De Moura Alvorcem 2018 Mitochondrion

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
De Moura Alvorcem L, Britto R, Parmeggiani B, Glanzel NM, Da Rosa-Junior NT, Cecatto C, Bobermin LD, Amaral AU, Wajner M, Leipnitz G (2018) Evidence that thiol group modification and reactive oxygen species are involved in hydrogen sulfide-induced mitochondrial permeability transition pore opening in rat cerebellum. Mitochondrion 47:141-50.

» PMID: 30399433

De Moura Alvorcem L, Britto R, Parmeggiani B, Glanzel NM, Da Rosa-Junior NT, Cecatto C, Bobermin LD, Amaral AU, Wajner M, Leipnitz G (2018) Mitochondrion

Abstract: 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.

Keywords: Cerebellum mitochondria, Cerebellum neurons, ETHE1 deficiency, Hydrogen sulfide, Mitochondrial permeability transition Bioblast editor: Plangger M O2k-Network Lab: BR Porto Alegre Souza DOG


Labels: MiParea: Respiration, Pharmacology;toxicology 

Stress:Permeability transition  Organism: Rat  Tissue;cell: Nervous system  Preparation: Homogenate 


Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS  HRR: Oxygraph-2k 

Labels, 2018-11