Induction of human NAD(P)H:quinone oxidoreductase (NQO1) gene expression by the flavonol quercetin

Valerio, Luis G.; Kepa, Jadwiga K.; Pickwell, George V.; Quattrochi, Linda C.

doi:10.1016/s0378-4274(00)00302-7

Cited by 105 publications

(54 citation statements)

References 24 publications

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“…The peroxynitrite-mediated decreases in Nrf2 levels correlated with a decrease in the levels of both subunits of GCL, and GCL loss was also prevented by fisetin treatment. These findings are in agreement with earlier studies which showed that fisetin could increase the expression of various ARE-dependent genes in multiple non-neuronal cell lines [34,65,89] as well as rat C6 glioma cells [17]. The precise mechanisms whereby fisetin increases Nrf2 levels are still under investigation.…”

Section: Mechanism Of Actionsupporting

confidence: 92%

Modulation of multiple pathways involved in the maintenance of neuronal function during aging by fisetin

Maher

2009

Genes Nutr

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Multiple factors have been implicated in the age-related declines in brain function. Thus, it is unlikely that modulating only a single factor will be effective at slowing this decline. A better approach is to identify small molecules that have multiple biological activities relevant to the maintenance of brain function. Over the last few years, we have identified an orally active, novel neuroprotective and cognition-enhancing molecule, the flavonoid fisetin. Fisetin not only has direct antioxidant activity but it can also increase the intracellular levels of glutathione, the major intracellular antioxidant. Fisetin can also maintain mitochondrial function in the presence of oxidative stress. In addition, it has anti-inflammatory activity against microglial cells and inhibits the activity of 5-lipoxygenase, thereby reducing the production of lipid peroxides and their pro-inflammatory by-products. This wide range of actions suggests that fisetin has the ability to reduce the age-related decline in brain function.

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Section: Mechanism Of Actionsupporting

confidence: 92%

Modulation of multiple pathways involved in the maintenance of neuronal function during aging by fisetin

Maher

2009

Genes Nutr

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“…Supporting the present findings, malathion also provoked alteration in antioxidant enzymes such as SOD, GPx following sub chronic exposure in animals (Akhgari et al, 2003;Abdollahi et al, 2004) may be due to hepato and neurotoxicity induced by several organophosphorus induced Reactive Oxygen Species (Mansour and Mossa, 2010; and associated with lipid peroxidation and phospholipids degradation (Mansour and Mossa, 2009), it has been previously reported that during liver damage there was an observed decrease in antioxidant defenses in the liver (Seven et al, 2004;Heikal et al (2012). In other hand in groups treated by malathion plus vitamine c or malathion plus green tea there were a significant decrease in activities of SOD, GSH and GPx in rat liver if compared with malathion treated group may be due to vitamin c is proposed to reduce oxidative stress from H2O2 potentially by reducing the free radical species generated from H2O2 and reduces oxidative DNA damage (Noroozi et al, 1998), more over green tea extract enhances the expression of intracellular endogenous antioxidants such as SOD and GPX by maintaining their activities higher compared to the malathion group and other antioxidants enzymes such as glutathione, glutathione reductase, glutathionereductase and quinone reductase (Valerio et al, 2001) Administration of green tea to ethanol-treated rats of different ages partly normalized the activity of enzymes and the level of non-enzymatic antioxidants (Khan et al, 2007). Our histopathological study revealed that the liver of the malathion administrated rat showed degenerative changes in the cytoplasm of hepatocytes and the kidney showed edema with inflammatory cells infiltration in the perivascular tissue at the cortex.…”

Section: Discussionmentioning

confidence: 99%

Protective Role of Vitamin C and Green Tea Extract on Malathion-Induced Hepatotoxicity and Nephrotoxicity in Rats

Elzoghby¹,

Hamoda²,

Aboubakr³

et al. 2014

American Journal of Pharmacology and Toxicology

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The present study was designed to determine the modulating effect of green tea and vitamin C against adverse effects of malathion. Animals were divided into four groups 5 rats /group). Group one was used as a control. Group two given malathion (50 mg/kg/day; 1/50 of the LD50 for four weeks). Group three and Group four were given malathion (50 mg/kg/day; 1/50 of the LD50 for four weeks) plus vitamin C (200 mg/kg/day) and plus green tea (36 mg/kg/day) respectively. At the end of the fourth week, the malathion-treated group had significantly lower Red Blood Cell count (RBCs), Hemoglobin concentration (Hb), Packed Cell Volume (PCV%) and leucocytes (WBCs) than the control group. Compared to the control group, the malathion-treated group had significantly higher serum Alkaline Phosphatase (ALP), Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Lactate Dehydrogenase (LDH), urea, creatinine and uric acid levels than the control group. The malathion treated rats also had significantly lower serum total protein, albumin and globulin levels than the control group, but the malathion plus vitamin C and malathion plus green tea groups did not differ from the control group in terms of these parameters. Moreover, concomitant vitamin C and green tea treatment significantly normalized, at least partially, all of the other hematological and biochemical parameters that were altered by malathion. Liver tissue homogenate in malathion treated group had lower Glutathione (GSH), Glutathione Peroxidase (GSH-PX) and Superoxide Dismutase (SOD) levels accompanied with higher level of Malondialdehyde (MDA) than the control group. Histopathological studies revealed that the malathion-treated, malathion plus vitamin C and malathion plus green tea treated groups exhibited histopathological changes in liver and kidney tissues, although some pathological features were only observed in the malathion-treated group. Thus, vitamin C and green tea can reduce malathion hepatotoxicity and nephrptoxicity.

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“…More recently, in vitro and animal model systems suggest that flavonoids influence signal transduction pathway (Morrow et al, 2001;Frigo et al, 2002), stimulate apoptosis (Choi et al, 2001), inhibit inflammation (Cho et al, 2001), and inhibit proliferation in human cancer cell lines (Manthey & Guthrie, 2002). Selected flavonoids may also increase transcription of phase II detoxifying enzymes, which supports a cancer protective effect via the clearance of procarcinogenic substances that are detoxified and eliminated by phase II enzyme products (Valerio et al, 2001). A study conducted with azoxymethane (AOM)-treated mice who were fed with either a standard diet, a standard diet plus rutin, or a standard diet plus quercetin showed that the flavonoids substantially decreased the number of focal areas of dysplasia that were induced by the AOM exposure (Yang et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Flavonoids and Cancer Prevention: What Is the Evidence in Humans?

Neuhouser

2004

Pharmaceutical Biology

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Diets high in fruits and vegetables are associated primarily with a reduced risk of human cancers of the gastrointestinal tract, as well as some other common cancers including those of the lung, breast, and prostate. Plants contain hundreds of bioactive substances, including flavonoids, which are a large group of compounds consisting of two phenolic benzene rings linked to a heterocyclic pyran or pyrone. This report reviews published epidemiologic studies that have examined associations of flavonoid intake with cancer risk in humans. Findings to date are extremely limited, but there is relatively consistent evidence from these studies that flavonoids, especially quercetin, reduce risk of lung cancer. Evidence is modest for other epithelial cancers. Further research is needed to confirm these findings before public health recommendations about flavonoids can be offered to consumers.

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Induction of human NAD(P)H:quinone oxidoreductase (NQO1) gene expression by the flavonol quercetin

Cited by 105 publications

References 24 publications

Modulation of multiple pathways involved in the maintenance of neuronal function during aging by fisetin

Modulation of multiple pathways involved in the maintenance of neuronal function during aging by fisetin

Protective Role of Vitamin C and Green Tea Extract on Malathion-Induced Hepatotoxicity and Nephrotoxicity in Rats

Flavonoids and Cancer Prevention: What Is the Evidence in Humans?

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