Oxygen Toxicity Induces Apoptotic Neuronal Death in Cultured Rat Hippocampal Neurons
Oxygen metabolism is the most important event for the aerobic energy metabolism and the redox-based biosynthesis. This means that cells are constantly exposed to oxidative stress during their life. As a consequence of a normal aerobic metabolism, several oxidants such as O 2 − , H2O2 and ·OH are produced by successive additions of electrons to O2. These byproducts cause ubiquitous cell damage and are thought to contribute to aging and to degenerative diseases (Ames, et al., 1993). It is well-known that the brain is one of the most energy consuming organs in mammalian body and exclusively depends on aerobic energy metabolism using oxygen and glucose. Thus, the oxygen molecule is not only an indispensable material for highly organized CNS activities but also a cytotoxic agent which constantly brings oxidative stresses to neurons during their long life without division. In addition, the brain readily undergoes oxidative damage as a result of cerebrovascular injury such as ischemia and this causes neuronal degeneration and death. Since mature neurons can not regenerate, once the survived neurons degenerate, neuronal activity is irreversibly declined. Thus, elucidation of the protection machinery of neuronal cells against oxidative damage is not only an important clue to understand the mechanism(s) of postmitotic neurons to be long-lived but also should provide useful information to design the cure for a number of neurological pathologies.
KeywordsNerve Growth Factor Hippocampal Neuron Neuronal Death Oxygen Atmosphere Oxygen Toxicity
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