Open AccessGlutathione depletion‐induced chromosomal DNA fragmentation associated with apoptosis and necrosis
Author(s) -
Higuchi Yoshihiro
Publication year - 2004
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2004.tb00470.x
Subject(s) - dna fragmentation , oxidative stress , apoptotic dna fragmentation , apoptosis , programmed cell death , necrosis , biology , reactive oxygen species , fragmentation (computing) , dna damage , glutathione , microbiology and biotechnology , chromatin , dna , biochemistry , genetics , enzyme , ecology
Chromosomal DNA and mitochondrial dysfunctions play a role on mammalian cell death induced by oxidative stress. The major biochemical dysfunction of chromosome is the presence of an ordered cleavage of the DNA backborn, which is separated and visualized as an electrophoretic pattern of fragments. Oxidative stress provides chromatin giant DNA, 200‐800 kb or 50‐300 kb high molecular weight (HMW) DNA and internucleosomal DNA fragments are produced during apoptosis or necrosis induced by oxidative stress such as gluthione (GSH) depletion in several types of mammalian cells. Reactive oxygen species (ROS)‐mediated DNA fragmentation is Mitochondrial dysfunction on decrease of trans membrane potential, accumulation of ROS, membrane permeability transition transition and release of apoptotic factors during apoptosis or necrosis has been implicated. This review refers to the correlation of chromo‐somal DNA fragmentation and apoptosis or necrosis induced by GSH depletion, and the possible mechanisms of oxidative stress‐induced cell death.