Evidence that thiol group modification and reactive oxygen species are involved in hydrogen sulfide-induced mitochondrial permeability transition pore opening in rat cerebellum
Autor: | Guilhian Leipnitz, Belisa Parmeggiani, Cristiane Cecatto, Renata Britto, Alexandre Umpierrez Amaral, Larissa Daniele Bobermin, Moacir Wajner, Nícolas Manzke Glänzel, Nevton Teixeira da Rosa-Junior, Leonardo de Moura Alvorcem |
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Rok vydání: | 2019 |
Předmět: |
Male
0301 basic medicine Ruthenium red Sulfide Hydrogen sulfide Oxidative phosphorylation Mitochondrion Mitochondrial Membrane Transport Proteins Permeability 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cerebellum Animals Hydrogen Sulfide Rats Wistar Molecular Biology chemistry.chemical_classification Reactive oxygen species Mitochondrial Permeability Transition Pore Cell Biology Rats 030104 developmental biology chemistry Mitochondrial permeability transition pore Cyclosporine Biophysics Molecular Medicine Calcium ETHE1 Mitochondrial Swelling Reactive Oxygen Species 030217 neurology & neurosurgery |
Zdroj: | Mitochondrion. 47:141-150 |
ISSN: | 1567-7249 |
Popis: | We report here the effects of hydrogen sulfide (sulfide), that accumulates in ETHE1 deficiency, in rat cerebellum. Sulfide impaired electron transfer and oxidative phosphorylation. Sulfide also induced mitochondrial swelling, and decreased ΔΨm and calcium retention capacity in cerebellum mitochondria, which were prevented by cyclosporine A (CsA) plus ADP, and ruthenium red, suggesting mitochondrial permeability transition (mPT) induction. Melatonin (MEL) and N-ethylmaleimide also prevented sulfide-induced alterations. Prevention of sulfide-induced decrease of ΔΨm and viability by CsA and MEL was further verified in cerebellum neurons. The data suggest that sulfide induces mPT pore opening via thiol modification and ROS generation. |
Databáze: | OpenAIRE |
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