Lowering of brain endothelial cell barrier function by exposure to 4'-iodo-α-pyrrolidinononanophenone.

Overuse of pyrrolidinophenones (PPs) is known to cause damage to vascular and central nervous systems, but little is known about its effect on brain endothelial barrier function. In this study, we found that exposure to 4'-iodo-α-pyrrolidinononanophenone (I-α-PNP), one of the most potently cytotoxic PPs, at sublethal concentrations decreases trans-endothelial electrical resistance and increases paracellular permeability across a monolayer of human brain microvascular endothelial cells. Treatment with I-α-PNP also elevated the production of superoxide anion.

Poly-phenylene jacketed tailor-made dendritic phenylazomethine ligand for nanoparticle synthesis.

Synthesizing metal clusters with a specific number of atoms on a preparative scale for studying advanced properties is still a challenge. The dendrimer templated method is powerful for synthesizing size or atomicity controlled nanoparticles. However, not all atomicity is accessible with conventional dendrimers.

Apoptotic mechanism in human brain microvascular endothelial cells triggered by 4'-iodo-α-pyrrolidinononanophenone: Contribution of decrease in antioxidant properties.

In this study, we newly synthesized four α-pyrrolidinononanophenone (α-PNP) derivatives [4'-halogenated derivatives and α-pyrrolidinodecanophenone (α-PDP)], and then performed the structure-cytotoxicity relationship analyses. The results showed the rank order for the cytotoxic effects, α-PNP < α-PDP < 4'-fluoro-α-PNP < 4'-chrolo-α-PNP < 4'-bromo-α-PNP < 4'-iodo-α-PNP (I-α-PNP), and suggest that cytotoxicities of 4'-halogenated derivatives were more intensive than that of elongation of the hydrocarbon chain (α-PDP). We also surveyed the apoptotic mechanism of I-α-PNP in brain microvascular endothelial (HBME) cells that are utilized as the in vitro model of the blood-brain barrier.

9,10-Phenanthrenequinone provokes dysfunction of brain endothelial barrier through down-regulating expression of claudin-5.

Chronic exposure to diesel exhaust particle (DEP) is considered to provoke dysfunction of the blood-brain barrier, but the detailed molecular mechanism remains unclear. In this study, we investigated the toxic effects of five DEP components against human vascular cells and found that, among them, 9,10-phenanthrenequinone (9,10-PQ), a major tricyclic quinone in DEP, most potently elicits the cellular toxicities. Additionally, treatment with 9,10-PQ at its cytolethal concentrations (more than 2 μM) facilitated the production of reactive oxygen species (ROS), caspase activation, and DNA fragmentation in human brain microvascular endothelial (HBME) cells, inferring that high concentrations of 9,10-PQ elicit the cell apoptosis through the ROS-dependent mechanism.

Photo-patternable electroluminescence based on one-way photoisomerization reaction of tetraoxidized triangle terarylenes.

Oxidized triangle terarylenes with asymmetric side-aryl units are synthesized, which show photo-induced turn-on yellow luminescence based on photochemical intramolecular ring-cyclization reaction in the solid state. A direct photo-patterning process for organic electroluminescent devices is successfully demonstrated with selective light irradiation through an appropriate mask-pattern.

Efficient oxidative cycloreversion reaction of photochromic dithiazolythiazole.

Electrochemical response of photochromic tearylenes was surveyed by means of cyclic voltammetry, DFT calculations, and spectroelectrochemistry. 4,5-Bis(2-phenyl-5-methylthiazolyl)-2-phenylthiazole was found to show electrochemical oxidative ring-cycloreversion reaction. The net current efficiency of the cycloreversion reaction under constant potential electrolysis was as high as 900%, which is ascribed to an electrochemical local-cell mechanism and a chain reaction mechanism.