Author(s): Arshed Shihad, Maksim Khancheuski, Aliaksei Sysa, Evgeniy Gritskevitch, Evgeniy Kvasyuk and Viktar Lemiasheuski

Abstract: Recently, it was postulated that antibacterial substances kill bacteria by a common mechanism involving the formation of reactive oxygen species, in addition to particular drug-target interactions (ROS). However, there is a lot of controversy about this mechanism that produces hydroxyl radicals. Different experimental approaches are anticipated to be the root of the inconsistent results because the role of ROS to antibiotic-mediated death most likely varies on the circumstances. In the current work, the bacteria strains Escherichia coli, Sarcina lutea, Bacillus cereus, and Proteus mirabilis were treated with nucleoside-based compounds, and the production of ROS was measured using the markers araC, araCMP, TTU, and cCMP. It was shown over times that, the formation of intracellular reactive oxygen species (ROS) was increased by the examined modified pyrimidine nucleoside derivatives (validated via DCFA-DA probe assay). For instance, after treatment with araC and cCMP but not after treatment with araCMP and TTU, an increase in the ROS was detected in E. coli. Results also vary depending on the species studied and the experimental setup. Despite this, our data strongly imply that using antioxidants as therapeutic agents to treat some infections is a viable option that is starting to be used against bacterial strains.

DOI: 10.33545/26174693.2022.v6.i2b.144