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Arachidonic Acid‐Induced Oxidative Injury to Cultured Spinal Cord Neurons
Author(s) -
Toborek Michal,
Malecki Andrzej,
Garrido Rosario,
Mattson Mark P.,
Hennig Bernhard,
Young Byron
Publication year - 1999
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.1471-4159.1999.0730684.x
Subject(s) - oxidative stress , arachidonic acid , spinal cord , intracellular , chemistry , glutathione , viability assay , calcium in biology , fatty acid , neuroprotection , calcium , spinal cord injury , endocrinology , medicine , biochemistry , biology , cell , neuroscience , enzyme
: Spinal cord trauma can cause a marked release of free fatty acids, in particular, arachidonic acid (AA), from cell membranes. Free fatty acids, and AA by itself, may lead to secondary damage to spinal cord neurons. To study this hypothesis, cultured spinal cord neurons were exposed to increasing concentrations of AA (0.01‐10 μ M ). AA‐induced injury to spinal cord neurons was assessed by measurements of cellular oxidative stress, intracellular calcium levels, activation of nuclear factor‐κB (NF‐κB), and cell viability. AA treatment increased cell intracellular calcium concentrations and decreased cell viability. Oxidative stress increased significantly in neurons exposed to 1 and 10 μ M AA. In addition, AA treatment activated NF‐κB and decreased levels of the inhibitory subunit, IκB. It is interesting that manganese superoxide dismutase protein levels and levels of intracellular total glutathione increased in neurons exposed to this fatty acid for 24 h, consistent with a compensatory response to increased oxidative stress. These results strongly support the hypothesis that free fatty acids contribute to the tissue injury observed following spinal cord trauma.