Singlet molecular oxygen (O21Δg)like other reactive oxygen species(ROS), can be generated in mammafian cells during oxidative stress by an energy transfer mechanism following the production of triplet species during the course of lipid peroxidation. Furthermore, the photodynamic action of some drugs is mediated by singlet oxygen. In this regard, mitochondria are important targets of ROS-promoted cell damage and play a key role in diseases sensitive to photodynamic therapy. This work characterizes the effect of O21Δg generated by NDPO 2 on rat liver mitochondria. NDPO2 inhibits mitochondrial respiration at sites I and II but not at site IV. NDPO2 treated mitochondria exhibits loss of transmembrane potential (Δψ) in a dose and exposition timedependent manner. This Δψ decrease is sensitive to the protective effect of EGTA, ADP, CyA and DTT. Alterations in membrane proteins were determined by SDS-PAGE electrophoresis of solubilized membrane proteins in the presence of eosin-5-maleimide. The results evidenced thiol groups oxidation that was prevented by dithiothreitol (DTT)and ADP. NDPO2-promoted mitochondrial damage was increased in D20 medium and prevented by histidine. Through this work, we suggested that singlet oxygen-promoted damage in rat liver mitochondria is mediated by Ca2+-dependent mitochondrial permeability transition pore (MPT) opening as demonstrated by the protective effect of EGTA, ADP and CyA. Supported by FAPESP, CNPq, PADCT and FAEP.
|Estado||Publicada - 1997|
Áreas temáticas de ASJC Scopus
- Agricultura y biología (miscelánea)
- Bioquímica, genética y biología molecular (todo)
- Biología celular
- Biología molecular