Genotoxicants target distinct molecular networks in neonatal neurons.

BACKGROUND: Exposure of the brain to environmental agents during critical periods of neuronal development is considered a key factor underlying many neurologic disorders. OBJECTIVES: In this study we examined the influence of genotoxicants on cerebellar function during early development by measuring...

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Publicado en:Environmental Health Perspectives Vol. 114; no. 11; pp. 1703 - 1713
Autores principales: Kisby GE, Olivas A, Standley M, Lu X, Pattee P, O'Malley J, Li X, Muniz J, Nagalla SR
Formato: Journal Article
Publicado: National Institute of Environmental Health Sciences Nov2006
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Nov2006
      vid: 114
      iid: 11
      pid: 56539
      pub: National Institute of Environmental Health Sciences
      place: Research Triangle Park, North Carolina
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        2009341481
        10.1289/ehp.9073
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        atl: Genotoxicants target distinct molecular networks in neonatal neurons.
      aug:
        au:
          Kisby GE
          Olivas A
          Standley M
          Lu X
          Pattee P
          O'Malley J
          Li X
          Muniz J
          Nagalla SR
      sug:
        subj:
          Alkylating Agents
          Animals
          Carcinogens
          Neurons Drug Effects
          Nitrogen Mustard Compounds
          Biochips
          Cell Physiology Drug Effects
          Cells Drug Effects
          Cells
          Cerebellum
          DNA
          Genetic Techniques
          Mice
          Neurons Metabolism
      ab: BACKGROUND: Exposure of the brain to environmental agents during critical periods of neuronal development is considered a key factor underlying many neurologic disorders. OBJECTIVES: In this study we examined the influence of genotoxicants on cerebellar function during early development by measuring global gene expression changes. METHODS: We measured global gene expression in immature cerebellar neurons (i.e., granule cells) after treatment with two distinct alkylating agents, methylazoxymethanol (MAM) and nitrogen mustard (HN2). Granule cell cultures were treated for 24 hr with MAM (10-1,000 microM) or HN2 (0.1-20 microM) and examined for cell viability, DNA damage, and markers of apoptosis. RESULTS: Neuronal viability was significantly reduced (p < 0.01) at concentrations > 500 microM for MAM and > 1.0 microM for HN2; this correlated with an increase in both DNA damage and markers of apoptosis. Neuronal cultures treated with sublethal concentrations of MAM (100 microM) or HN2 (1.0 microM) were then examined for gene expression using large-scale mouse cDNA microarrays (27,648). Gene expression results revealed that a) global gene expression was predominantly up-regulated by both genotoxicants; b) the number of down-regulated genes was approximately 3-fold greater for HN2 than for MAM; and c) distinct classes of molecules were influenced by MAM (i.e, neuronal differentiation, the stress and immune response, and signal transduction) and HN2 (i.e, protein synthesis and apoptosis). CONCLUSIONS: These studies demonstrate that individual genotoxicants induce distinct gene expression signatures. Further study of these molecular networks may explain the variable response of the developing brain to different types of environmental genotoxicants.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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