Antimutagenic evaluation of vitamins B1, B6 and B12 in vitro and in vivo, with the Ames test

被引:10
|
作者
Arriaga-Alba, Myriam [1 ]
Janett Ruiz-Perez, Nancy [1 ]
Sanchez-Navarrete, Jaime [1 ]
Lopez de Angel, Beatriz [1 ]
Flores-Lozada, Jorge [1 ]
Luis Blasco, Jose [2 ]
机构
[1] Hosp Juarez Mexico, Microbiol Res Lab, Mexico City 07760, DF, Mexico
[2] Univ Politecn Pachuca, Municipio De Zempoala 43830, Hidalgo, Mexico
关键词
Quinolones; Vitamin B; Urinary mutagens; Ames test; ESCHERICHIA-COLI; MUTAGENICITY; MODULATION; CANCER; NORFLOXACIN; MECHANISMS; PREVENTION; QUINOLONE; ACID;
D O I
10.1016/j.fct.2012.11.028
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
The aim of this work is to evaluate vitamins B antimutagenic effect against alkylatings methyl-N-nitro-N-nitrosoguanidine (MNNG), ethyl-N-nitro-N'- nitrosoguanidine (ENNG), frameshift mutagens 2-aminoanthracene (2AA) and 2-acetyl-amino-fluorene (2AF) and ROS-generating antibiotics norfloxacin (NOR) and nalidixic acid (NLX), using the in vitro Ames test. In vivo antimutagenesis studies were performed against urinary mutagens induced by NOR (70 mg/kg) or NLX (100 mg/kg) in CD1 mice. Vitamin B1 was antimutagenic against alkylatings MNNG (P < 0.05) or ENNG (P < 0.001). In fact as per the results observed during the current study, none of the vitamins reduced mutagenesis caused by frameshift mutagens. All of them reduced mutagenesis of NOR or NIX (P < 0.001). In vivo studies showed that vitamins B1 and B6 (10 or 100 mg/kg) reduced urinary mutagens from NOR (P < 0.001) or NLX (P < 0.02) either free or beta-glucoronidase-conjugates. None of the studied samples were toxic for the employed antimutagenic system. Vitamin B12 (4 mg/kg) reduced urinary mutagens of NOR or NIX (P < 0.02). Vitamins B inhibited DNA mutations induced by ROS generated by NLX or NOR, both in vitro and in vivo. Vitamin B1 is antimutagenic against mutations induced by the alkylating MNNG or ENNG. Based on the observations, employment of vitamins B in vivo can be a promising alternative to reduce genotoxic risk exposure to ROS. Published by Elsevier Ltd.
引用
收藏
页码:228 / 234
页数:7
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