Mitochondria, oxygen free radicals, and apoptosis Journal Articles

abstract

• AbstractReactive oxygen species (ROS) generated by mitochondria are produced as by‐products of normal oxidative metabolism. The fate of these species is governed by a number of factors that vary from tissue to tissue in mammals and may be involved in the pathogenesis of disease. Reactive oxygen species are also invoked as agents that are important in the processes which become active in cells undergoing apoptosis. Integration of knowledge surrounding these different aspects of ROS generation is difficult and reveals considerable gaps in our understanding. © 2001 Wiley‐Liss, Inc.

authors

• Raha, Sandeep
• Robinson, Brian H

status

• published 

publication date

• March 2001

has subject area

• 0604 Genetics (FoR)
• 1103 Clinical Sciences (FoR)
• Animals (MeSH)
• Apoptosis (MeSH)
• Carrier Proteins (MeSH)
• Cytochrome c Group (MeSH)
• Electron Transport (MeSH)
• Free Radicals (MeSH)
• Genes, p53 (MeSH)
• Humans (MeSH)
• Membrane Proteins (MeSH)
• Mice (MeSH)
• Mitochondria (MeSH)
• Models, Biological (MeSH)
• Oxygen (MeSH)
• Reactive Oxygen Species (MeSH)
• Superoxides (MeSH)

published in

• American Journal of Medical Genetics, Part A  Journal

keywords

• Animals
• Apoptosis
• Carrier Proteins
• Cytochrome c Group
• Electron Transport
• Free Radicals
• Genes, p53
• Humans
• Membrane Proteins
• Mice
• Mitochondria
• Models, Biological
• Oxygen
• Reactive Oxygen Species
• Superoxides

Digital Object Identifier (DOI)

• 10.1002/ajmg.1398

PubMed ID

• 11579426

start page

• 62

end page

• 70

volume

• 106

issue

• 1