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Insult dependent oxidative‐induced cell death
Author(s) -
Osborne N.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.01365
Subject(s) - necroptosis , oxidative stress , programmed cell death , sodium azide , reactive oxygen species , oxidative phosphorylation , mitochondrion , apoptosis , chemistry , hydrogen peroxide , microbiology and biotechnology , nadph oxidase , biochemistry , biology
Summary Mitochondrial dysfunction caused by inhibition of oxidative phosphorylation results both in reduced ATP production and oxidative stress because of a significant elevation of ROS . In the reported studies oxidative stress to cultures of cells ( RGC ‐5 cells) was initiated by inhibition of mitochondrial phosphorylation (blue light, sodium azide) or by use of hydrogen peroxide known to induce superoxide through the activation of cellular NADPH oxidase. While all insults resulted in cell death and attenuated by the antioxidant EGCG differences occurred in various measured biochemical parameters implicated in cell death. For example, blue light‐induced apoptosis was attenuated by the presence of the mitochondrial the uncoupler M3778 but potentiated by the presence of cobalt. In contrast, hydrogen‐peroxide‐induced apoptosis was unaffected by M3778 but attenuated by cobalt. Also, blue light‐induced cell death occurs via necroptosis, in that it was inhibited by necrostatin‐1 and was caspase‐independent. This was not the case for sodium azide, where the death process was caspase‐dependent, occurred via apoptosis and was unaffected by necrostatin‐1.