Antimycin A and lipopolysaccharide cause the leakage of superoxide radicals from rat liver mitochondria.
Here we show that both Antimycin A, a respiratory chain inhibitor inducing apoptosis, and endotoxic shock, a syndrome accompanied by both necrosis and apoptosis, cause not only an increase but also the leakage of superoxide radicals (O(2)(*-)) from rat heart mitochondria (RHM), while O(2)(*-) generated in intact RHM do not escape from mitochondria. This was shown by a set of O(2)(*-)-sensitive spin probes with varying hydrophobicity. The levels of O(2)(*-) detected in intact RHM gradually increase as the hydrophobicity of spin probes increases and were not sensitive to superoxide dismutase (SOD) added to the incubation medium. Both Antimycin A and endotoxic shock elevated O(2)(*-) levels. Elevated O(2)(*-) levels became sensitive to SOD but in a different manner. The determination of O(2)(*-) with water-soluble PPH was fully sensitive to SOD, while the determination of O(2)(*-) with the more hydrophobic CMH and CPH was only partially sensitive to SOD, suggesting the release of a portion of O(2)(*-) into the surrounding medium.
Piskernik
Christina
C
Ludwig Boltzmann Institute for Experimental and Clinical Traumatology in the Research Center of AUVA, Vienna, Austria.
Haindl
Susanne
S
Behling
Tricia
T
Gerald
Zanoni
Z
Kehrer
Ingeborg
I
Redl
Heinz
H
Kozlov
Andrey V
AV
D000818:Animals; D000968:Antimycin A / Q000494:pharmacology*; D017209:Apoptosis; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects; D008930:Mitochondria, Liver / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012772:Shock, Septic / Q000378:metabolism; D013482:Superoxide Dismutase / Q000494:pharmacology
D008070:Lipopolysaccharides; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D000968:Antimycin A; D013482:Superoxide Dismutase