Antioxidant enzymatically modified isoquercitrin suppresses the development of liver preneoplastic lesions in rats induced by β-naphthoflavone

Shimada, Yuko; Dewa, Yasuaki; Ichimura, Ryohei; Suzuki, Terumasa; Mizukami, Sayaka; Hayashi, Shim-mo; Shibutani, Makoto; Mitsumori, Kunitoshi

doi:10.1016/j.tox.2009.12.019

Cited by 39 publications

(23 citation statements)

References 27 publications

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“…6). In previous studies, it was suggested that AhR activation by exogenous ligands induces anti-inflammatory effects in liver cells [22,30]. In addition, AhR agonists were found to mediate anti-inflammatory responses through interference with the NFjB signaling pathway and the suppression of IL6 induction [31,32].…”

Section: Discussionmentioning

confidence: 99%

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A Role of the Aryl Hydrocarbon Receptor in Attenuation of Colitis

et al. 2011

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Section: Discussionmentioning

confidence: 99%

“…Next, we examined whether AhR activation induced by b-naphthoflavone (bNF), a non-toxic AhR activator [22], attenuated DSS-induced colitis.…”

Section: Introductionmentioning

confidence: 99%

A Role of the Aryl Hydrocarbon Receptor in Attenuation of Colitis

et al. 2011

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“…The results showed that the oxidative activity of BNF contributed to the formation of liver preneoplastic lesions while EMIQ demonstrated a protective effect by reducing the by reducing glutathione Stransferase P (GSTP)positive cellular foci and cyclooxygenase (COX)2 production. In addition, it suppressed encoding genes for proteins such as glutathione Stransferase mu 1 (GSTM1, drugs metabolizing enzyme), serpine1, COX2, and nuclear factor kappalightchainenhancer of activated B cells (NfκB), which are enzymes involved in inflammatory processes [86] . BNF is a strong inducer of CYP1A enzymes and exerts liver tumorpromoting activity through the enhancement of oxidative stress responses in rats.…”

Section: Liver Cancermentioning

confidence: 99%

Review of anticancer mechanisms of isoquercitin

Orfali¹,

Duarte²,

Bonadio³

et al. 2016

WJCO

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This review was based on a literature search of PubMed and Scielo databases using the keywords "quercetin, rutin, isoquercitrin, isoquercitin (IQ), quercetin-3-glucoside, bioavailability, flavonols and favonoids, and cancer" and combinations of all the words. We collected relevant scientific publications from 1990 to 2015 about the absorption, bioavailability, chemoprevention activity, and treatment effects as well as the underlying anticancer mechanisms of isoquercitin. Flavonoids are a group of polyphenolic compounds widely distributed throughout the plant kingdom. The subclass of flavonols receives special attention owing to their health benefits. The main components of this class are quercetin, rutin, and IQ, which is a flavonoid and although mostly found as a glycoside, is an aglycone (lacks a glycoside side chain). This compound presents similar therapeutic profiles to quercetin but with superior bioavailability, resulting in increased efficacy compared to the aglycone form. IQ has therapeutic applications owing to its wide range of pharmacological effects including antioxidant, antiproliferative, anti-inflammatory, anti-hypertensive, and anti-diabetic. The protective effects of IQ in cancer may be due to actions on lipid peroxidation. In addition, the antitumor effect of IQ and its underlying mechanism are related to interactions with Wnt signaling pathway, mixed-lineage protein kinase 3, mitogen-activated protein kinase, apoptotic pathways, as well proinflammatory protein signaling. This review contributed to clarifying the mechanisms of absorption, metabolism, and actions of IQ and isoquercitrin in cancer.

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“…The chosen dosage of OTA has been shown to induce karyomegaly in the proximal tubules of the OSOM after 28-day treatment in rats (Taniai et al, 2012a). The chosen dosage of EMIQ has been shown to suppress the promotion of hepatic preneoplastic lesions through restoring the cellular redox balance in rats (Shimada et al, 2010). Lower dosage of ALA than the chosen dosage here has been shown to enhance erythrocyte antioxidant defense and reduced nephrotoxicity by co-administration with ␣-tocopherol in cyclosporine A-treated rats (Lexis et al, 2006), but has also been shown to promote the growth of hepatic preneoplastic lesions in rats (Perra et al, 2008).…”

Section: Animal Experimentsmentioning

confidence: 99%