Otsuji N, Endo H
Mutat Res. 1978 Jan;49(1):9-18. doi: 10.1016/0027-5107(78)90073-8.
The mode of mutagenic action of 4-benzoylamido- and 4-acetamido- 4-carboxamido-n(N-nitroso)-butylcyanamide (BCNBC, ACNBC) was studied using Escherichia coli K12 strains. The strains carrying defects in DNA-repair mechanism, AB2463 (recA) and P3478 (polA) were more sensitive than their parent strains to both compounds, while AB1886 (uvrA) showed the same sensitivity as the parental strain. About 90% of tryptophan revertants from BE1043 (trpambphoamb) by both compounds were due to mutation in suppressor genes. Suppressor analysis by using BE1047 (trpambphooch) revealed that the most frequently occurring reversion was due to a mutation in suppressor gene, supE. This implies that these two alkylnitrosocyanamides predominantly induce GC leads to AT transition.
使用大肠杆菌K12菌株研究了4-苯甲酰氨基-和4-乙酰氨基-4-羧酰胺基-N-(N-亚硝基)-丁基氰胺(BCNBC,ACNBC)的诱变作用模式。携带DNA修复机制缺陷的菌株AB2463(recA)和P3478(polA)比其亲本菌株对这两种化合物更敏感,而AB1886(uvrA)表现出与亲本菌株相同的敏感性。两种化合物使BE1043(trpambphoamb)产生的色氨酸回复突变体中约90%是由于抑制基因的突变。使用BE1047(trpambphooch)进行的抑制分析表明,最常见的回复突变是由于抑制基因supE的突变。这意味着这两种烷基亚硝基氰胺主要诱导GC向AT的转变。