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[未稀释、稀释(75%)和无酒精红酒对潜在致癌金属铬(VI)诱导的遗传毒性损伤的体内效应]

[IN VIVO EFFECT OF RED WINE UNDILUTED, DILUTED (75%) AND ALCOHOL-FREE ON THE GENOTOXIC DAMAGE INDUCED BY POTENTIAL CARCINOGENIC METALS: CHROMIUM [VI]].

作者信息

García Rodríguez María del Carmen, Mateos Nava Rodrigo Aníbal, Altamirano Lozano Mario

机构信息

Unidad de Investigación en Genética y Toxicología Ambiental (UNIGEN), Facultad de Estudios Superiores "Zaragoza", Universidad Nacional Autónoma de México (UNAM). México..

出版信息

Nutr Hosp. 2015 Oct 1;32(4):1645-52. doi: 10.3305/nh.2015.32.4.9520.

DOI:10.3305/nh.2015.32.4.9520
PMID:26545530
Abstract

INTRODUCTION

the carcinogenesis may be initiated and promoted by the oxidative DNA damage. The compounds of chrome (Cr [VI]) cause oxidative stress (EOx) and are recognized as carcinogens in humans. In this sense, it is proposed that drinks with a high antioxidative potential, such as red wine, may have protective or modulatory effects on the oxidative DNA damage.

OBJECTIVE

to study the effects of the administration in vivo of undiluted, diluted (75%) and alcohol-free red wine on the genotoxic damage induced by carcinogenic metals (Cr [VI]), by evaluating the micronucleus (MN) in polychromatic erythrocytes (EPC) in mice (CD-1).

MATERIAL AND METHOD

it was randomly organized the follow groups: (i) control, (ii) undiluted, diluted and alcohol-free red wine (free access), (iii) CrO3 (20 mg/kg by intraperitoneal route) and (iv) CrO3-red wine. The evaluations were made in blood samples obtained from the caudal vein, in which it was identified the MN and EPC before, during and after treatments.

RESULTS AND DISCUSSION

the red wine (diluted and alcohol-free) was capable of decreasing the averages of MN induced by CrO3, demonstrating its modular capacity in vivo in the oxidative DNA damage caused by EOx-induced carcinogens. The administration of only undiluted red wine presented toxic effects.

CONCLUSIONS

our results raises expectations on the use of substances like the red wine for the protection or modulation of genotoxic damage, encouraging its application in the carcinogenic and mutagenic processes.

摘要

引言

氧化DNA损伤可能引发并促进癌症发生。铬(Cr[VI])化合物会导致氧化应激(EOx),并被公认为人类致癌物。从这个意义上说,有人提出具有高抗氧化潜力的饮品,如红酒,可能对氧化DNA损伤具有保护或调节作用。

目的

通过评估CD-1小鼠多染性红细胞(EPC)中的微核(MN),研究未稀释、稀释(75%)和无醇红酒的体内给药对致癌金属(Cr[VI])诱导的遗传毒性损伤的影响。

材料与方法

随机分组如下:(i)对照组,(ii)未稀释、稀释和无醇红酒(自由饮用)组,(iii)CrO3(腹腔注射20mg/kg)组,(iv)CrO3-红酒组。对从尾静脉采集的血样进行评估,在处理前、处理期间和处理后识别MN和EPC。

结果与讨论

红酒(稀释和无醇)能够降低CrO3诱导的MN平均值,表明其在体内对EOx诱导的致癌物引起的氧化DNA损伤具有调节能力。仅给予未稀释红酒会产生毒性作用。

结论

我们的结果提高了对使用红酒等物质保护或调节遗传毒性损伤的期望,鼓励其在致癌和诱变过程中的应用。

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