These are the damaging actions of free radicals and their product peroxynitrite, the actions of the Ca 2+-dependent protease calpain, the activity of phospholipases, the activity of poly-ADPribose polymerase (PARP), and the activation of the apoptotic pathway. These changes lead to the activation of five damaging events, termed perpetrators. These include inhibition (and subsequent reactivation) of electron transport, decreased ATP, decreased pH, increased cell Ca 2+, release of glutamate, increased arachidonic acid, and also gene activation leading to cytokine synthesis, synthesis of enzymes involved in free radical production, and accumulation of leukocytes. The first, the induction stage, includes several changes initiated by ischemia and reperfusion that are very likely to play major roles in cell death. The cell death process has four major stages. Death may also occur by autophagocytosis. Death also occurs via an apoptotic-like pathway that is characterized, minimally, by DNA laddering and a dependence on caspase activity and, optimally, by those properties, additional characteristic protein and phospholipid changes, and morphological attributes of apotosis. Cell death occurs by a necrotic pathway characterized by either ischemic/homogenizing cell change or edematous cell change. These are the two principal rodent models for human disease. ![]() ![]() This review is directed at understanding how neuronal death occurs in two distinct insults, global ischemia and focal ischemia.
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