Document Detail


Reactive oxygen species: from health to disease.
MedLine Citation:
PMID:  22903797     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Upon reaction with electrons, oxygen is transformed into reactive oxygen species (ROS). It has long been known that ROS can destroy bacteria and destroy human cells, but research in recent decades has highlighted new roles for ROS in health and disease. Indeed, while prolonged exposure to high ROS concentrations may lead to non-specific damage to proteins, lipids, and nucleic acids, low to intermediate ROS concentrations exert their effects rather through regulation of cell signalling cascades. Biological specificity is achieved through the amount, duration, and localisation of ROS production. ROS have crucial roles in normal physiological processes, such as through redox regulation of protein phosphorylation, ion channels, and transcription factors. ROS are also required for biosynthetic processes, including thyroid hormone production and crosslinking of extracellular matrix. There are multiple sources of ROS, including NADPH oxidase enzymes; similarly, there are a large number of ROS-degrading systems. ROS-related disease can be either due to a lack of ROS (e.g., chronic granulomatous disease, certain autoimmune disorders) or a surplus of ROS (e.g., cardiovascular and neurodegenerative diseases). For diseases caused by a surplus of ROS, antioxidant supplementation has proven largely ineffective in clinical studies, most probably because their action is too late, too little, and too non-specific. Specific inhibition of ROS-producing enzymes is an approach more promising of clinical efficacy.
Authors:
K Brieger; S Schiavone; Jr Miller; Kh Krause
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-8-17
Journal Detail:
Title:  Swiss medical weekly     Volume:  142     ISSN:  1424-3997     ISO Abbreviation:  Swiss Med Wkly     Publication Date:  2012  
Date Detail:
Created Date:  2012-8-20     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100970884     Medline TA:  Swiss Med Wkly     Country:  -    
Other Details:
Languages:  ENG     Pagination:  0     Citation Subset:  -    
Affiliation:
Department of Pathology and Immunology, University of Geneva Faculty of Medicine and Department of Genetic and Laboratory Medicine, Geneva University Hospitals, Switzerland; katharine.brieger@unige.ch.
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