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抗坏血酸体外和体内致突变活性的研究。

Studies on the mutagenic activity of ascorbic acid in vitro and in vivo.

作者信息

Norkus E P, Kuenzig W, Conney A H

出版信息

Mutat Res. 1983 Apr;117(1-2):183-91. doi: 10.1016/0165-1218(83)90166-0.

DOI:10.1016/0165-1218(83)90166-0
PMID:6403856
Abstract

In vitro data are presented to show that ascorbic acid does not have intrinsic mutagenicity towards strain TA100 of S. typhimurium if deionized water is used to prepare the incubation medium. The addition of Cu2+ ions to the bacterial medium that contains ascorbic acid, or the use of tap water and ascorbic acid alone, causes a mutagenic and cytotoxic response that is blocked by EDTA. Additional in vitro data demonstrate that hydrogen peroxide is mutagenic to S. typhimurium strain TA100 and it is suggested that ascorbic acid may be mutagenic and cytotoxic through the generation of hydrogen peroxide. In vivo studies using a sensitive intrahepatic host-mediated mutagenicity assay indicate that ascorbic acid is not genotoxic in guinea pigs even when the dietary intake of vitamin C is above the level required for tissue saturation (5000 mg/kg body weight/day).

摘要

体外实验数据表明,如果使用去离子水制备培养介质,抗坏血酸对鼠伤寒沙门氏菌TA100菌株没有内在致突变性。向含有抗坏血酸的细菌培养基中添加铜离子,或者单独使用自来水和抗坏血酸,会引起诱变和细胞毒性反应,而这种反应可被乙二胺四乙酸(EDTA)阻断。更多体外实验数据表明,过氧化氢对鼠伤寒沙门氏菌TA100菌株具有致突变性,并且有人提出抗坏血酸可能通过产生过氧化氢而具有致突变性和细胞毒性。使用灵敏的肝内宿主介导的致突变性试验进行的体内研究表明,即使豚鼠饮食中维生素C的摄入量高于组织饱和所需水平(5000毫克/千克体重/天),抗坏血酸对豚鼠也没有遗传毒性。

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