双歧杆菌及其表面分子对MNNG诱导SOS反应的抑制作用

INHIBITORY EFFECT OF BIFIDOBACTERIUM BIFIDUM AND ITS SURFACE MOLECULES ON THE SOS REACTION INDUCED BY MNNG

化学物质对细菌的基因毒作用与其对哺乳动物的致突变性和致癌性密切相关。为探讨双歧杆菌抗致癌作用的机理，本文研究了双歧杆菌及其表面分子———酯磷壁酸、细胞壁肽聚糖和双歧杆菌培养乏液对已知致癌剂Ｎ－甲基Ｎ′－硝基－Ｎ－亚硝基胍（ＭＮＮＧ）诱导ＥｃｏｌｉＰＱ３７菌株ＳＯＳ反应的抑制作用。结果表明，双歧杆菌全菌、脂磷壁酸、细胞壁肽聚糖、培养乏液均能不同程度地抑制ＭＮＮＧ的诱变性，其中以脂磷壁酸作用最强，细胞壁肽糖与全菌相当，培养乏液也有一定的抗诱变作用，未培养过双歧杆菌的原培养液无抗诱变性。双歧杆菌及其表面分子的这种体外抗诱变作用机理，可能是通过与诱变剂发生结合作用掩盖了诱变剂的活性基团或使诱变剂降解，使之丧失活性。

It has been known that there is a close correlation between the genotoxic effect of chemicals on the bacteria and their mutagenesis or carcinogenesis on mammals. In order to investigate the mechanisms of the anticarcinogenicity effect of Bifidobacteria, the inhibitor effect of Bi fidobacterium bifidum(Bif1101) and its surface molecules -Lipoteichoic acid(LTA), whole cell peptidoglycan(WPG) and Spent Culture (SC) on the SOS reaction of E.coli PQ37 induced by NmethylN′nitroNnitrosoguanidine(MNNG) was studied. The results indicate that all of the tested Bifi1101 related materials appeared significant inhibition on the SOS response induced by MNNG, but the most effective components was LTA, the following WPG, Bif1101, SC. The uninoculated BL medium had not appeared effect of antimutagenicity. This kind of in vitro antimutagenicity of Bifidobacteria and its surface is probably occured by binding or cleaving the active center of mutagens.