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首页> 外文期刊>Photodiagnosis and photodynamics therapy >Mechanistic insight of the photodynamic inactivation of Escherichia coli by a tetracationic zinc(ll) phthalocyanine derivative
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Mechanistic insight of the photodynamic inactivation of Escherichia coli by a tetracationic zinc(ll) phthalocyanine derivative

机译：四阳离子锌（II）酞菁衍生物对大肠杆菌进行光动力学灭活的机理研究

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Photodynamic inactivation (PDI) of Escherichia coli has been studied in cultures treated with zinc(ll) 2,9,16,23-tetrakis[4-(N-methylpyridyloxy)]phthalocyanine (ZnPPc~(+4)) to obtain insight about the mechanism of damage. This phthalocyanine is rapidly bound to cells, reaching a value of ～0.8nmol/10~6 cells when the cultures were incubated with 2μM sensitizer. After 30min of irradiation, a 4 log decrease of E. coli survival was observed. The photocytotoxic action was investigated in plasmid and genomic DNA by electrophoretic analysis. Absorption spectroscopic studies showed that this cationic phthalocyanine interacts strongly with DNA (K_(dna) = 4.7 × 10~6 M~(-1)). Photocleavage of calf thymus DNA sensitized by ZnPPc~+4 was not found even after long irradiation periods. Similar results were also observed in genomic DNA extracted from E. coli cells after PDI treatment. Modifications of plasmid DNA isolated from bacteria were only observed after long irradiation periods. However, under these conditions transmission electron microscopy of the PDI bacteria revealed an aggregation of cytoplasmic macromolecules and irregularities in cell barriers. Also, scanning electron microscopy showed a shrunken appearance in cells after PDI. Even so, retease of intracellular biopolymers was not detected by absorption. On the other hand, outer and inner membranes permeabilization assays showed an increase in the permeability. Consequently, alterations in the cell membrane functionality induced by ZnPPc~(+4) appear to be the major cause of f. coli inactivation upon PDI.
机译：在用锌（II）2,9,16,23-四[4-（N-甲基吡啶氧基）]酞菁（ZnPPc〜（+4））处理的培养物中，研究了大肠杆菌的光动力学灭活（PDI），以了解损坏的机制。将酞菁与细胞快速结合，当将培养物与2μM敏化剂一起孵育时，其值达到〜0.8nmol / 10〜6个细胞。照射30分钟后，观察到大肠杆菌存活率下降了4 log。通过电泳分析质粒和基因组DNA中的光细胞毒性作用。吸收光谱研究表明，该阳离子酞菁与DNA有很强的相互作用（K_（dna）= 4.7×10〜6 M〜（-1））。 ZnPPc〜+ 4致敏的小牛胸腺DNA即使长时间照射也未发生光裂解。在PDI处理后从大肠杆菌细胞提取的基因组DNA中也观察到了相似的结果。从细菌分离的质粒DNA的修饰仅在长时间照射后才能观察到。但是，在这些条件下，PDI细菌的透射电子显微镜显示细胞质大分子的聚集和细胞屏障的不规则性。而且，扫描电子显微镜显示PDI后细胞中的皱缩外观。即使这样，也不能通过吸收检测细胞内生物聚合物的蛋白酶。另一方面，外膜和内膜的通透性测定表明通透性增加。因此，ZnPPc〜（+4）诱导的细胞膜功能改变似乎是f的主要原因。 PDI使大肠杆菌失活。

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