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Rapid Communication: Oxidative Stress Induces Apoptosis in Embryonic Cortical Neurons
Author(s) -
Ratan Rajiv R.,
Murphy Timothy H.,
Baraban Jay M.
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62010376.x
Subject(s) - dna laddering , glutathione , oxidative stress , apoptosis , microbiology and biotechnology , programmed cell death , fragmentation (computing) , biology , dna fragmentation , chromatin , glutamate receptor , dna damage , neurodegeneration , biochemistry , chemistry , dna , medicine , ecology , receptor , enzyme , disease
Glutamate‐induced glutathione depletion in immature embryonic cortical neurons has been shown to lead to oxidative stress and cell death. We have used this in vitro model to investigate the mechanism(s) by which free radicals induce neuronal degeneration. We find that glutathione depletion leads to hypercondensation and fragmentation of chromatin into spherical or irregular shapes, a morphologic signature of apoptosis. These morphologic changes are accompanied by laddering of DNA into multiple oligonucleosomal fragments and can be prevented by the antioxidants idebenone and butylated hydroxyanisole. Cell death induced by glutathione depletion can also be prevented by inhibitors of macromolecular synthesis. Taken together, these observations suggest that oxidative stress can induce apoptosis in neurons.