The phenyldimethylsilyl-cuprate reagent reacts with secondary allyl acetates stereospecifically anti, and with secondary and tertiary allyl urethanes stereospecifically syn; these reactions can be used to synthesise either enantiomer of an optically active allylsilane from a single enantiomer of an optically active allyl alcohol.
The liver is a major target for both short- and long-term actions of ethanol. The mechanisms that mediate the response of cells and tissues to chronic intake of ethanol are unknown, but it is likely that both adaptive and deleterious responses are triggered by short-term interactions of the cell with ethanol. Cellular signaling processes are candidates to mediate the connection between short- and long-term actions of ethanol. Receptor-coupled signal transduction systems in the plasma membrane of many different cell types are affected by ethanol. In the liver, the signaling processes associated with phospholipases C and D are particularly responsive to ethanol. In this review, we investigate the direct and indirect short-term effects of ethanol on the signal transduction systems in liver and discuss the possible implications for the responses of the liver to chronic ethanol exposure.
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The activation properties of inositol 1,4,5-trisphosphate (InsP3)-sensitive Ca2+ stores in permeabilized and intact hepatocytes were investigated by monitoring Mn2+ quench of fura-2 compartmentalized within these stores, as Mn2+ passed through InsP3-activated channels in a retrograde manner. In cells permeabilized in suspension the InsP3-sensitive pool size was dependent on InsP3 dose, and there was a large unresponsive compartment. By contrast, essentially all of the compartmentalized dye was accessible following activation of a small fraction of the InsP3 receptors in carefully permeabilized attached cells. After loading the cytosol of intact hepatocytes with Mn2+, both submaximal and maximal vasopressin doses caused complete quench of the entire intracellular pool of compartmentalized fura-2. Vasopressin-induced Mn2+ quench occurred in a stepwise manner at doses that gave cytosolic Ca2+ oscillations, reflecting periodic opening of intracellular Ca2+ channels. Pretreatment with thapsigargin to eliminate feedback effects of Ca2+ fluxes converted the steps to a continuous quench. The data suggest that Ca2+ stores in attached permeabilized and intact hepatocytes are luminally connected, making the entire store accessible to InsP3. In cells permeabilized in suspension, GTP increased InsP3-sensitive pool size, and this effect was inhibited by cytochalasin B. GTP did not change the initial rate of Mn2+ quench but increased the proportion of slowly accessible stores in the InsP3-sensitive compartment, apparently by recruitment of InsP3-insensitive stores. Preincubation on ice or with cytoskeletal inhibitors dissociated slowly accessible compartments from the InsP3-sensitive stores in both intact and subsequently permeabilized attached hepatocytes. Addition of GTP to permeabilized cells reversed this disruption of store continuity. It is suggested that GTP- and cytoskeleton-dependent luminal communication between Ca2+ stores is an important determinant of function, which could modulate the availability of Ca2+ for release.
Unsymmetrical secondary allylic acetates and urethanes react with the dimethyl(phenyl)silylcuprate reagent to give allylsilanes with fair to good regioselectivity.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.