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CHEMILUMINESCENT DIPHENYLACETALDEHYDE OXIDATION BY MITOCHONDRIA IS PROMOTED BY CYTOCHROMES and LEADS TO OXIDATIVE INJURY OF THE ORGANELLE
Author(s) -
Nantes Isbli L.,
Cilento Giuseppe,
Bechara Etelvino J. H.,
Vercesi Aníbal E.
Publication year - 1995
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1995.tb02378.x
Subject(s) - rotenone , cyanide , mitochondrion , antimycin a , chemistry , oxidative phosphorylation , cytochrome , cytochrome c , biochemistry , cytochrome c oxidase , chemiluminescence , respiratory chain , enzyme , organic chemistry
— Plant and animal mitochondria promote the aerobic oxidation of diphenylacetaldehyde (DPAA). This process is accompanied by chemiluminescence and rotenone‐insensitive oxygen uptake. Tn rat liver and potato tubers, mitochondrial swelling is concurrently detected. Light emission and oxygen consumption decreased (about 50%) in cytochrome c‐depleted mitochondria. A model system–cytochrome c or b5/dihexadecylphosphate liposomes–was also able to oxidize DPAA with parallel reduction of the cytochrome. Reduction of respiratory complex I or I plus II by addition of rotenone or antimycin A, respectively, did not prevent DPAA oxidation. However, when all cytochrome was reduced by addition of cyanide, aldehyde oxidation was completely suppressed. Altogether these data indicate that respiratory cytochromes are responsible for DPAA oxidation with production of excited species and consequent mitochondrial permeabilization.