2022/10/01 by T. A. Seregina, Т. А. Серегина, К. В. Лобанов +5 · 21 citations
Biochemistry, Genetics and Molecular Biology · Chemistry · Environmental Science · #Antibiotics #Bacteria #Biochemistry #Biofilm #Biology #Chemistry #Enzyme #Hydrogen sulfide #Microbiology #Multidrug tolerance #Oxidative stress #Pharmaceutical and Antibiotic Environmental Impacts #Polyamine Metabolism and Applications #Sulfide #Sulfur Compounds in Biology
paper · pdf · doi:10.1134/s0026893322050120
published in Molecular Biology 56(5), 638-648 (Pleiades Publishing)
crossref issued 2022/10/01 · crossref published 2022/10/01 · crossref published-print 2022/10/01 · openalex publication_date 2022/10/01 · crossref published-online 2022/10/05 · crossref created 2022/10/05 · openalex created_date 2025/10/10 · crossref deposited 2026/03/29 · crossref indexed 2026/07/30 · openalex updated_date 2026/07/31
Abstract Counteraction of the origin and distribution of multidrug-resistant pathogens responsible for intra-hospital infections is a worldwide issue in medicine. In this brief review, we discuss the results of our recent investigations, which argue that many antibiotics, along with inactivation of their traditional biochemical targets, can induce oxidative stress (ROS production), thus resulting in increased bactericidal efficiency. As we previously showed, hydrogen sulfide, which is produced in the cells of different pathogens protects them not only against oxidative stress but also against bactericidal antibiotics. Next, we clarified the interplay of oxidative stress, cysteine metabolism, and hydrogen sulfide production. Finally, demonstrated that small molecules, which inhibit a bacterial enzyme involved in hydrogen sulfide production, potentiate bactericidal antibiotics including quinolones, beta-lactams, and aminoglycosides against bacterial pathogens in in vitro and in mouse models of infection. These inhibitors also suppress bacterial tolerance to antibiotics by disrupting the biofilm formation and substantially reducing the number of persister bacteria, which survive the antibiotic treatment. We hypothesise that agents which limit hydrogen sulfide biosynthesis are effective tools to counteract the origin and distribution of multidrug-resistant pathogens.