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π-Extended Donor-Acceptor Porphyrins and Metalloporphyrins for Antimicrobial Photodynamic Inactivation.

ABSTRACT: Free base, zinc and palladium π-extended porphyrins containing fused naphthalenediamide units were employed as photosensitizers in antimicrobial photodynamic therapy (aPDT). Their efficacy, assessed by photophysical and in vitro photobiological studies on Gram-positive bacteria, was found to depend on metal coordination, showing a dramatic enhancement of photosensitizing activity for the palladium complex.

SUBMITTER: Galstyan A

PROVIDER: S-EPMC7384002 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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π-Extended Donor-Acceptor Porphyrins and Metalloporphyrins for Antimicrobial Photodynamic Inactivation.

Galstyan Anzhela A Maurya Yogesh Kumar YK Zhylitskaya Halina H Bae Youn Jue YJ Wu Yi-Lin YL Wasielewski Michael R MR Lis Tadeusz T Dobrindt Ulrich U Stępień Marcin M

Chemistry (Weinheim an der Bergstrasse, Germany) 20200608 37

Free base, zinc and palladium π-extended porphyrins containing fused naphthalenediamide units were employed as photosensitizers in antimicrobial photodynamic therapy (aPDT). Their efficacy, assessed by photophysical and in vitro photobiological studies on Gram-positive bacteria, was found to depend on metal coordination, showing a dramatic enhancement of photosensitizing activity for the palladium complex. ...[more]

PMID: 31968144

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Project description:A promising alternative to antibiotics for treatment of Staphylococcus aureus infections is photodynamic inactivation (PDI), which employs a photosensitizer (PS) that produces cytotoxic reactive oxygen species (ROS) when exposed to molecular oxygen and antimicrobial blue light in the spectrum of 400-470 nm. Although the precise mechanistic basis of PDI has not been defined, the formation of ROS and free radicals that oxidize a number of cellular targets, including membrane lipids, damage to proteins and nucleic acids result in inactivation of essential cellular functions and subsequent cell death. Because PDI is non-selective and affects multiple cellular targets, development of resistance or tolerance to PDI has been considered to be unlikely and attempts to induce S. aureus resistance or tolerance upon repeated sub-lethal doses of PDI have not succeeded. However, multiple aspects of PDI suggest that development of tolerance is highly probable, in particular when PDI is used for treatment of infections where the environment at the infection site prevents penetration of PDI at a level sufficient to cause death of all bacteria and with tolerant phenotypes emerging from the surviving bacteria. In this study, we sought to identify the mechanisms that contribute to PDI tolerance in S. aureus. S. aureus HG003 and the isogenic HG003DmutSL strain with defects in DNA mismatch repair were used to evaluate the response of S. aureus and the roles of DNA mismatch repair and gene regulatory networks to repeated sublethal doses of PDI. Global transcriptome and genome analyses were used in an agnostic approach to identify the underlying transcriptional responses and genetic adaptations that occur as a result of repeated PDI and contribute to PDI tolerance. Our results reveal multiple metabolic, transport and cell wall biogenesis pathways that contribute to PDI tolerance, and a S. aureus regulatory gene likely responsible for the adaptive transcriptional response to PDI.

Dataset Information

π-Extended Donor-Acceptor Porphyrins and Metalloporphyrins for Antimicrobial Photodynamic Inactivation.

Publications

π-Extended Donor-Acceptor Porphyrins and Metalloporphyrins for Antimicrobial Photodynamic Inactivation.

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