Reusser F
J Bacteriol. 1968 Oct;96(4):1285-90. doi: 10.1128/jb.96.4.1285-1290.1968.
Melinacidin, a new antibacterial agent, blocked the synthesis of nicotinic acid and its amide in Bacillus subtilis cells. The inhibitory activity of the agent was reversed by nicotinic acid, its amide, or nicotinamide adenine dinucleotides, but not by l-kynurenine, l-3-hydroxykynurenine, l-hydroxyanthranilic acid, or quinolinic acid. These properties indicated that the antibiotic interferes with the conversion of quinolinic acid to nicotinate ribonucleotide by the enzyme quinolinate phosphoribosyl-transferase. However, the activity of a purified preparation of this enzyme derived from a Pseudomonas strain was not impaired by the antibiotic. This suggested that, in B. subtilis, melinacidin interferes with a reaction which occurs before the formation of quinolinic acid in the biosynthetic pathway leading to nicotinic acid. Failure of quinolinic acid to reverse melinacidin inhibition in B. subtilis cultures might be due to insufficient penetration of the cell membranes by quinolinate.
新型抗菌剂美里西丁可阻断枯草芽孢杆菌细胞中烟酸及其酰胺的合成。该药剂的抑制活性可被烟酸、其酰胺或烟酰胺腺嘌呤二核苷酸逆转，但不能被L-犬尿氨酸、L-3-羟基犬尿氨酸、L-羟基邻氨基苯甲酸或喹啉酸逆转。这些特性表明，该抗生素通过喹啉酸磷酸核糖基转移酶干扰喹啉酸向烟酸核糖核苷酸的转化。然而，源自假单胞菌菌株的该酶纯化制剂的活性并未受到该抗生素的损害。这表明，在枯草芽孢杆菌中，美里西丁干扰了在导致烟酸的生物合成途径中喹啉酸形成之前发生的反应。喹啉酸无法逆转枯草芽孢杆菌培养物中美里西丁的抑制作用，可能是由于喹啉酸对细胞膜的穿透不足。
