首页> 外文期刊>RSC Advances >Mechanistic insight into the photodynamic effect mediated by porphyrin-fullerene C-60 dyads in solution and in Staphylococcus aureus cells
【24h】

Mechanistic insight into the photodynamic effect mediated by porphyrin-fullerene C-60 dyads in solution and in Staphylococcus aureus cells

机译:对卟啉 - 富勒烯C-60二元溶液中介导的光动力学效应和金黄色葡萄球菌细胞的机械洞察

获取原文
获取原文并翻译 | 示例
           

摘要

The photodynamic action mechanism sensitized by a non-charged porphyrin-fullerene C-60 dyad (TCP-C-60) and its tetracationic analogue (TCP-C-60(4+)) was investigated in solution and in Staphylococcus aureus cells. The ability of both dyads to form a photoinduced charge-separated state was evidenced by the reduction of methyl viologen in N,N-dimethylformamide (DMF). Moreover, the formation of superoxide anion radicals induced by these dyads was detected by the reduction of nitro blue tetrazolium. Also, photosensitized decomposition of l-tryptophan (Trp) was investigated in the presence of reactive oxygen species (ROS) scavengers. The addition of -carotene and sodium azide had a slight effect on reaction rate. However, photooxidation of Trp mediated by TCP-C-60 was negligible in the presence of d-mannitol, while no protection was found using TCP-C-60(4+). In a polar medium, these dyads mainly act by a contribution of type I pathway with low generation of singlet molecular oxygen, O-2((1)(g)). In S. aureus cell suspensions, an aerobic atmosphere was required for the photokilling of this bacterium. The photocytotoxicity induced by TCP-C-60 was increased in D2O with respect to water, while a small effect was found using TCP-C-60(4+). Furthermore, photoinactivation of microbial cells was negligible in the presence of sodium azide. The addition of d-mannitol did not affect the photoinactivation induced by TCP-C-60. In contrast, S. aureus cells were protected by d-mannitol when TCP-C-60(4+) was used as a photosensitizer. Also, generation of O-2((1)(g)) in the S. aureus cells was higher for TCP-C-60 than TCP-C-60(4+). Therefore, TCP-C-60 appears to act in microbial cells mainly through the mediation of O-2((1)(g)). Although, a contribution of the type I mechanism was found for cell death induced by TCP-C-60(4+). Therefore, these dyads with high capacity to produce photoinduced charge-separated state represent interesting photosensitizers to inactivate microorganisms by type I or type II mechanisms. In particular, TCP-C-60 may be located in a non-polar microenvironment in the cells favoring a type II pathway, while a contribution of the type I mechanism was produced using the cationic TCP-C-60(4+).
机译:在溶液和金黄色葡萄球菌中,研究了不带卟啉 - 富勒林-60α-60α-60α-和其旋转卟啉类二酮(TCP-C-60)及其旋翼类化合物(TCP-C-60(4+)的光动力作用机制。通过在N,N-二甲基甲酰胺(DMF)中的甲基Viologen还原,证明了两种二元形成光致电荷分离状态的能力。此外,通过减少硝基蓝四唑鎓检测这些二元的超氧化物阴离子的形成。此外,在活性氧(ROS)清除剂存在下,研究了L-色氨酸(TRP)的光敏分解。加入-Carotene和叠氮化钠对反应速率略有效果。然而,在D-甘露醇存在下,TCP-C-60介导的TRP的光氧化可以忽略不计,而使用TCP-C-60(4+)没有发现任何保护。在极性培养基中,这些二元主要通过具有低产生单态分子氧,O-2((1)(g))的I型途径的贡献起作用。在金黄色葡萄球菌细胞悬浮液中,需要一种有氧气氛来对该细菌的光吸管。通过TCP-C-60诱导的光致毒性相对于水,在D2O中增加,而使用TCP-C-60(4+)发现少量效果。此外,在叠氮化钠存在下微生物细胞的光灭绝可忽略不计。添加D-甘露醇的添加不影响TCP-C-60诱导的光灭活。相比之下,当使用TCP-C-60(4+)作为光敏剂时,S.UUREUS细胞受到D-甘露醇的保护。此外,对于TCP-C-60的OUREUS细胞中O-2((1)(G))的产生比TCP-C-60(4+)更高。因此,TCP-C-60似乎主要通过O-2的中介((1)(g))中的微生物细胞作用。尽管,发现I型机理的贡献是由TCP-C-60(4+)诱导的细胞死亡。因此,这些具有高容量产生光诱导的电荷分离状态的二元代表了有趣的光敏剂,通过类型I或II型机制灭活微生物。特别地,TCP-C-60可以位于有利于II型途径的细胞中的非极性微环境中,同时使用阳离子TCP-C-60(4+)产生I型机理的贡献。

著录项

  • 来源
    《RSC Advances》 |2018年第41期|共11页
  • 作者单位

    Univ Nacl Rio Cuarto Fac Ciencias Exactas Fis Quim &

    Nat Dept Quim Ruta Nacl 36 Km 601 X5804BYA Cordoba Argentina;

    Univ Nacl Rio Cuarto Fac Ciencias Exactas Fis Quim &

    Nat Dept Quim Ruta Nacl 36 Km 601 X5804BYA Cordoba Argentina;

    Univ Nacl Rio Cuarto Fac Ciencias Exactas Fis Quim &

    Nat Dept Quim Ruta Nacl 36 Km 601 X5804BYA Cordoba Argentina;

    Univ Nacl Rio Cuarto Fac Ciencias Exactas Fis Quim &

    Nat Dept Quim Ruta Nacl 36 Km 601 X5804BYA Cordoba Argentina;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 化学;
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号