Swedberg G, Sköld O
J Bacteriol. 1980 Apr;142(1):1-7. doi: 10.1128/jb.142.1.1-7.1980.
Plasmid-borne resistance to sulfonamides was studied in both newly isolated and earlier characterized R plasmids. Two different classes of drug-resistant dihydropteroate synthases were found to be responsible for most cases of plasmid-mediated sulfonamide resistance. The plasmid-coded enzymes could be completely separated from their chromosomal counterpart and also showed differences in heat stability and molecular size. The resistant and chromosomal enzymes could bind the normal substrate, p-aminobenzoic acid, with equal efficiency. In contrast, sulfonamide binding was about 10,000 times lower with the plasmid-coded enzymes than with the chromosomal enzyme. Another substrate analog, p-aminosalicylic acid, on the other hand, inhibited chromosomal and plasmid-mediated enzymes to a similar extent. Evidence was also found for the existence of a plasmid-borne resistance mechanism independent of drug-insensitive enzymes.
对新分离的和先前已鉴定的R质粒中的质粒介导的磺胺耐药性进行了研究。发现两类不同的耐药二氢蝶酸合酶是大多数质粒介导的磺胺耐药性的原因。质粒编码的酶可以与它们的染色体对应物完全分离,并且在热稳定性和分子大小上也表现出差异。耐药酶和染色体酶能以相同效率结合正常底物对氨基苯甲酸。相比之下,质粒编码的酶与磺胺的结合能力比染色体酶低约10000倍。另一方面,另一种底物类似物对氨基水杨酸对染色体和质粒介导的酶的抑制程度相似。还发现了一种独立于药物不敏感酶的质粒介导耐药机制的证据。