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A potent and selective activator of large-conductance Ca2+-activated K+ channels induces preservation of mitochondrial function after hypoxia and reoxygenation by handling of calcium and transmembrane potential.
de Souza, Itanna Isis Araujo; da Silva Barenco, Thais; Pavarino, Maria Eduarda Maciel Fernandes; Couto, Marcos Tadeu; de Resende, Gabriel Oliveira; de Oliveira, Dahienne Ferreira; Ponte, Cristiano Gonsalves; Nascimento, José Hamilton Matheus; Maciel, Leonardo.
Afiliación
  • de Souza IIA; Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.
  • da Silva Barenco T; Programa de Pós-Graduação Em Cardiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.
  • Pavarino MEMF; Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.
  • Couto MT; Programa de Pós-Graduação Em Cardiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.
  • de Resende GO; Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.
  • de Oliveira DF; Instituto Federal de Educação, Ciência e Tecnologia do Rio de Janeiro, Rio de Janeiro, Brasil.
  • Ponte CG; Instituto Federal de Educação, Ciência e Tecnologia do Rio de Janeiro, Rio de Janeiro, Brasil.
  • Nascimento JHM; Instituto de Bioquímica Médica Leopoldo De Meis, Universidade Federal do Rio de Janeiro, Duque de Caxias, Brasil.
  • Maciel L; Instituto Federal de Educação, Ciência e Tecnologia do Rio de Janeiro, Rio de Janeiro, Brasil.
Acta Physiol (Oxf) ; 240(6): e14151, 2024 06.
Article en En | MEDLINE | ID: mdl-38676357
ABSTRACT

AIMS:

Ischaemic heart disease remains a significant cause of mortality globally. A pharmacological agent that protects cardiac mitochondria against oxygen deprivation injuries is welcome in therapy against acute myocardial infarction. Here, we evaluate the effect of large-conductance Ca2+-activated K+ channels (BKCa) activator, Compound Z, in isolated mitochondria under hypoxia and reoxygenation.

METHODS:

Mitochondria from mice hearts were obtained by differential centrifugation. The isolated mitochondria were incubated with a BKCa channel activator, Compound Z, and subjected to normoxia or hypoxia/reoxygenation. Mitochondrial function was evaluated by measurement of O2 consumption in the complexes I, II, and IV in the respiratory states 1, 2, 3, and by maximal uncoupled O2 uptake, ATP production, ROS production, transmembrane potential, and calcium retention capacity.

RESULTS:

Incubation of isolated mitochondria with Compound Z under normoxia conditions reduced the mitochondrial functions and induced the production of a significant amount of ROS. However, under hypoxia/reoxygenation, the Compound Z prevented a profound reduction in mitochondrial functions, including reducing ROS production over the hypoxia/reoxygenation group. Furthermore, hypoxia/reoxygenation induced a large mitochondria depolarization, which Compound Z incubation prevented, but, even so, Compound Z created a small depolarization. The mitochondrial calcium uptake was prevented by the BKCa activator, extruding the mitochondrial calcium present before Compound Z incubation.

CONCLUSION:

The Compound Z acts as a mitochondrial BKCa channel activator and can protect mitochondria function against hypoxia/reoxygenation injury, by handling mitochondrial calcium and transmembrane potential.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Calcio / Mitocondrias Cardíacas Límite: Animals Idioma: En Revista: Acta Physiol (Oxf) Asunto de la revista: FISIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Calcio / Mitocondrias Cardíacas Límite: Animals Idioma: En Revista: Acta Physiol (Oxf) Asunto de la revista: FISIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Reino Unido