Quercetin Affects Erythropoiesis and Heart Mitochondrial Function in Mice.

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

doi:10.1155/2015/836301

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.

Highlights

The generation of reactive oxygen species (ROS) due to normal cell metabolism and the accumulative damage they cause to DNA, proteins, and lipid membranes have been associated with the development of many acquired diseases and aging
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
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 its potential use as a dietary supplement should be reexamined

Summary

Introduction

The generation of reactive oxygen species (ROS) due to normal cell metabolism and the accumulative damage they cause to DNA, proteins, and lipid membranes have been associated with the development of many acquired diseases and aging. In vivo studies of the antioxidant properties of dietary flavonoids have shown some paradoxical effects on human health [1] making important to investigate further and deeper the mechanism of action of these supplements. Quercetin is one of the most abundant dietary flavonoids, with the highest antioxidant capability [2, 3], modulating the expression of different antioxidant enzymes such a catalase and superoxide dismutase, and increasing the intracellular levels of glutathione [4,5,6]. During ROS scavenging process, quercetin gets oxidized, and it further reacts with glutathione and the protein thiol groups, leading to consumption of Oxidative Medicine and Cellular Longevity glutathione, an increase in cytosolic calcium concentration and lactate dehydrogenase leakage [11]

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Conclusion