TY - CHAP
T1 - Alcohol, neuron apoptosis, and oxidative stress
AU - Henderson, George I.
AU - Stewart, Jennifer
AU - Schenker, Steven
N1 - Publisher Copyright:
© 2009 Springer Science+Business Media, LLC. All rights reserved.
PY - 2009
Y1 - 2009
N2 - The aim of this chapter is to present a contemporary overview of ethanol-induced apoptosis in the brain, with a focus on the potential role of oxidative stress and some new concepts related to glia-mediated neuroprotection and selective vulnerability of neurons to ethanol. While ethanol-related oxidative stress and neuron apoptotic death have been documented in the adult brain, the vast majority of reports have centered on the developing organ (Schenker et al., 1990). We address both settings and offer several potential explanations for the high sensitivity of the fetal brain to these toxic responses to ethanol. Of note is that neurotoxic responses to ethanol have been recognized for several decades yet the mechanisms underlying these often devastating effects remain controversial. The following material abundantly illustrates that the setting is multifactorial with multiple ethanol-related perturbations at play, likely with each impacting to different degrees on various brain areas as well as on different neuron and glia populations. Finally, neuron survival and functions are intimately connected to the glia with which neurons are commingled. Such interactions may often be essential to neuron survival and we include a brief overview of recent studies addressing ethanol effects on neuroprotective glia/neuron interactions.
AB - The aim of this chapter is to present a contemporary overview of ethanol-induced apoptosis in the brain, with a focus on the potential role of oxidative stress and some new concepts related to glia-mediated neuroprotection and selective vulnerability of neurons to ethanol. While ethanol-related oxidative stress and neuron apoptotic death have been documented in the adult brain, the vast majority of reports have centered on the developing organ (Schenker et al., 1990). We address both settings and offer several potential explanations for the high sensitivity of the fetal brain to these toxic responses to ethanol. Of note is that neurotoxic responses to ethanol have been recognized for several decades yet the mechanisms underlying these often devastating effects remain controversial. The following material abundantly illustrates that the setting is multifactorial with multiple ethanol-related perturbations at play, likely with each impacting to different degrees on various brain areas as well as on different neuron and glia populations. Finally, neuron survival and functions are intimately connected to the glia with which neurons are commingled. Such interactions may often be essential to neuron survival and we include a brief overview of recent studies addressing ethanol effects on neuroprotective glia/neuron interactions.
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U2 - 10.1007/978-0-387-79112-8_13
DO - 10.1007/978-0-387-79112-8_13
M3 - Chapter
AN - SCOPUS:84919840044
SN - 9780387791098
SP - 261
EP - 279
BT - Metabolic Encephalopathy
PB - Springer New York
ER -