No

Cell Death

Figure 3 Diagram of pathways for free radical generation after subarachnoid hemorrhage. Source: From Ref. 16.

of DNA and mitochondria are other consequences of oxidative stress that have been implicated in the etiology of cerebral vasospasm after SAH (94). Lipid peroxidation, in particular, brings about the activation of membrane phospholipase A2, release of arachidonic acid (AA), intercellular accumulation of diacylglycerol, and activation of protein kinase C (95,96).

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