Kondo I, Ishikawa T, Nakahara H
J Bacteriol. 1974 Jan;117(1):1-7. doi: 10.1128/jb.117.1.1-7.1974.
Resistance of Staphylococcus aureus mediated by the penicillinase (Pc-ase) plasmid to divalent metal ions of Hg and Cd was found to be controlled by different mechanisms. The Hg resistance of the Pc-ase plasmid-carrying organisms is based upon a process of changing the ion incorporated in the cell into a somewhat innocuous form. This process is independent of temperature and seems to be controlled by an inducible enzyme. The killing effect of Hg salts was not influenced by the coexistence of other di- or monovalent ions such as MgCl(2), CaCl(2), MnCl(2), and NaCl. No vaporization of Hg, which explains the resistance mechanism such as that proposed by Komura et al. for R factor-mediated Hg resistance in enterobacilli, was found in the case of Hg resistance in staphylococci. On the other hand, the resistance to Cd ion is mediated by some protective mechanism to retain the ion outside the cell. Pc-sensitive organisms not carrying the Pc-ase plasmid incorporate Cd ions into the cells, whereas the Pc-ase plasmid-carrying organisms do not. The incorporation of this ion is temperature dependent and does not take place at 4 C. When incubated with this ion at 4 C, Pc-sensitive organisms as well as Pc-resistant organisms are also able to show a resistance. The addition of CaCl(2) could eliminate the killing effect of CdCl(2) with a dose-effective response.
由青霉素酶（Pc-ase）质粒介导的金黄色葡萄球菌对汞和镉二价金属离子的抗性被发现受不同机制控制。携带Pc-ase质粒的生物体对汞的抗性基于将细胞内掺入的离子转变为某种无害形式的过程。该过程与温度无关，似乎受一种诱导酶控制。汞盐的杀伤作用不受其他二价或一价离子如氯化镁、氯化钙、氯化锰和氯化钠共存的影响。在葡萄球菌对汞的抗性情况中，未发现汞的汽化现象，而在肠杆菌中，小村等人提出的R因子介导的汞抗性的抗性机制是基于汞的汽化。另一方面，对镉离子的抗性由某种保护机制介导，以将离子保留在细胞外。不携带Pc-ase质粒的对青霉素敏感的生物体将镉离子掺入细胞，而携带Pc-ase质粒的生物体则不会。这种离子的掺入依赖于温度，在4℃时不会发生。当在4℃下与这种离子一起孵育时，对青霉素敏感的生物体以及对青霉素抗性的生物体也能够表现出抗性。添加氯化钙可以以剂量效应反应消除氯化镉的杀伤作用。
