Reimer K, Schreier H, Erdos G, König B, König W, Fleischer W
Mundipharma GmbH, Limburg.
Zentralbl Hyg Umweltmed. 1998 Feb;200(5-6):423-34.
The microbicidal activity of the broad spectrum antimicrobial agent povidone-iodine is due to the strong oxidizing effects of free iodine on functional groups of amino acids, nucleotides and double bonds of unsaturated fatty acids. While the chemical mechanism of action of PVP-iodine is well understood, the actual sequence of events on the cellular and molecular level that causes rapid cell death has not been fully understood. The aim of this study was to elucidate effects of povidone-iodine on cell ultrastructure by electron microscopy and to monitor changes in enzyme activity and nucleotide efflux. Staphylococcus aureus, E. coli and C. albicans, medically relevant gram-positive, gram-negative and yeast micro-organisms, served as models. In the presence of povidone-iodine, rapid partitioning of the cytoplasm and pronounced coagulation of nuclear material was noted. Especially C. albicans exhibited a rapid, dose-dependent "loosening" of the cell wall; cells remained intact without lysis, rupture or wall breakage. Changes in beta-galactosidase and nucleotide concentrations were measured in E. coli. A rapid and dose-dependent loss of cellular beta-galactosidase activity was found, with no increase in the supernatant; loss of cellular nucleotides corresponded with an increase in the supernatant. Electron microscopy and biochemical observations support the conclusion that povidone-iodine interacts with cell walls of micro-organisms causing pore formation or generating solid-liquid interfaces at the lipid membrane level which lead to loss of cytosol material, in addition to enzyme denaturation. The chemical mechanism of action explains the fact that povidone-iodine does never generate resistance in micro-organisms.
广谱抗菌剂聚维酮碘的杀菌活性归因于游离碘对氨基酸官能团、核苷酸以及不饱和脂肪酸双键的强氧化作用。虽然聚维酮碘的化学作用机制已为人熟知，但在细胞和分子水平上导致细胞快速死亡的实际事件序列尚未完全明了。本研究的目的是通过电子显微镜阐明聚维酮碘对细胞超微结构的影响，并监测酶活性和核苷酸外排的变化。金黄色葡萄球菌、大肠杆菌和白色念珠菌，这些医学上相关的革兰氏阳性、革兰氏阴性和酵母微生物，用作模型。在聚维酮碘存在的情况下，观察到细胞质快速分离和核物质明显凝固。尤其是白色念珠菌表现出细胞壁快速、剂量依赖性的“松弛”；细胞保持完整，没有裂解、破裂或细胞壁破损。在大肠杆菌中测量了β-半乳糖苷酶和核苷酸浓度的变化。发现细胞β-半乳糖苷酶活性快速且剂量依赖性丧失，而上清液中没有增加；细胞核苷酸的丧失与上清液中的增加相对应。电子显微镜和生化观察结果支持以下结论：聚维酮碘与微生物细胞壁相互作用，导致在脂质膜水平形成孔隙或产生固液界面，除了酶变性外，还会导致细胞质物质流失。其化学作用机制解释了聚维酮碘在微生物中从不产生耐药性这一事实。
