Abstract
Metal ferrite nanoparticles (NPs) attracted much attention due to their superparamagnetic, catalytic properties and surface area to volume ratio. Among these spinel ferrite NPs have shown immense potential in nanomedicine. The objective of present research work was the synthesis of chromium-substituted spinel copper ferrite NPs [(CuCrxFe2-xO4 (0.0x1.0)] by coprecipitation method and characterization of their antibacterial activity against E. coli. The synthesized ferrite NPs were characterized by X-ray diffraction, FT-IR, UV- Vis diffuse reflectance, SEM, Brunauer-Emmett-Teller (BET) and Barrett-Joyner-Halenda (BJH) techniques. XRD analysis confirmed that the all the samples were cubic spinel in structure with crystal size of 43.3-20.2nm. It has been found that as the amount of dopant (Cr) increases, size of the NPs decreased. The E-g values were found in the range of 1.20-1.80eV for CuCrxFe(2-x)O(4) (0.0x1.0) NPs as analyzed by UV-Visible diffuse reflectance spectroscopy. The BET surface area of Cr-substituted ferrite NPs decreases as Cr content increased while the pore diameter increases when moved from CuFe2O4 to CuCrFeO2 analyzed by BJH. The antibacterial activity increases as the concentration of dopant (Cr) increased. It has been found that CuCrxFe2-xO4 NPs inhibit bacterial growth in a size dependent manner i.e., small size NPs (CuCrxFe2-xO4; 20.2nm; x=1.0) exhibit strong antibacterial activity (MIC; 2.5mg/ml), whereas large size NPs (CuCrxFe2-xO4; 43.3nm; x=0.0) inhibit bacterial growth at concentration of more 16mg/ml. SEM micrograph shows that CuCrxFe2-xO4 NPs get adhered to bacterial cell surfaces and damaged the cell membrane due to interaction between NPs and cell membrane. Cells treated with CuCrxFe2-xO4 NPs were irregular and abnormal in shape with distorted cell membrane. CuCrxFe2-xO4 NPs severely damaged E. coli cells might be because of formation of pits, indentation, deformation and distortion of cell wall and membrane, indicating significant loss of membrane integrity that may lead to cell death.