Redox Regulation of Programmed Cell Death in Lymphocytes
作者:
ButtkeThomas M.,
SandstromPaul A.,
期刊:
Free Radical Research
(Taylor Available online 1995)
卷期:
Volume 22,
issue 5
页码: 389-397
ISSN:1071-5762
年代: 1995
DOI:10.3109/10715769509147548
出版商: Taylor&Francis
数据来源: Taylor
摘要:
A redox imbalance caused by an over-production of prooxidants or a decrease in antioxidants seems to play a role in the programmed cell death that occurs in various developmental programs. Such a physiological function for oxidative stress is particularly applicable to the immune system, wherein individual lymphocytes undergo continuous scrutiny to determine if they should be preserved or programmed to die. Following activation, lymphocytes produced increased levels of reactive oxygen species (ROS) which may serve as intracellular signaling molecules. The ultimate outcome of this increased ROS formation, i.e., lymphocyte proliferation versus programmed cell death, may be dictated by macrophage-derived costimulatory molecules that bolster or diminish lymphocyte antioxidant defenses. HIV-1-infected individuals display multiple symptoms of redox imbalance consistent with their being in oxidative stress, and lymphocytes from such individuals are more prone to undergo apoptosisin vitro. It is suggested that oxidative stress is a physiological mediator of programmed cell death in lymphoid cells, and that HIV disease represents an extreme case of what can happen when regulatory safeguards are compromised.
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