genes.

Annette E Maczurek1, Rebekka Wild, Daunia Laurenti, Megan L Steele, Lezanne Ooi, Gerald Münch.   

Abstract

Oxidative stress has been suggested to play an important role in the pathogenesis of various neurodegenerative diseases including Alzheimer's disease (AD). Hydrogen peroxide (H2O2), one of the main reactive oxygen species, is converted into the highly toxic ·OH radical in the presence of redox-active transition metals, which then oxidises nucleic acids, lipids and proteins, leading to neurodegeneration and cell death. There is an urgent need to gain more knowledge about relevant therapeutic targets to combat oxidative stress and it neurotoxic effects, and how this knowledge can be utilized to develop novel neuroprotective therapies for AD. One way to identify new mechanisms combating oxidative stress was via the creation of H2O2-resistant cell lines and identification of the mechanisms responsible for their resistance. However, in most cases catalase overexpression or increased glutathione content was identified as the primary mode of H2O2 resistance in these cell lines. In this study, we have generated six different resistant neuronal cell lines or populations (from the same original murine Neuro2a neuroblastoma line) by exposing cells to increasing concentrations of H2O2 and performing continuous selection for survivors over a period of several months, which appear to have acquired H2O2 resistance based on other, novel mechanisms. These six populations showed a significant, but differential resistance against H2O2 when compared with the parental cell line. Using combinations of catalase-, glutathione synthesis- and glutathione peroxidase-inhibitors it was shown that the increased resistance of Neuro2a-HR cells is not solely based on an increased activity of catalase or the glutathione system, suggesting that their resistance might be based on yet unknown, novel defence mechanisms.

Entities:  

Mesh:

Substances:

Year:  2013        PMID: 23653222     DOI: 10.1007/s00702-013-0995-z

Source DB:  PubMed          Journal:  J Neural Transm (Vienna)        ISSN: 0300-9564            Impact factor:   3.575


  23 in total

Review 1.  Optimizing reduced-intensity conditioning regimens for myeloproliferative neoplasms.

Authors:  Aravind Ramakrishnan; Brenda M Sandmaier
Journal:  Expert Rev Hematol       Date:  2010-02-01       Impact factor: 2.929

2.  The expression of key oxidative stress-handling genes in different brain regions in Alzheimer's disease.

Authors:  M Y Aksenov; H M Tucker; P Nair; M V Aksenova; D A Butterfield; S Estus; W R Markesbery
Journal:  J Mol Neurosci       Date:  1998-10       Impact factor: 3.444

3.  Involvement of glutathione peroxidase and catalase in the disposal of exogenous hydrogen peroxide by cultured astroglial cells.

Authors:  R Dringen; B Hamprecht
Journal:  Brain Res       Date:  1997-06-06       Impact factor: 3.252

4.  Increased peroxidation and reduced antioxidant enzyme activity in Alzheimer's disease.

Authors:  D L Marcus; C Thomas; C Rodriguez; K Simberkoff; J S Tsai; J A Strafaci; M L Freedman
Journal:  Exp Neurol       Date:  1998-03       Impact factor: 5.330

Review 5.  Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteins.

Authors:  D A Butterfield; J Kanski
Journal:  Mech Ageing Dev       Date:  2001-07-15       Impact factor: 5.432

6.  Elevated thiobarbituric acid-reactive substances and antioxidant enzyme activity in the brain in Alzheimer's disease.

Authors:  M A Lovell; W D Ehmann; S M Butler; W R Markesbery
Journal:  Neurology       Date:  1995-08       Impact factor: 9.910

Review 7.  Glutathione metabolism during aging and in Alzheimer disease.

Authors:  Honglei Liu; Hong Wang; Swapna Shenvi; Tory M Hagen; Rui-Ming Liu
Journal:  Ann N Y Acad Sci       Date:  2004-06       Impact factor: 5.691

8.  Advanced glycation end products contribute to amyloidosis in Alzheimer disease.

Authors:  M P Vitek; K Bhattacharya; J M Glendening; E Stopa; H Vlassara; R Bucala; K Manogue; A Cerami
Journal:  Proc Natl Acad Sci U S A       Date:  1994-05-24       Impact factor: 11.205

Review 9.  Amyloid beta-protein toxicity and oxidative stress in Alzheimer's disease.

Authors:  C Behl
Journal:  Cell Tissue Res       Date:  1997-12       Impact factor: 5.249

10.  Inhibition of glycogen synthase kinase 3 beta is involved in the resistance to oxidative stress in neuronal HT22 cells.

Authors:  Monika Schäfer; Sharon Goodenough; Bernd Moosmann; Christian Behl
Journal:  Brain Res       Date:  2004-04-16       Impact factor: 3.252

View more
  1 in total

1.  Benzothiazole aniline tetra(ethylene glycol) and 3-amino-1,2,4-triazole inhibit neuroprotection against amyloid peptides by catalase overexpression in vitro.

Authors:  Amrutha Chilumuri; Mark Odell; Nathaniel G N Milton
Journal:  ACS Chem Neurosci       Date:  2013-09-09       Impact factor: 4.418

  1 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.