TY - CHAP
T1 - Neuroinflammation and oxidative injury in developmental neurotoxicity
AU - Milatovic, Dejan
AU - Zaja-Milatovic, Snjezana
AU - Brockett, Mirjana Milosevic
AU - Breyer, Richard M.
AU - Aschner, Michael
AU - Montine, Thomas J.
N1 - Publisher Copyright:
© 2022 Elsevier Inc. All rights reserved.
PY - 2022/1/1
Y1 - 2022/1/1
N2 - 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 are associated with increased levels of prostaglandins (PGs), particularly PGE2. The 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.
AB - 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 are associated with increased levels of prostaglandins (PGs), particularly PGE2. The 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.
KW - Developmental neurotoxicity
KW - Neuroinflammation
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=85131497658&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85131497658&partnerID=8YFLogxK
U2 - 10.1016/B978-0-323-89773-0.00056-4
DO - 10.1016/B978-0-323-89773-0.00056-4
M3 - Chapter
AN - SCOPUS:85131497658
SN - 9780323915601
SP - 1129
EP - 1140
BT - Reproductive and Developmental Toxicology
PB - Elsevier
ER -