Synthesis and bacteriostatic properties of ciprofloxacin-modified α-cobalt-substituted Keggin-structured polyoxometalate isomer single-crystal materials

Given the international restrictions on the use of antibiotics, there is an urgent need to develop new antibacterial materials in the field of antibacterial inhibition that exhibit excellent performance, while ensuring safety, stability, and resistance to drug development. These materials should be designed to minimize the risk of drug resistance. Polyoxometalate isomers show good application prospects as green bacteriostatic agents with unique properties. In this study, we synthesize polyoxometalate isomer (α-SiW11CoO39) single crystal materials (α-SiW11CoO39-CF) materials with ciprofloxacin (CF) as a modifying ligand by the hydrothermal method. The synthesized single-crystal materials are further characterized by X-ray crystal diffraction. To evaluate the bacteriostatic properties of the single-crystal material, we conduct tests using the disc diffusion method, the colony counting method, and minimum inhibitory concentration (MIC) method. The experimental results demonstrate that the materials exhibit effective bacteriostatic properties against Escherichia coli (E. coli: MIC = 12 μg mL−1, diameter of inhibition circle (D) = 3.15 cm, inhibition rate (I%) = 99.57%), Bacillus subtilis (B. subtilis: MIC = 45 μg mL−1, D =2.95 cm, I% = 99.43%), and Staphylococcus aureus (S. aureus: MIC = 56 μg mL−1, D = 2.75 cm, I% = 98.56%). Moreover, the materials displays greater bacteriostatic activity against Gram-negative bacteria (E. coli) compare to Gram-positive bacteria (B. subtilis and S. aureus). In this study, the antimicrobial mechanisms of single-crystal materials are investigated. It is found that these materials can disrupt the bacterial cell wall, which in turn affects the normal production of Adenosine triphosphate (ATP), the energy system of the bacteria. Additionally, the presence of single-crystal materials increases the level of reactive oxygen species (ROS), which further interferes with the normal metabolism of the bacterial cell. Ultimately, these disruptions and disturbances lead to bacterial death.