RESUMEN
A multi-functional anti-pathogen coating with "release-killing", "contact-killing" and "anti-adhesion" properties was prepared from biocompatible polymer encapsulated chlorine dioxide (ClO2) which protected the active ingredient from the outside environment. A slow sustained-release of ClO2 from micelles over fifteen days was detected for long-term release-killing. Micelles only release ClO2 on demand in minimum inhibitory concentrations. We prepared nanoparticles which were covalently clustered on micelle surfaces to improve contact-killing as well as to improve the stability of the micelle. Copper nanoparticles were generated using the biosynthesis method including l-vitamin C, which avoids the toxicity and allows for the preparation of copper nanoparticles in a green environment. Synergistic anti-pathogen activity could be generated by a combination of micelle released ClO2 and ascorbic acid. In addition to release-killing and contact-killing, a pluronic polymer coated surface also provides an additional "anti-adhesion" property through its protein-repelling ability. In this research, the designed coating demonstrated a broad-spectrum of activity to kill drug-resistant bacteria, viruses and spores in short period of time. Based on scanning electron microscopy (SEM), transmission electron microscopy (TEM) and anti-oxidase assays, we found that the designed coatings killed the pathogens via bio-oxidation. We also carried out acute respiratory toxicity tests in this research. Analysis of blood samples, lung function and histopathological slices indicated that the synthesized micelles allowed a controlled and sustained release of ClO2 to kill pathogens while maintaining an overall ClO2 concentration in the air within a safe range.
RESUMEN
The aim of this study was to explore the mechanism of the nervous system lesions induced by formaldehyde (FA). Male Balb/c mice were exposed to gaseous formaldehyde for 7 days (8 h/d) with three different concentrations (0, 0.5 and 3.0 mg/m(3)). A group of animals injected with the nitric oxide synthase inhibitor L-NMMA (0.01 mL/g) was also set and exposed to 3.0 mg/m(3) FA. The concentrations of cAMP, cGMP, NO and the activity of NOS in cerebral cortex, hippocampus and brain stem were determined by corresponding assay kits. The results showed that, compared with the control (0 mg/m(3) FA) group, the cAMP contents in cerebral cortex and brain stem were significantly increased in 0.5 mg/m(3) FA group (P < 0.05), but decreased in 3.0 mg/m(3) FA group (P < 0.05); The concentration of cAMP in hippocampus was significantly decreased in 3.0 mg/m(3) FA group (P < 0.05). In comparison with the control group, L-NMMA group showed unchanged cAMP contents and NOS activities in different brain regions, but showed increased cGMP contents in hippocampus and NO contents in cerebral cortex (P < 0.05). In addition, compared with 3.0 mg/m(3) FA group, L-NMMA group showed increased contents of cAMP and reduced NOS activities in different brain regions, as well as significantly decreased cGMP contents in cerebral cortex and brain stem and NO content in brain stem. These results suggest that the toxicity of FA on mouse nervous system is related to NO/cGMP and cAMP signaling pathways.