Antimicrobial Resistance and Inorganic Nanoparticles.

Antibiotics are being less effective, which leads to high mortality in patients with infections and a high cost for the recovery of health, and the projections that are had for the future are not very encouraging which has led to consider antimicrobial resistance as a global health problem and to be the object of study by researchers. Although resistance to antibiotics occurs naturally, its appearance and spread have been increasing rapidly due to the inappropriate use of antibiotics in recent decades. A bacterium becomes resistant due to the transfer of genes encoding antibiotic resistance. Bacteria constantly mutate; therefore, their defense mechanisms mutate, as well. Nanotechnology plays a key role in antimicrobial resistance due to materials modified at the nanometer scale, allowing large numbers of molecules to assemble to have a dynamic interface. These nanomaterials act as carriers, and their design is mainly focused on introducing the temporal and spatial release of the payload of antibiotics. In addition, they generate new antimicrobial modalities for the bacteria, which are not capable of protecting themselves. So, nanoparticles are an adjunct mechanism to improve drug potency by reducing overall antibiotic exposure. These nanostructures can overcome cell barriers and deliver antibiotics to the cytoplasm to inhibit bacteria. This work aims to give a general vision between the antibiotics, the nanoparticles used as carriers, bacteria resistance, and the possible mechanisms that occur between them.

Cell wall damage and oxidative stress in Candida albicans ATCC10231 and Aspergillus niger caused by palladium nanoparticles.

In this work the toxic effect of Palladium nanoparticles (PdNPs) was investigated in two eukaryotic cell models, Candida albicans and Aspergillus niger. PdNPs were synthesized by chemical reduction method, obtaining spherical NPs with a primary size ranging from 3 to 15 nm. PdNPs showed a hydrodynamic size of 1548 nm in Lee's minimum media. Minimal inhibitory concentration was determined at 200 and 250 ppm for Candida albicans and Aspergillus niger respectively, revealing a significant cell growth inhibition (ANOVA and tukey analysis, α = 0.5). Reactive Oxygen Species levels were increased in both microorganisms. Confocal, scanning and transmission electron microscopy studies revealed cell wall damage and cellular morphology changes, induced by the interaction of PdNPs, in both microorganisms.

Oxidative damage to Pseudomonas aeruginosa ATCC 27833 and Staphylococcus aureus ATCC 24213 induced by CuO-NPs.

The cytotoxicity of nanoparticles (NPs) and their properties are important issues in nanotechnology research. Particularly, NPs affect the metabolism of microorganisms due to NP interactions with some biomolecules. In order to assess the mechanisms underlying NPs toxicity, we studied the damage caused by copper oxide nanoparticles (CuO-NPs) on Staphylococcus aureus ATCC 24213 and Pseudomonas aeruginosa ATCC 27833. Spherical CuO-NPs characterized by their diameter (13 ± 3 nm) were synthesized with a maximum of 254 nm. These NPs reduced cell viability, with a minimum inhibitory concentration (MIC) of 500 and 700 ppm for Staphylococcus aureus and Pseudomonas aeruginosa, respectively. Surfactant was added to reduce the NP agglomeration, but it did not present any effect. The mechanism of CuO-NPs as antimicrobial agent was assessed by analyzing solubilized Cu2+, quantifying DNA release in the culture media, and measuring intracellular reactive oxygen species (ROS). CuO-NPs induced severe damage on cells as revealed by confocal optical microscopy and scanning electron microscopy (SEM). Our results indicated that CuO-NPs interacted with bacteria, triggering an intracellular signaling network which produced oxidative stress, leading to ROS generation. Finally, we concluded that CuO-NPs exhibited higher antibacterial activity on Gram-negative bacteria than on Gram-positive ones.