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ABSTRACT: Background
Traumatic brain injury (TBI) induces arachidonic acid (ArA) release from cell membranes. ArA metabolites form a class of over 50 bioactive eicosanoids that can induce both adaptive and/or maladaptive brain responses. The dynamic metabolism of ArA to eicosanoids, and how they affect the injured brain, is poorly understood due to their diverse activities, trace levels, and short half-lives. The eicosanoids produced in the brain postinjury depend upon the enzymes present locally at any given time. Eicosanoids are synthesized by heme-containing enzymes, including cyclooxygenases, lipoxygenases, and arachidonate monoxygenases. The latter comprise a subset of the cytochrome P450 "Cyp" gene family that metabolize fatty acids, steroids, as well as endogenous and exogenous toxica
SUBMITTER: Birnie M
PROVIDER: S-EPMC3658912 | biostudies-literature | 2013 May
REPOSITORIES: biostudies-literature