Quercetin and the mitochondria: A mechanistic view

Oliveira, Marcos Roberto de; Nabavi, Seyed Mohammad; Braidy, Nady; Setzer, William N.; Ahmed, Touqeer

doi:10.1016/j.biotechadv.2015.12.014

Cited by 201 publications

(101 citation statements)

References 220 publications

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“…Additionally it is reported that quercetin is accumulated in mitochondria and modulates mitochondrial function (Fiorani et al, ). Several studies indicated that quercetin prevents mitochondria from oxidative damage by various mechanisms (De Oliveira et al, ). Quercetin restored mitochondrial complex I activity in rotenone and 3‐nitropropionic acid treated rats (Karuppagounder et al, ; Sandhir & Mehrotra, ).…”

Section: Discussionmentioning

confidence: 99%

Quercetin ameliorates chlorpyrifos-induced oxidative stress in the rat brain: Possible involvment of PON2 pathway

2018

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In the present study, protective effect of quercetin against chlorpyrifos-induced oxidative stress in the brain of rat and possible involvement of paraoxanase2 (PON2) pathway was investigated. The experimental groups include control, CPF (10 mg/kg), quercetin (20 mg/kg), and CPF 1 quercetin.All treatments were orally administered once per day for 1 month. The PON2 gene expression in brain was quantified by real time PCR method and oxidative stress markers in the brain and AChE activity in the brain and serum were measured. AChE activity significantly decreases in the brain and serum of CPF-treated groups indicating CPF exposure. Quercetin restored the increased lipid peroxidation and decreased antioxidant enzyme activities and total thiol content which were induced by CPF. These results indicate the reduction of oxidative stress by quercetin. Also, quercetin unregulated the expression of PON2 gene more potently in CPF-treated group. Practical applicationsPON2 is a lactonase expressed in brain and has antioxidant and anti-inflammatory activities. It is reported that quercetin, a flavonoid with antioxidant and neuroprotective activities, increases expression of paraoxanase2 enzyme (PON2) in cultured neural cells which resulted in neuroprotection against oxidative insults. Chlorpyrifos (CPF) is a neurotoxic organophosphate pesticide which can induce oxidative damage in the brain and trigger neurodegeneration. The aim of the present study was to evaluate the protective effect of quercetin against CPF-induced oxidative stress in the brain of rat and possible involvement of PON2 pathway was also investigated. Results of the present study indicate that quercetin improves CPF-induced oxidative stress and this effect may be achieved through upregulation of PON2 gene and potentiation of cellular antioxidant defense.Therefore, quercetin can be used as a dietary supplement to people at risk for CPF exposure such as farmers in order to reduce CPF-induced brain oxidative damage and consecutive disorders. K E Y W O R D S chlorpyrifos, oxidative stress, paraoxonase2, quercetin

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Section: Discussionmentioning

confidence: 99%

Quercetin ameliorates chlorpyrifos-induced oxidative stress in the rat brain: Possible involvment of PON2 pathway

2018

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“…So, mitochondria targeted chemotherapeutic agents and polyphenolic compounds have been reported to decrease mitochondrial membrane fluidity (Gorlach et al, ). Quercetin‐induced mitochondria‐dependent cell death in diverse cancer cells originating from bone, brain, breast, cervix, lung, prostate and skin by increasing loss of MMP, release of cytochrome c, PARP cleavage and activation of caspase‐3 and caspase‐9 (de Oliveira et al, ). The current study showed that quercetin decreased MMP and increased ROS in JAR and JEG3 cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Quercetin on Progression of Human Choriocarcinoma Cells Are Mediated Through PI3K/AKT and MAPK Signal Transduction Cascades

Lim

Yang

Park

et al. 2016

Journal Cellular Physiology

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As a major dietary flavonol, quercetin mitigates proliferation and progression of cancer due to its anti-angiogenic, anti-inflammatory, anti-oxidant, and apoptotic biological effects on cells. Although its apoptotic effects have been reported for various cancers, little is known of the functional role of quercetin in gestational choriocarcinoma. Results of the present study indicated that quercetin reduced proliferation and induced cell death in two choriocarcinoma cell lines, JAR and JEG3 cells, with an increase in the sub-G phase of the cell cycle. In addition, quercetin induced mitochondrial dysfunction significantly reduced mitochondrial membrane potential (MMP) and increased production of reactive oxygen species (ROS) in both JAR and JEG3 cells. Further, quercetin inhibited phosphorylation of AKT, P70S6K and S6 proteins whereas, it increased phosphorylation of ERK1/2, P38, JNK and P90RSK proteins in JAR and JEG3 cells. The decrease in viability of choriocarcinoma cells treated with quercetin was confirmed by using combinations of quercetin and pharmacological inhibitors of the PI3K and MAPK signaling pathways. Classical chemotherapeutic agents, cisplatin (a platinum-based drug) and paclitaxel (a taxene-based drug), inhibited proliferation of JAR and JEG3 cells, and when combined with quercetin, the antiproliferative effects of cisplatin and paclitaxel were enhanced for both choriocarcinoma cell lines. Collectively, these results suggest that quercetin prevents development of choriocarcinoma and may be a valuable therapeutic agent for treatment of choriocarcinoma through its regulation of PI3K and MAPK signal transduction pathways. J. Cell. Physiol. 232: 1428-1440, 2017. © 2016 Wiley Periodicals, Inc.

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“…It is present at varying concentration levels in different fruits and vegetables (Table 3). Isoquercetin (quercetin-3-glucoside) is one of the glycoside forms of quercetin that is present in plants [98]. Reports have suggested that quercetin exhibits anti-cancer effects in breast cancer [99][100][101], however the literature on the epigenetic modifying activity of quercetin in breast cancer is limited.…”

Section: Quercetin Modulates Brca1 Expression Levelmentioning

confidence: 99%

Flavonoids and Other Polyphenols Act as Epigenetic Modifiers in Breast Cancer

et al. 2020

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Breast cancer is a common cancer that occurs due to different epigenetic alterations and genetic mutations. Various epidemiological studies have demonstrated an inverse correlation between breast cancer incidence and flavonoid intake. The anti-cancer action of flavonoids, a class of polyphenolic compounds that are present in plants, as secondary metabolites has been a major topic of research for many years. Our review analysis demonstrates that flavonoids exhibit anti-cancer activity against breast cancer occurring in different ethnic populations. Breast cancer subtype and menopausal status are the key factors in inducing the flavonoid’s anti-cancer action in breast cancer. The dose is another key factor, with research showing that approximately 10 mg/day of isoflavones is required to inhibit breast cancer occurrence. In addition, flavonoids also influence the epigenetic machinery in breast cancer, with research demonstrating that epigallocatechin, genistein, and resveratrol all inhibited DNA methyltransferase and altered chromatin modification in breast cancer. These flavonoids can induce the expression of different tumor suppressor genes that may contribute to decreasing breast cancer progression and metastasis. Additional studies are required to confirm the contribution of epigenetic modifications by flavonoids to breast cancer prevention.

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Quercetin and the mitochondria: A mechanistic view

Cited by 201 publications

References 220 publications

Quercetin ameliorates chlorpyrifos-induced oxidative stress in the rat brain: Possible involvment of PON2 pathway

Quercetin ameliorates chlorpyrifos-induced oxidative stress in the rat brain: Possible involvment of PON2 pathway

Inhibitory Effects of Quercetin on Progression of Human Choriocarcinoma Cells Are Mediated Through PI3K/AKT and MAPK Signal Transduction Cascades

Flavonoids and Other Polyphenols Act as Epigenetic Modifiers in Breast Cancer

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