Apoptosis and free radicals.
Necrotic cell death is usually a consequence of extensive insult to the cell, leading to release of intracellular contents and an inflammatory response. Apoptosis, however, is a physiological response to damaging influences that requires sufficient maintenance of homeostasis to allow execution of the pathway. Apoptosis circumvents the induction of an inflammatory response, which can be disadvantageous and, therefore, would be more beneficial than necrosis under many circumstances. The apoptotic response appears complicated and involves many factors, including the mitotic rate, the stage of differentiation, the type and strength of the initiating stimulus, and exogenous factors. Recent evidence, however, implicates free radicals as a causal agent in some types of apoptosis, both physiologically and pathologically.
Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
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Wood
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Youle
D000818:Animals; D017209:Apoptosis; D002490:Central Nervous System / Q000473:pathology / Q000502:physiology*; D003907:Dexamethasone / Q000494:pharmacology; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D009336:Necrosis; D009474:Neurons / Q000166:cytology* / Q000473:pathology / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013950:Thymus Gland / Q000166:cytology / Q000648:ultrastructure
D005609:Free Radicals; D017382:Reactive Oxygen Species; D003907:Dexamethasone