C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2015-05-14

AUTHORS

Berenice Fernández-Rojas, Daniela Sarai Rodríguez-Rangel, Luis Fernando Granados-Castro, Mario Negrette-Guzmán, Juan Carlos León-Contreras, Rogelio Hernández-Pando, Eduardo Molina-Jijón, José L. Reyes, Cecilia Zazueta, José Pedraza-Chaverri

ABSTRACT

The potential of C-phycocyanin (C-PC) to prevent cisplatin (CP)-induced kidney mitochondrial dysfunction was determined in CD-1 male mice. The CP-induced mitochondrial dysfunction was characterized by ultrastructural abnormalities and by decrease in the following parameters in isolated kidney mitochondria: adenosine diphosphate (ADP)-induced oxygen consumption (state 3), respiratory control ratio, ADP/oxygen (ADP/O) ratio, adenosine triphosphate synthesis, membrane potential, calcium retention, glutathione (GSH) content, and activity of respiratory complex I, aconitase, catalase, and GSH peroxidase. These mitochondria also showed increase in hydrogen peroxide production, malondialdehyde, and 3-nitrotyrosine protein adducts content. The above-described changes, as well as CP-induced nephrotoxicity, were attenuated in mice pretreated with a single injection of C-PC. Our data suggest that the attenuation of mitochondrial abnormalities is involved in the protective effect of C-PC against CP-induced nephrotoxicity. This is the first demonstration that C-PC pretreatment prevents CP-induced mitochondrial dysfunction in mice. More... »

PAGES

183-197

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11010-015-2436-9

DOI

http://dx.doi.org/10.1007/s11010-015-2436-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1039656205

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25971372


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36 schema:description The potential of C-phycocyanin (C-PC) to prevent cisplatin (CP)-induced kidney mitochondrial dysfunction was determined in CD-1 male mice. The CP-induced mitochondrial dysfunction was characterized by ultrastructural abnormalities and by decrease in the following parameters in isolated kidney mitochondria: adenosine diphosphate (ADP)-induced oxygen consumption (state 3), respiratory control ratio, ADP/oxygen (ADP/O) ratio, adenosine triphosphate synthesis, membrane potential, calcium retention, glutathione (GSH) content, and activity of respiratory complex I, aconitase, catalase, and GSH peroxidase. These mitochondria also showed increase in hydrogen peroxide production, malondialdehyde, and 3-nitrotyrosine protein adducts content. The above-described changes, as well as CP-induced nephrotoxicity, were attenuated in mice pretreated with a single injection of C-PC. Our data suggest that the attenuation of mitochondrial abnormalities is involved in the protective effect of C-PC against CP-induced nephrotoxicity. This is the first demonstration that C-PC pretreatment prevents CP-induced mitochondrial dysfunction in mice.
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45 CP
46 GSH peroxidase
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