Anti-BHMT (aa 391-402) polyclonal antibody

Upconverting nanoparticles (UCNPs) of beta-NaYF4, co-doped with Yb3+ and Tm3+ and 21-36 nm large, were synthesized using a modified thermal decomposition method. The as-synthesized UCNPs were coated with oleic acid and dispersed in nonpolar media. Their morphology, size and crystal structure were analysed with transmission electron microscopy and X-ray diffraction. The UCNPs showed a fluorescence emission spectrum characteristic of Tm3+. Their dissolution in water (pH similar to 4-5) and phosphate buffered saline (PBS, pH = 7.4) was determined from the fraction of dissolved fluoride ions using a fluoride-ion-selective electrode. The dissolution of bare UCNPs was much more prominent in PBS than in water. Two amphiphilic coatings, poly(maleic anhydride-alt-1-octadecene)-bis(hexamethylene) triamine (PMAOBHMT) and D-alpha-tocopheryl polyethylene glycol succinate (TPGS) were tested for their effects on the dissolution of the UCNPs. The coatings were formed directly on the as-synthesized UCNPs as was confirmed with electrokinetic measurements, infrared spectroscopy and thermogravimetric analyses. Both coatings enabled the dispersion of UCNPs in water, and improved the fluorescence emission intensity with respect to the bare UCNPs. However, only the PMAO-BHMT coating provided an effective protection against the dissolution of the UCNPs and long-term colloidal stability in PBS, and did not show cytotoxicity in EAhy926 endothelial cells.

Formaldehyde (FA) inhalation is hazardous to human health; but the exact molecular mechanisms associated with FA hepatotoxicity remain poorly unknown. Thus, the present study was addressed to gain better understanding of the intimate mechanisms of FA hepatotoxicity. Adult female W istar rats were distributed into 5 groups: (1) control, (2) FA; 10 ppm for 15 days, (3) FA; 10 ppm for 30 days, (4): FA; 20 ppm for 15 days and (5): FA; 20 ppm for 30 days. At the end of the experiment, liver samples from all studied groups were obtained and preserved for histopathological description, immune histo chemical examination and molecular genetics analysis. Histopathological findings of liver tissue sections revealed several adverse histopathological changes including sinusoidal congestion, liver necrosis and liver fibrosis depending on dose and duration of FA exposure. Immuno histochemical investigation of liver tissue sections immune stained with the antibody for PCNA showed strong positive immunoreactivity within numerous nuclei. Immuno histochemical investigation of liver tissue sections immunostained with the antibody for cytochrome c showed positive immune reactivity within the cytoplasm of numerous cells. On the gene expression level, exposure of rat to FA (10 or 20 ppm) for 15 days evoked down regulation in the expression level of liver Cyp2c6 and Bhmt genes. However, exposure of rat to FA (10 or 20 ppm) for 30 days elicited up regulation in the expression level of liver Cyp2c6 and Bhmt genes. Rats exposed to FA (20 ppm) for 15 or 30 days experienced down regulation in the expression level of liver Mapk12 gene. The expression of HLA-A and GSTP1 genes in liver of rats exposed to FA (10 or 20 ppm) for 15 and 30 days showed up regulation except for 10 ppm of FA at 15 days. In conclusion, this study provides cellular and molecular evidences for formaldehyde-induced hepatotoxicity. Formaldehyde confers multi mechanistic approaches in promoting hepatotoxicity. It is reasonable to assume that apoptosis, oxidative stress and inflammation be involved in formaldehyde-induced hepatotoxicity.