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没食子酸表没食子儿茶素(EGCG)、槲皮素和芦丁对三氧化铬诱导的小鼠外周血多染红细胞微核的抗原毒性作用。

Antigenotoxic effects of (-)-epigallocatechin-3-gallate (EGCG), quercetin, and rutin on chromium trioxide-induced micronuclei in the polychromatic erythrocytes of mouse peripheral blood.

机构信息

a Unidad de Investigación en Genética y Toxicología Ambiental, Facultad de Estudios Superiores "Zaragoza," Universidad Nacional Autónoma de México , México , D.F , México.

出版信息

J Toxicol Environ Health A. 2014;77(6):324-36. doi: 10.1080/15287394.2013.865006.

Abstract

This study was conducted to investigate the modulating effects of (-)-epigallocatechin-3-gallate (EGCG), quercetin, and rutin on the genotoxic damage induced by Cr(VI) in polychromatic erythrocytes of CD-1 mice. The animals were divided into the following groups: (i) vehicle only; (ii) flavonoids (10 mg/kg EGCG, 100 mg/kg quercetin, 625 mg/kg rutin, or 100-625 mg/kg quercetin-rutin); (iii) Cr(VI) (20 mg/kg of CrO3); and (iv) flavonoids concomitantly with Cr(VI). All of the treatments were administered intraperitoneally (i.p.). The genotoxic damage was evaluated based on the number of micronucleated polychromatic erythrocytes (MN-PCE) obtained from the caudal vein 0, 24, 48, and 72 h after treatment. Groups treated with EGCG and quercetin exhibited no significant statistical changes in induction of MN-PCE. However, CrO3 treatment significantly increased MN-PCE induction 24 and 48 h after injection. Treatment with flavonoids prior to CrO3 exposure decreased MN-PCE induction compared with CrO3 only. The magnitudes of the potency of flavonoids were in the following order: rutin (82%) > quercetin (64%) > quercetin-rutin (59%) and EGCG (44%). The group treated with rutin significantly reduced genotoxic damage in mice treated with Cr(VI) (antioxidant effect). However rutin exerted a marginal genotoxic effect when administered alone (pro-oxidant effect). Our findings suggest protective effects of EGCG, quercetin, and rutin against genotoxic damage induced by Cr(VI).

摘要

本研究旨在探讨(-)-表没食子儿茶素没食子酸酯(EGCG)、槲皮素和芦丁对六价铬(Cr(VI))诱导的 CD-1 小鼠多染红细胞遗传毒性损伤的调节作用。动物分为以下几组:(i)仅给予载体;(ii)类黄酮(10mg/kg EGCG、100mg/kg 槲皮素、625mg/kg 芦丁或 100-625mg/kg 槲皮素-芦丁);(iii)Cr(VI)(20mg/kg CrO3);和(iv)类黄酮与 Cr(VI)同时给药。所有处理均经腹腔注射(i.p.)。基于尾静脉中微核多染红细胞(MN-PCE)的数量来评估遗传毒性损伤,在处理后 0、24、48 和 72 小时从尾静脉中获得 MN-PCE。用 EGCG 和槲皮素处理的组中 MN-PCE 的诱导没有明显的统计学变化。然而,CrO3 处理显著增加了注射后 24 和 48 小时 MN-PCE 的诱导。在暴露于 CrO3 之前用类黄酮处理可降低与仅 CrO3 处理相比的 MN-PCE 诱导。类黄酮的效力大小顺序如下:芦丁(82%)>槲皮素(64%)>槲皮素-芦丁(59%)和 EGCG(44%)。用芦丁处理的组显著降低了 Cr(VI)处理的小鼠的遗传毒性损伤(抗氧化作用)。然而,芦丁单独给药时具有边缘遗传毒性作用(促氧化作用)。我们的研究结果表明 EGCG、槲皮素和芦丁对 Cr(VI)诱导的遗传毒性损伤具有保护作用。

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