Quercetin Affects Erythropoiesis and Heart Mitochondrial Function in Mice

Lina M Ruiz, Celia Salazar, Erik Jensen, Paula Ruiz Hincapie, William Tiznado, Rodrigo A Quintanilla, Marlen Barreto, Alvaro A Elorza

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)
48 Downloads (Pure)

Abstract

Quercetin, a dietary flavonoid used as a food supplement, showed powerful antioxidant effects in different cellular models. However, recent in vitro and in vivo studies in mammals have suggested a prooxidant effect of quercetin and described an interaction with mitochondria causing an increase in O2 (∙-) production, a decrease in ATP levels, and impairment of respiratory chain in liver tissue. Therefore, because of its dual actions, we studied the effect of quercetin in vivo to analyze heart mitochondrial function and erythropoiesis. Mice were injected with 50 mg/kg of quercetin for 15 days. Treatment with quercetin decreased body weight, serum insulin, and ceruloplasmin levels as compared with untreated mice. Along with an impaired antioxidant capacity in plasma, quercetin-treated mice showed a significant delay on erythropoiesis progression. Heart mitochondrial function was also impaired displaying more protein oxidation and less activity for IV, respectively, than no-treated mice. In addition, a significant reduction in the protein expression levels of Mitofusin 2 and Voltage-Dependent Anion Carrier was observed. All these results suggest that quercetin affects erythropoiesis and mitochondrial function and then its potential use as a dietary supplement should be reexamined.

Original languageEnglish
Article number836301
Number of pages12
JournalOxidative medicine and cellular longevity
Volume2015
DOIs
Publication statusPublished - 28 May 2015

Keywords

  • Animals
  • Antioxidants
  • Body Weight
  • Bone Marrow Cells
  • Ceruloplasmin
  • Erythropoiesis
  • Ferritins
  • GTP Phosphohydrolases
  • Insulin
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria
  • Myocardium
  • Quercetin
  • Transcription Factors

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