Jayawardene A, Farkas-Himsley H
J Bacteriol. 1970 May;102(2):382-8. doi: 10.1128/jb.102.2.382-388.1970.
The mechanism of action of vibriocin, a bacteriocin produced by Vibrio comma, was investigated. Its lethal action (as defined by the loss in colony-forming ability) was reversed by tryptic digestion within 7 to 10 min after adsorption. The bacteriocin had a pronounced inhibitory effect on deoxyribonucleic acid (DNA) synthesis, whereas ribonucleic acid (RNA) and protein synthesis continued, although at a reduced rate. Chloramphenicol protected sensitive bacteria from the lethal action. Degradation of bacterial DNA prelabeled with (3)H-thymidine, as measured by changes in acid-precipitable radioactivity, occurred 10 min after treatment with vibriocin. The bacteriocin per se had no detectable deoxyribonuclease activity. Observation of vibriocin-treated cells by phase-contrast microscopy, measurement of ultraviolet light-absorbing capacity of extracellular fluid, and (42)K-efflux studies indicated a damaged bacterial membrane. This impairment of membrane function occurred in the presence of chloramphenicol and thus, unlike the lethal effect of vibriocin, was independent of protein synthesis.
对由霍乱弧菌产生的细菌素弧菌素的作用机制进行了研究。其致死作用(通过集落形成能力的丧失来定义)在吸附后7至10分钟内通过胰蛋白酶消化得以逆转。该细菌素对脱氧核糖核酸(DNA)合成有明显的抑制作用,而核糖核酸(RNA)和蛋白质合成仍在继续,尽管速率有所降低。氯霉素可保护敏感细菌免受致死作用。用(3)H-胸腺嘧啶预标记的细菌DNA的降解,通过酸沉淀放射性的变化来测量,在弧菌素处理后10分钟发生。该细菌素本身没有可检测到的脱氧核糖核酸酶活性。通过相差显微镜观察经弧菌素处理的细胞、测量细胞外液的紫外线吸收能力以及(42)K外流研究表明细菌膜受损。这种膜功能的损害在氯霉素存在的情况下发生,因此,与弧菌素的致死作用不同,它与蛋白质合成无关。