Neuroinflammation and oxidative injury in developmental neurotoxicity

Dejan Milatovic, Snjezana Zaja-Milatovic, Richard M. Breyer, Michael Aschner, Thomas J. Montine

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations

Abstract

Neuroinflammation is a complex response to brain injury involving the activation of glia, release of inflammatory mediators, such as cytokines and chemokines, and generation of reactive oxygen and nitrogen species. Inflammatory responses in the brain also are associated with increased levels of prostaglandins (PGs), particularly PGE2. PGE2 signaling is mediated by interactions with four distinct G protein-coupled receptors, EP1, EP2, EP3, and EP4, which are differentially expressed on neuronal and glial cells throughout the central nervous system. Elevated PGE2 and inflammatory mediators are also inherent to the aging brain. An increased state of neuroinflammation renders the aged brain more vulnerable to the disruptive effects of both intrinsic and extrinsic factors such as disease, infection, toxicants, or stress. This chapter characterizes processes of neuroinflammation and related oxidative injury and discusses neuroinflammatory changes associated with aging.

Original languageEnglish (US)
Title of host publicationReproductive and Developmental Toxicology
PublisherElsevier
Pages1051-1061
Number of pages11
ISBN (Electronic)9780128042397
DOIs
StatePublished - Jan 1 2017

Keywords

  • Developmental neurotoxicity
  • Neuroinflammation
  • Oxidative stress
  • Oxidative stress biomarkers

ASJC Scopus subject areas

  • Medicine(all)

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  • Cite this

    Milatovic, D., Zaja-Milatovic, S., Breyer, R. M., Aschner, M., & Montine, T. J. (2017). Neuroinflammation and oxidative injury in developmental neurotoxicity. In Reproductive and Developmental Toxicology (pp. 1051-1061). Elsevier. https://doi.org/10.1016/B978-0-12-804239-7.00055-X