Antimicrobial potential of bismuth lipophilic nanoparticles embedded into chitosan-based membrane.

The objective of this work was to analyze the antimicrobial and antibiofilm activities of bismuth lipophilic nanoparticles (BisBAL NPs) incorporated into chitosan-based membranes. Chitosan-based membranes were homogeneously embedded with BisBAL NPs, confirming the bismuth presence by scanning electron microscopy. The tensile strength of chitosan-based membrane alone or with BisBAL NPs showed similar results as elongation, suggesting that BisBAL NP addition did not affect membrane mechanical properties. Chitosan-based membranes complemented with 100 µM of BisBAL NPs caused a complete inhibition of biofilm formation and a 90-98% growth inhibition of six different oral pathogens. Cytotoxicity studies revealed that 80% of human gingival fibroblasts were viable after a 24-h exposure to the chitosan-based membrane with 100 µM of BisBAL NPs and collagen. Altogether, we conclude that the biological properties of chitosan-based membranes supplemented with BisBAL NPs could be a very interesting option for tissue regeneration.

In vitro evaluation of the antitumor effect of bismuth lipophilic nanoparticles (BisBAL NPs) on breast cancer cells.

AIM: The objective of this study was to evaluate the antitumor activity of lipophilic bismuth nanoparticles (BisBAL NPs) on breast cancer cells. MATERIALS AND METHODS: The effect of varying concentrations of BisBAL NPs was evaluated on human MCF-7 breast cancer cells and on MCF-10A fibrocystic mammary epitheliocytes as noncancer control cells. Cell viability was evaluated with the MTT assay, plasma membrane integrity was analyzed with the calcein AM assay, genotoxicity with the comet assay, and apoptosis with the Annexin V/7-AAD assay. RESULTS: BisBAL NPs were spherical in shape (average diameter, 28 nm) and agglomerated into dense electronic clusters. BisBAL NP induced a dose-dependent growth inhibition. Most importantly, growth inhibition was higher for MCF-7 cells than for MCF-10A cells. At 1 µM BisBAL NP, MCF-7 growth inhibition was 51%, while it was 11% for MCF-10A; at 25 µM BisBAL NP, the growth inhibition was 81% for MCF-7 and 24% for MCF-10A. With respect to mechanisms of action, a 24-hour exposure of 10 and 100 µM BisBAL NP caused loss of cell membrane integrity and fragmentation of tumor cell DNA. BisBAL NPs at 10 µM were genotoxic to and caused apoptosis of breast cancer cells. CONCLUSION: BisBAL NP-induced growth inhibition is dose dependent, and breast cancer cells are more vulnerable than noncancer breast cells. The mechanism of action of BisBAL NPs may include loss of plasma membrane integrity and a genotoxic effect on the genomic DNA of breast cancer cells.