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11.
12.
Abstract— The convulsant action of allylglycine (2-amino-4-pentenoic acid) is due to the metabolic conversion of allylglycine to 2-keto-4-pentenoic acid, a more potent glutamic acid decarboxylase inhibitor and more potent convulsant than the parent compound. We report regional changes in cerebral GABA concentration in rats after administration of d - and l -allylglycine. d -Allylglycine (3.75 mmol/kg) induced convulsions in 95–115 min, characterised by repeated clonic limb movements and rapid rotation around the head to tail axis. GABA concentrations were only reduced in cerebellum and ponsmedulla during the pre and post-convulsive periods. The localised reduction of GABA concentration is consistent with the enzymic conversion of d -allylglycine to 2-keto-4-pentenoic acid catalysed by cerebral d -amino acid oxidase, an enzyme known to be localised to the hind brain and spinal cord. l -allylglycine (1.2mmol/kg i.p.) induced convulsions in 65 -90 min, characterised by violent running followed by tonic flexion and extension. During the pre-convulsive period, GABA concentrations were reduced in all brain areas studied except the globus pallidus and ventral midbrain. The widespread decreases in GABA concentration suggest that the enzyme(s) which catalyse the conversion of l -allylglycine to 2-keto-4-pentenoic acid are widely distributed within the brain. 相似文献
13.
Prevention of thromboxane B2-induced hepatocyte plasma membrane bleb formation by certain prostaglandins and a proteinase inhibitor 总被引:1,自引:0,他引:1
Isolated hepatocytes incubated in the presence of thromboxane B2 developed many plasma membrane blebs which are a characteristic feature of toxic or ischaemic cell injury. When hepatocytes were incubated in the presence of both thromboxane B2 and the non-lysosomal proteinase inhibitor, leupeptin, were also well protected from the formation of blebs. This implies that thromboxane B2 is able to activate non-lysosomal proteinases which appear to attack certain cytoskeletal proteins. The data presented are consistent with thromboxane B2 acting as an intermediary in a proposed mechanism of cell injury and death in which elevated cytosolic free Ca2+ levels activate phospholipase A2 and the arachidonic acid cascade. 相似文献
14.
Abstract: An enzymic lipid peroxidation system has been demonstrated in the microsomal fraction of rat brain and the requirements and optimal conditions for assay determined. The involvement of NADPH-cytochrome c reductase was demonstrated in vesicles reconstituted with lipids extracted from the brain microsomal fraction. Further characterization of the system made use of substances shown to inhibit the liver microsomal system. α-Tocopherol was shown to be an effective inhibitor of lipid peroxidation in the brain microsomal system, whereas Na2 SO3 had no effect, which is indicative that free radical transfer occurs only in the hydrophobic regions. Neither superoxide dismutase nor catalase inhibited lipid peroxidation. The implications of an NADPH-cytochrome c reductase-dependent lipid peroxidation system that is not linked to a drug hydroxylation system and appears to differ from the liver microsomal system in a number of other ways are discussed. 相似文献
15.
Intact lipopolysaccharide antigens isolated from seven different immunotypes of Pseudomonas aeruginosa have been examined by 31P-NMR spectroscopy. These macromolecular complexes contain phosphorus covalently attached to the carbohydrate residues present in the lipid A moiety and the ‘core’ oligosaccharide region. The spectral signals for various ortho- and pyro-phosphoric esters were observed. All phosphate groups appeared to be mono-esterified. Certain shifts characteristic for phosphate diester groups, observed in lipopolysaccharide complexes from other Gram-negative bacteria, were absent. Furthermore, no evidence was found to indicate that phosphate groups are involved in the covalent linkage of individual lipopolysaccharide complexes to form dimers or trimers. 相似文献
16.
17.
Derek Horton 《Carbohydrate research》1978,67(2):357-370
Addition of phenyl azide to 3,5-di-O-acetyl-6,7-dideoxy-1,2-O-isopropylidene-β-l-idio-hept-6-ynofuranose (1) and subsequent saponification gave a 4-substituted 1-phenyl-1,2,3-triazole derivative (3) whose optical rotatory dispersion (o.r.d.) curve was positive. The α-d-gluco analog (5) of 1 similarly gave the 5-epimer (7) of 3; its o.r.d. curve was negative. Both 3 and 7 were degraded to the known 1-phenyl-1,2,3-triazole-4-carboxaldehyde. Similarly, addition of 2,4,6-trimethylbenzonitrile N-oxide to 1 or 5 gave the corresponding, crystalline 3-mesitylisoxazoles as single products; 13C-n.m.r. spectroscopy was used to establish the orientation of addition. Related 3-mesitylisoxazoles (11 and 13) were obtained from 1,2:3,4-di-O-isopropylidene-d-glycero-α-d-galacto-oct-7-ynopyranose (10) and its l-glycero 6-epimer (12), respectively; 11 showed the expected, large levorotation, and the 6-epimer 13 was also levorotatory. Benzonitrile (N-phenyl)imine, prepared in situ from 1-(α-chlorobenzylidene)-2-phenylhydrazine and base, did not react with 10 (or its 6-epimer 12), but did react with the 6-keto analog to give a 5-substituted 1,3-diphenyl-1,2-diazole. 相似文献
18.
—The convulsant action of methyldithiocarbazinate (MDTC), thiocarbohydrazide (TCH) and thiosemicarbazide (TSC) has been studied in mice. The relationship between dose and time to convulsions indicated that MDTC has a dual action and is more potent than TSC. Pretreatment of mice with pyridoxal phosphate (0.25 mmol/kg) protected against convulsions and death produced by low doses of MDTC or TCH, and low or high doses of TSC. Pretreatment with pyridoxine hydrochloride (0.25 mmol/kg) protected mice against TSC but not against TCH. It protected against low doses of MDTC (0.12 mmol/kg), but shortened the latency to convulsions after intermediate doses of MDTC (0.37 mmol/kg). Glutamate decarboxylase activity (GAD, EC 4.1.1.15) in whole brain homogenates from mice killed at the onset of seizures, was significantly reduced by all 3 drugs at all doses. This inhibition did not exceed 30% after any dose of TSC or TCH, but was 64% in mice killed 4 min after the injection of MDTC (0.98 mmol/kg). The addition of pyridoxal phosphate to brain homogenates abolished GAD inhibition after MDTC but not after TCH. In vitro brain GAD was 50% inhibited by 10−4m -MDTC, 18% by 10−4m -TSC and 8% by 10 −4m -TCH. Kinetic studies suggested that at low concentrations MDTC inhibits by competing with pyridoxal phosphate. At the onset of convulsions the cerebral content of pyridoxal phosphate was reduced after low or high doses of TSC (0.27 and 2.2 mmol/kg) and after high doses of MDTC (0.98 mmol/kg). All three drugs (at 10−5−10−4m ) inhibited pyridoxal phosphokinase (EC 2.7.1.35) in vitro. Short latency convulsions after MDTC (0.37–0.98 mmol/kg) very probably arise from inhibition of cerebral GAD, due to competition for coenzymic sites and/or unavailability of coenzyme. Long-latency convulsions after MDTC (0.12–0.37 mmol/kg) are comparable to those seen after TSC (0.27–2.2 mmol/kg) and may depend on a mechanism additional to inhibition of GAD. 相似文献
19.
The chemical-ionization (ci) mass spectra of the carbohydrate antibiotic lincomycin (1), its 7(S)-chloro analog clindamycin (2), and its N-deacylated derivative methyl 1-thiolincosaminide (3), produced with isobutane or ammonia as the reagent gas, display in each instance the protonated molecular-ion as the most abundant species. Only a few fragment-ions are observed, and these arise largely from low-energy, nonskeletal cleavage-reactions of the major ion, or through thermal breakdown of the original molecule; characteristic differences in the patterns of charge capture are observed as a function of the reagent gas. The spectra contrast sharply with those obtained by electron-impact (ei) mass spectrometry, wherein extreme fragmentation occurs and few prominent fragments of high mass are observed. The ci-ms technique offers considerable potential as a micro method for determining the purity of antibiotics, for analyzing them in admixture, and for monitoring reactions performed by chemical or biochemical methods to effect structural modification of antibiotics. 相似文献
20.
Focused glycomic analysis of the N-linked glycan biosynthetic pathway in ovarian cancer 总被引:1,自引:0,他引:1
Abbott KL Nairn AV Hall EM Horton MB McDonald JF Moremen KW Dinulescu DM Pierce M 《Proteomics》2008,8(16):3210-3220