Premium
Oxidative‐induced RGC‐5 cell death culture involves mitochondrial dysfunction and can be attenuated by hydrogen sulphide
Author(s) -
OSBORNE N
Publication year - 2013
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.1755-3768.2013.2261.x
Subject(s) - mitochondrion , poly adp ribose polymerase , programmed cell death , apoptosis , oxidative phosphorylation , microbiology and biotechnology , cytochrome c , apoptosis inducing factor , hydrogen peroxide , reactive oxygen species , chemistry , inner mitochondrial membrane , caspase , membrane potential , cell culture , biology , biochemistry , polymerase , enzyme , genetics
Exposure of cells in culture to light (1000lux, 400‐760nm) results in cell death but only if their mitochondria are functional. A comparison between the death mechanisms of RGC‐5 cells in culture caused by light or hydrogen peroxide (H2O2) showed them to be almost identical involving the stimulation of ROS and the activation and cleavage of both poly(ADP‐ribose) polymerase‐1 (PARP‐1) and apoptosis‐inducing factor (AIF) but not caspase‐3. Their death processes are inhibited by similar substances that included hydrogen sulphide (H2S). The protective mechanism for H2S appears to involve the preservation of mitochondrial function deduced from the analysis of ATP, the mitochondrial membrane potential, the release of cytochrome c and the analysis of oxidative phosphorylation components in cells exposed to H2O2. This supports the notion that one way for H2S to act as a protective agent is to channel electrons into the electron transport chain of mitochondria.