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Review
. 2017 Jan 31;5(1):e00294.
doi: 10.1002/prp2.294. eCollection 2017 Feb.

Effects of resveratrol on drug- and carcinogen-metabolizing enzymes, implications for cancer prevention

Ariane R Guthrie  1 , H-H Sherry Chow  2 , Jessica A Martinez  1   2
Affiliations
Review

Effects of resveratrol on drug- and carcinogen-metabolizing enzymes, implications for cancer prevention

Ariane R Guthrie et al. Pharmacol Res Perspect. .

Abstract

Resveratrol is a polyphenol found in grape skins and peanuts that has demonstrated many health benefits including protection against aging, cardiovascular and metabolic disease, neurological decline, and cancer. The anticancer properties of resveratrol have been attributed to a variety of mechanisms, including its general inhibition of phase I metabolism and induction of phase II metabolism VSports手机版. The effects of resveratrol on these enzymes, however, are still unclear, as in vitro evidence often contrasts with animal studies and clinical trials. Reasons for these variances could include the low bioavailability of resveratrol and the effects of resveratrol metabolites. Due to resveratrol's interactions with drug-metabolizing enzymes and drug transporters, individuals concurrently taking pharmacological doses of resveratrol with other supplements or medications could potentially experience nutrient-drug interactions. This review summarizes the known effects of resveratrol and its main metabolites on drug metabolism in order to help characterize which populations might benefit from resveratrol for the prevention of cancer, as well as those that may need to avoid supplementation due to potential drug interactions. .

Keywords: Chemoprevention; cytochrome P450; resveratrol V体育安卓版. .

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Figures (V体育平台登录)

Figure 1
Figure 1
Structure of transresveratrol, a trihydroxystilbene naturally found in red wine and peanuts.
Figure 2
Figure 2
Structures of resveratrol's main metabolites. (A) transresveratrol‐4′‐O‐sulfate (main metabolite found in mice) (B) transresveratrol‐3‐O‐sulfate (main metabolite found in humans) (C) transresveratrol‐3‐O‐4′‐O‐disulfate (D) transresveratrol‐3‐O‐glucuronide (major glucuronide product) (E) transresveratrol‐4′‐O‐glucuronide, (F) piceatannol (a minor resveratrol metabolite that is quickly metabolized by phase II enzymes).
Figure 3
Figure 3
Systemic effects of resveratrol on drug‐ and carcinogen‐metabolizing enzymes. Solid lines within the figure refer to effects that have been demonstrated in both preclinical and clinical models. Dotted lines indicate effects that have only been demonstrated in cell culture and/or animal studies. 1 Denotes the exception of CYP1A2, which was induced by resveratrol in a clinical study (Chow et al. 2010).2 Concentration of resveratrol in stool ranges from 0 to 23 μg resveratrol/g dry weight feces, with the concentration of metabolites <1% (Boocock et al., 2007). 3 77% of all urinary species excreted within 4 h post consumption, likely due to enterohepatic recirculation (Boocock et al., 2007).CYP, cytochrome P450; GST, glutathione S‐transferase; NQO1, NAD(P)H dehydrogenase, quinone 1; P‐gp, P‐glycoprotein; UGT, Uridine diphosphate.
Figure 4
Figure 4
Proposed mechanisms for resveratrol's suppression of CYP1 induction. An early model showed that resveratrol inhibited the transformation of the AHR to its nuclear form by forming a complex with the ARNT. Resveratrol has also been shown to act later in the pathway, inhibiting the binding of the nuclear AHR complex to the XRE or inhibiting the recruitment of RNA polymerase II to the DNA. These mechanisms block the transcription of CYP1A1 and CYP1B1. Still, others have proposed that CYP1 inhibition occurs posttranscriptionally. AHR, aryl hydrocarbon receptor; ARNT, aryl hydrocarbon receptor nuclear translocator; CYP, cytochrome P450; XRE, xenobiotic response element.
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References (VSports app下载)

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