首页   按字顺浏览 期刊浏览 卷期浏览 Redox Regulation of Programmed Cell Death in Lymphocytes
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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