Synthesis of 2-[(2-pyridyl)amino]ethyl beta-D-lactosaminide and evaluation of its acceptor ability for sialyltransferase: a comparison with 4-methylumbelliferyl and dansyl beta-D-lactosaminide

We reported the synthesis of beta-D-lactosaminide with a 2-aminopyridyl group that is linked to a glycosyl tether at the reducing end. This fluorescent disaccharide acts as an acceptor for both alpha-(2-->6)- and alpha-(2-->3)-sialyltransferases. In addition, the acceptor ability of this disaccharide was evaluated and compared with that of beta-D-lactosaminide having a dansyl or a 4-methylumbelliferyl group.     

Role of ICAM-1 in chronic ethanol consumption-enhanced liver injury after gut ischemia-reperfusion in rats

Intercellular adhesion molecule-1 (ICAM-1) has been implicated in the hepatic microvascular dysfunction elicited by gut ischemia-reperfusion (I/R). Although the effects of chronic ethanol (EtOH) consumption on the liver are well known, it remains unclear whether this condition renders the hepatic microcirculation more vulnerable to the deleterious effects of gut and/or hepatic I/R. The objectives of this study were to determine whether chronic EtOH consumption alters the severity of gut I/R-induced hepatic microvascular dysfunction and hepatocellular injury and to determine whether ICAM-1 contributes to this response. Male Wistar rats, pair fed for 6 wk a liquid diet containing EtOH or an isocaloric control diet, were exposed to gut I/R. Intravital video microscopy was used to monitor leukocyte recruitment in the hepatic microcirculation, the number of nonperfused sinusoids (NPS), and plasma concentrations of endotoxin and tumor necrosis factor-alpha. Plasma alanine aminotransferase (ALT) levels were measured 6 h after the onset of reperfusion. In control rats, gut I/R elicited increases in the number of stationary leukocytes, NPS, and plasma endotoxin, tumor necrosis factor-alpha, and ALT. In EtOH-fed rats, the gut I/R-induced increases in NPS and leukostasis were blunted in the midzonal region, while exaggerated leukostasis was noted in the pericentral region and terminal hepatic venules. Chronic EtOH consumption also enhanced the gut I/R-induced increase in plasma endotoxin and ALT. The exaggerated responses to gut I/R normally seen in EtOH-fed rats were largely prevented by pretreatment with a blocking anti-ICAM-1 monoclonal antibody. In conclusion, these results suggest that chronic EtOH consumption enhances gut I/R-induced hepatic microvascular dysfunction and hepatocellular injury in the pericentral region and terminal hepatic venules via an enhanced hepatic expression of ICAM-1.     

A zigzag chain coordination polymer consisting of silver(I) ion having square planar geometry

Silver(I) complexes of hexakis(tolylsulfanyl)benzene (htsb), [Ag(htsb)](PF₆) (1), have been prepared and their molecular structures were determined by X-ray crystallography. In 1, the silver ion prefers a square planar coordination geometry comprized of four S atoms from two different htsb molecules and producing a zigzag chain structure of AgS in the silver coordination polymer. Based on the thermo-gravimetry analysis results, two tolylsulfanyl groups were easily eliminated at approximately 211 °C. However, [Ag(htsb)(2-butanone)] (PF₆) (2), which were obtained by the reactions in different solvents, showed a different colors and thermal degradation behaviors.     

Syntheses and crystal structures of mononuclear [2.2]paracyclophane complexes of rhodium and iridium supported by the pentamethylcyclopentadienyl ligand [M(η-pcp)(η-C5Me5)](BF4)2 (M=Rh and Ir)

Mononuclear [2.2]paracyclophane complexes of Rh and Ir, [M(η⁶-pcp)(η⁵-C₅Me₅)](BF₄)₂ (M=Rh (1) and Ir (2); pcp=[2.2]paracyclophane) were crystallized and their structures were first characterized crystallographically. On both pcp complexes the metal atom is bonded to the benzene ring on one side of the pcp ligand in the η⁶-coordination mode. The metal atom is also supported by the η⁵-C₅Me₅ ligand to afford a triple-decker sandwich structure. In Rh pcp complex 1 the average RhC(pcp) and RhC(C₅Me₅) distances are 2.284(2) and 2.161(2) Å, respectively. The average C(pcp)C(pcp) distance of 1.407(4) Å with the Rh atom is longer than that (1.388(4) Å) without a Rh atom. Similarly, the average IrC(pcp) and IrC(C₅Me₅) distances in Ir pcp complex 2 are 2.275(3) and 2.174(3) Å, respectively. The average C(pcp)C(pcp) distance of 1.410(4) Å with the Ir atom is longer than that (1.388(4) Å) without an Ir atom. It is interesting that the average interannular distances of 2.97 Å for 1 and 2 between two decks of the pcp ligand are shorter than that (3.09 Å) of the metal-free pcp ligand, indicative of the decrease of the repulsive π-interaction between benzene rings. The Rh pcp complex gave the well-resolved ¹H NMR signals of [Rh(η⁶-pcp)(η⁵-C₅Me₅)]²⁺, whereas the Ir pcp complex exhibited two kinds of ¹H NMR signals which were assigned as [Ir(η⁶-pcp)(η⁵-C₅Me₅)]²⁺ and [Ir₂(η⁶-pcp)(η⁵-C₅Me₅)₂]⁴⁺ in (CD₃)₂CO at 23 °C.     

GBF1, a guanine nucleotide exchange factor for ADP-ribosylation factors,is localized to the cis-Golgi and involved in membrane association of the COPI coat

Formation of coated carrier vesicles, such as COPI-coated vesicles from the cis -Golgi, is triggered by membrane binding of the GTP-bound form of ADP-ribosylation factors. This process is blocked by brefeldin A, which is an inhibitor of guanine nucleotide exchange factors for ADP-ribosylation factor. GBF1 is one of the guanine nucleotide-exchange factors for ADP-ribosylation factor and is localized in the Golgi region. In the present study, we have determined the detailed subcellular localization of GBF1. Immunofluorescence microscopy of cells treated with nocodazole or incubated at 15 °C has suggested that GBF1 behaves similarly to proteins recycling between the cis -Golgi and the endoplasmic reticulum. Immunoelectron microscopy has revealed that GBF1 localizes primarily to vesicular and tubular structures apposed to the cis -face of Golgi stacks and minor fractions to the Golgi stacks. GBF1 overexpressed in cells causes recruitment of class I and class II ADP-ribosylation factors onto Golgi membranes. Furthermore, overexpressed GBF1 antagonizes various effects of brefeldin A, such as inhibition of membrane recruitment of ADP-ribosylation factors and the COPI coat, and redistribution of Golgi-resident and itinerant proteins. These observations indicate that GBF1 is involved in the formation of COPI-coated vesicles from the cis -Golgi or the pre-Golgi intermediate compartment through activating ADP-ribosylation factors.     

Mutagenic target for hydroxyl radicals generated in Escherichia coli mutant deficient in Mn- and Fe- superoxide dismutases and Fur,a repressor for iron-uptake systems

We previously reported that mutations in Mn- and Fe-superoxide dismutases and Fur, a repressor for iron uptake systems, simulated generation of hydroxyl radicals, and caused hypermutability in Escherichia coli. The predominant type of spontaneous mutation was GC --> TA, followed by AT --> CG, suggesting the involvement of 7,8-dihydro-8-oxoguanine (8-oxoG) and 1,2-dihydro-2-oxoadenine (2-oxoA) in DNA as well as 7,8-dihydro-8-oxodeoxyguanosine triphosphate (8-oxodGTP) and 1,2-dihydro-2-oxodeoxyadenosine triphosphate (2-oxodATP) in the nucleotide pool. To determine the targets contributing to oxidative mutagenesis, DNA or nucleotides, we characterized spontaneous mutations and compared the distribution to those in mutMY and mutT strains, in which GC --> TA and AT --> CG were predominantly induced, respectively. The hotspots and sequence contexts where AT --> CG occurred frequently in sodAB fur strain were almost identical to those in mutT strain,whereas, those where GC --> TA occurred frequently in sodAB fur strain were quite different from those in mutMY strain. These observations suggested that AT --> CG is due to 8-oxodGTP, while GC --> TA is produced by some other lesion(s). The 2-oxodATP is also a major oxidative lesion in nucleotides, and strongly induces GC --> TA. The expression of cDNA for MTH1, which can hydrolyze 2-oxodATP as well as 8-oxodGTP, partially but significantly, suppressed the GC --> TA mutator phenotype of the sodAB fur strain, whereas, it did not for the mutMY strain. Additionally, the sequence contextby 2-oxodATP in E. coli was similar to that in sodAB fur strain. These results suggested that the targets contributing to oxidative mutagenesis in sodAB fur strain are nucleotides such as dGTP and dATP, rather than DNA.     

Starch-dependent sodium accumulation in the leaves of Vigna riukiuensis

Journal of Plant Research - This research provides insight into a unique salt tolerance mechanism of Vigna riukiuensis. V. riukiuensis is one of the salt-tolerant species identified from the genus...     

On the chromaffin cells in dog adrenal medulla; with special reference to the small granule chromaffin cells (SGC cells)

Small granule chromaffin cells (SGC cells) were identified in the adrenal medulla of adult dogs. They were small in size and usually showed a high nucleo-cytoplasmic ratio. Cytoplasmic projections were occasionally observed in some of these cells. They contained a variable number of small secretory granules with diameters ranging from 70 to 300 nm, but mostly from 100 to 200 nm. The densities of the secretory granules were variable, ranging from highly dense to less dense. These adrenal SGC cells were rich in free ribosomes and polysomes, but were relatively poor in other cell organelles. Chromaffin cells which were intermediate in their characteristics (IM cells) between the SGC cells and the typical A and N cells were also identified. These IM cells contained both highly electron dense and less dense granules in various proportions. The IM cells were classified into two subgroups, according to the proportions of adrenaline type granules and noradrenaline type granules. One group resembled A cells (IM-A cells) and the other resembled N cells (IM-N cells). Light microscopic histochemical studies of A cells stained with the ammoniacal silver solution demonstrated that they contained a small number of darkly stained granules. Electron microscopic cytochemistry revealed that the electron dense granuls in the SGC cells, IM cells and A cells reacted positively with both the potassium dichromate solution at pH 4.1 and the ammoniacal silver solution.     

Silver(I) tetraiodoethylene complexes with twisted olefin moiety

The reactions of silver perchlorate and tetraiodoethylene in different solvents, namely, benzene and toluene, isolated two silver(I)–iodocarbon complexes, [Ag(C₂I₄)(C₆H₆)₂(ClO₄)] (1) and [Ag(C₂I₄)(ClO₄)] (2). Both compounds contain intact iodoalkenes which coordinate via σ-donation of a halogen lone pair and retain their carbon–iodine bonds. Owing to the participation of the benzene molecules in coordination, complex 1 is found to be a discrete monomer in which the five-coordinate geometry of the silver ion is comprised of two benzene molecules, one C₂I₄ group and one perchlorate ion. In contrast, the unsaturated coordination environment of the metal ion in 2 is filled by the second iodocarbon group leading to a two-dimensional framework. The coordinated tetraiodoethylene molecules involve severe twisting of the C=C double bond, causing the C=C stretching band to move to a lower frequency.     

XRCC1 interactions with multiple DNA glycosylases: a model for its recruitment to base excision repair

Repair of chemically modified bases in DNA is accomplished through base excision repair (BER). This pathway is initiated by a specific DNA glycosylase that recognizes and excises the altered base to yield an abasic (AP) site. After cleavage of the AP site by APE1, repair proceeds through re-synthesis and ligation steps. In mammalian cells, the XRCC1 protein, essential for the maintenance of genomic stability, is involved in both base excision and single-strand break repair. XRCC1 participates in the first step of BER by interacting with the human DNA glycosylases hOGG1 and NEIL1. To analyze the possibility of a general mechanism involving the interaction of XRCC1 with DNA glycosylases we used XRCC1 to pull-down DNA glycosylases activities from human cell extracts. XRCC1 co-purifies with DNA glycosylase activities capable of excising hypoxanthine and dihydrothymine, in addition to 8-oxoguanine, but not uracil. Biochemical analyses with the purified proteins confirmed the interactions between XRCC1 and MPG, hNTH1 or hNEIL2. Furthermore, XRCC1 stimulates the activities of these enzymes. In vivo localization studies show that after genotoxic treatments these DNA glycosylases can be found associated with XRCC1 foci. Our results support a BER model in which XRCC1 is recruited to the repair of alkylated or oxidized bases by the enzyme recognizing the lesion. XRCC1 would then coordinate the subsequent enzymatic steps and modulate the activities of all the proteins involved.