Trends in Structure and Ethylene Polymerization Reactivity of Transition-Metal Permethylindenyl-phenoxy (PHENI*) Complexes.

A family of ansa-permethylindenyl-phenoxy (PHENI*) transition-metal chloride complexes has been synthesized and characterized (1-7; {(η5-C9Me6)Me(R″)Si(2-R-4-R'-C6H2O)}MCl2; R,R' = Me, tBu, Cumyl (CMe2Ph); R″ = Me, nPr, Ph; M = Ti, Zr, Hf). The ancillary chloride ligands could readily be exchanged with halides, alkyls, alkoxides, aryloxides, or amides to form PHENI* complexes [L]TiX2 (8-17; X = Br, I, Me, CH2SiMe3, CH2Ph, NMe2, OEt, ODipp). The solid-state crystal structures of these PHENI* complexes indicate that one of two conformations may be preferred, parametrized by a characteristic torsion angle (TA'), in which the η5 system is either disposed away from the metal center or toward it. Compared to indenyl PHENICS complexes, the permethylindenyl (I*) ligand appears to favor a conformation in which the metal center is more accessible. When heterogenized on solid polymethylaluminoxane (sMAO), titanium PHENI* complexes exhibit exceptional catalytic activity toward the polymerization of ethylene. Substantially greater activities are reported than for comparable PHENICS catalysts, along with the formation of ultrahigh-molecular-weight polyethylenes (UHMWPE). Catalyst-cocatalyst ion pairing effects are observed in cationization experiments and found to be significant in homogeneous catalytic regimes; these effects are also related to the influence of the ancillary ligand leaving groups in slurry-phase polymerizations. Catalytic efficiency and polyethylene molecular weight are found to increase with pressure, and PHENI* catalysts can be categorized as being among the most active for the controlled synthesis of UHMWPE.

Gill histopathologies following exposure to nanosilver or silver nitrate.

Fish gill is the site for many crucial physiological functions. It is among the first sites of xenobiotic exposure, and gill histopathological alterations may be detected soon after toxicant exposure. Silver (Ag) is one of the most toxic metals to aquatic organisms mainly due to its ability to disrupt ionic regulation. The goal of this study was to determine the effect of ionic and nanoscale Ag on fathead minnow gills by examining gill histology and Na(+)/K(+)-ATPase immunoreactivity. Fathead minnows were exposed to two measured concentrations of silver nitrate (AgNO3: 1.3 or 3.7 µg/L as Ag(+)), citrate silver nanoparticles (citrate-AgNP: 15 or 39 µg/L), and polyvinylpyrrolidone-AgNP (PVP-AgNP) (AgNP: 11 or 50 µg/L). Circulatory disturbances were the most prevalent gill alterations detected and were significantly increased in all Ag treatment groups compared to control. AgNO3 (1.3 µg/L) was the only treatment that significantly elevated the number of total mucous goblet cells present. In all other Ag treatments, the percent of degenerated goblet cells was significantly increased compared to control. When the sum of all histopathological abnormalities (weighted index) was calculated, all Ag groups displayed a significantly higher index, with citrate-AgNP having the highest toxicity (index of 10 ± 0.32 versus 2.4 ± 0.6 in controls). Gill Na(+)/K(+)-ATPase immunoreactivity was decreased by Ag. These results indicated that both AgNO3 and AgNP created similar disruptions in gill structure and ionic regulation, possibly due to the ionic Ag portion of each treatment.

Alteration in Pimephales promelas mucus production after exposure to nanosilver or silver nitrate.

The fish gill's ability to produce mucus effectively is a critical part of the stress response and protection against xenobiotic toxicity. Adult fathead minnows were exposed to silver nitrate (0.82 µg/L or 13.2 µg/L), polyvinylpyrrolidone-coated silver nanoparticles (11.1 µg/L or 208 µg/L), and citrate-coated silver nanoparticles (10.1 µg/L or 175 µg/L) for 96 h. Mucus concentrations based on glucose as a surrogate were determined at 0 h, 1 h, 2 h, 3 h, 4 h and 24 h after re-dosing each day. Higher mucus production rates following silver treatment were observed at the beginning as compared to controls and compared to after 3 d of exposure. Control fish produced consistent mucus concentrations throughout the exposure (0.62 mg/L and 0.40 mg/L at 24 h and 96 h, respectively). Following 24 h of exposure, all silver treatment groups produced significantly more mucus than controls. Following 96 h of exposure, mucus concentrations in treatment groups were significantly reduced compared with each respective treatment at 24 h. Reduced mucus production following long-term silver exposure could prevent the gills from removing silver, and thus increase toxicity.