The Fe-Cyclam-DerivedCompound [Fe(cyclam)sal]PF₆ Restrains Drug-Resistant Staphylococcus aureus Proliferation and Biofilm Formation

Staphylococcus aureus is a bacterium found on the skin and mucous membranes of humans and animals. This micro-organism is classified as an opportunistic pathogen and causes infections in both hospital and community settings. The increase in antibiotic resistance, especially methicillin-resistant S. aureus (MRSA), is a major challenge for clinical and epidemiological practice. The present study aims to investigate the potential antibacterial and antibiofilm activities of the compound [Fe(cyclam)sal]PF6 against drug-resistant strains of S. aureus. The minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) against S. aureus strains ATCC 25904, S. aureus ATCC 33591, and S. aureus 05–0052 were determined for [Fe(cyclam)sal]PF₆. First, bacterial abundance, viability, and cell envelope damage in planktonic cultures were investigated in response to this compound. Second, its potential effect on biofilm proliferation and adhesion was evaluated using different approaches: optical density (OD), scanning electron microscopy (SEM), and biochemical analysis of the extracellular polymeric matrix. The complex [Fe(cyclam)sal]PF₆ inhibited bacterial growth and induced an increase in cell death. The compound disrupted the integrity of the cell membrane, resulting in the release of cytoplasmic contents into the extracellular medium. Remarkably, the metal complex reduced the pre-established S. aureus biofilm and impaired its adhesion. Furthermore, it is not toxic to mammalian cells. The compound [Fe(cyclam)sal]PF₆ affects both the proliferation and biofilm formation of drug-resistant strains of S. aureus, demonstrating strong potential for the design of novel antimicrobial agents.