Gichner T, Voutsinas G, Patrineli A, Kappas A, Plewa M J
Institute of Experimental Botany, Prague, Czech Republic.
Mutat Res. 1994 Sep 1;309(2):201-10. doi: 10.1016/0027-5107(94)90093-0.
The m-, o- and p-isomers of aminobenzoic acid (ABA) repressed the mutagenicity of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in Salmonella typhimurium TA100. Their antimutagenic potency was in the order of o-ABA > m-ABA > p-ABA. The mechanism of this antimutagenicity is ascribed mainly to the decomposition of MNNG induced by the aminobenzoic acid isomers outside or within the bacterial cells. The inhibition of plant cell peroxidases and bacterial acetyltransferases that are required for the plant activation of 2-aminofluorene (2-AF) to mutagenic product(s) may participate in the repression of 2-AF mutagenesis by the aminobenzoic acids in S. typhimurium strain YG1024. The aminobenzoic acid isomers exhibited no inhibitory effects towards the direct-acting agent 2-acetoxy-2-acetylaminofluorene, the stable diacetylated metabolic product of 2-AF.
氨基苯甲酸（ABA）的间位、邻位和对位异构体抑制了鼠伤寒沙门氏菌TA100中N-甲基-N'-硝基-N-亚硝基胍（MNNG）的诱变性。它们的抗诱变效力顺序为邻位ABA＞间位ABA＞对位ABA。这种抗诱变作用的机制主要归因于氨基苯甲酸异构体在细菌细胞外或细胞内诱导的MNNG分解。对植物将2-氨基芴（2-AF）激活为诱变产物所需的植物细胞过氧化物酶和细菌乙酰转移酶的抑制作用，可能参与了氨基苯甲酸对鼠伤寒沙门氏菌YG1024菌株中2-AF诱变作用的抑制。氨基苯甲酸异构体对直接作用剂2-乙酰氧基-2-乙酰氨基芴（2-AF的稳定二乙酰化代谢产物）没有抑制作用。
