This review shows how beta-lactam antibiotics affect reactive oxygen species in cellular oxidative stress, suggesting new therapeutic strategies.
Reactive oxygen species (ROS) play a pivotal role in cellular damage and the signaling processes, with their production significantly influenced by antimicrobial agents such as β-lactam antibiotics. This review explores the dual role of β-lactam antibiotics and comparable agents, where relevant in antimicrobial therapy, and their significant impact on cellular oxidative stress through the production of ROS. These antibiotics not only disrupt bacterial cell wall synthesis by binding to DD-transpeptidase domains but also induce the formation of ROS, leading to protein damage via chemical modifications into quinone-like products. This process generates advanced oxidation protein products (AOPPs) that influence gene expression related to protein repair. Furthermore, β-lactam antibiotics uniquely expedite the degradation of cellular proteins, affecting the solute carrier family and leading to transcriptional reprogramming. Despite their efficacy in combating bacterial infections, the production of ROS by these antibiotics also poses risks, including oxidative damage and potential antibiotic resistance. Understanding these mechanisms provides insights into optimizing therapeutic strategies and mitigating adverse effects associated with β-lactam and comparable agents, where relevant.
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Basu et al. (2025) studied this question.
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