Cytotoxicity of quercetin is related to mitochondrial respiration impairment in Saccharomyces cerevisiae.

Saccharomyces cerevisiae cytochrome c cytotoxicity mitochondrial respiration quercetin ubiquinone pool

Journal

Yeast (Chichester, England)
ISSN: 1097-0061
Titre abrégé: Yeast
Pays: England
ID NLM: 8607637

Informations de publication

Date de publication:
11 2022
Historique:
revised: 07 10 2022
received: 18 03 2022
accepted: 21 10 2022
pubmed: 27 10 2022
medline: 7 12 2022
entrez: 26 10 2022
Statut: ppublish

Résumé

Quercetin is a flavonol ubiquitously present in fruits and vegetables that shows a potential therapeutic use in non-transmissible chronic diseases, such as cancer and diabetes. Although this phytochemical has shown promising health benefits, the molecular mechanism behind this compound is still unclear. Interestingly, quercetin displays toxic properties against phylogenetically distant organisms such as bacteria and eukaryotic cells, suggesting that its molecular target resides on a highly conserved pathway. The cytotoxicity of quercetin could be explained by energy depletion occasioned by mitochondrial respiration impairment and its concomitant pleiotropic effect. Thereby, the molecular basis of quercetin cytotoxicity could shed light on potential molecular mechanisms associated with its health benefits. Nonetheless, the evidence supporting this hypothesis is still lacking. Thus, this study aimed to evaluate whether quercetin supplementation affects mitochondrial respiration and whether this is related to quercetin cytotoxicity. Saccharomyces cerevisiae was used as a study model to assess the effect of quercetin on energetic metabolism. Herein, we provide evidence that quercetin supplementation: (1) decreased the exponential growth of S. cerevisiae in a glucose-dependent manner; (2) affected diauxic growth in a similar way to antimycin A (complex III inhibitor of electron transport chain); (3) suppressed the growth of S. cerevisiae cultures supplemented with non-fermentable carbon sources (glycerol and lactate); (4) promoted a glucose-dependent inhibition of the basal, maximal, and ATP-linked respiration; (5) diminished complex II and IV activities. Altogether, these data indicate that quercetin disturbs mitochondrial respiration between the ubiquinone pool and cytochrome c, and this phenotype is associated with its cytotoxic properties.

Identifiants

pubmed: 36285422
doi: 10.1002/yea.3818
doi:

Substances chimiques

Quercetin 9IKM0I5T1E
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

617-628

Informations de copyright

© 2022 John Wiley & Sons Ltd.

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Auteurs

Andres Carrillo-Garmendia (A)

Universidad Autónoma de Querétaro, Cerro de las Campanas, Santiago de Querétaro, Qro, Mexico.

Cecilia Martinez-Ortiz (C)

Universidad Autónoma de Querétaro, Cerro de las Campanas, Santiago de Querétaro, Qro, Mexico.

Melina Canizal-Garcia (M)

Tecnológico Nacional de México/Instituto Tecnológico de Morelia, Morelia, Michoacán, Mexico.

Juan Carlos González-Hernández (JC)

Tecnológico Nacional de México/Instituto Tecnológico de Morelia, Morelia, Michoacán, Mexico.

Sofia Maria Arvizu-Medrano (SM)

Universidad Autónoma de Querétaro, Cerro de las Campanas, Santiago de Querétaro, Qro, Mexico.

Jorge Gracida (J)

Universidad Autónoma de Querétaro, Cerro de las Campanas, Santiago de Querétaro, Qro, Mexico.

Luis Alberto Madrigal-Perez (LA)

Tecnológico Nacional de México/Instituto Tecnológico Superior de Ciudad Hidalgo, Ciudad Hidalgo, Michoacán, Mexico.

Carlos Regalado-Gonzalez (C)

Universidad Autónoma de Querétaro, Cerro de las Campanas, Santiago de Querétaro, Qro, Mexico.

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