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PubMed2005

Total synthesis of (-)-colchicine via a Rh-triggered cycloaddition cascade.

[reaction: see text] A synthesis of the antimitotic alkaloids (-)-colchicine and (-)-isocolchicine is reported. Important steps are (a) enantioselective transfer-hydrogenation of an alkynone, (b) iodine/magnesium exchange with subsequent aromatic acylation, (c) Rh-catalyzed transformation of an alpha-diazoketone into an oxatetracyclic key intermediate through intramolecular [3 + 2]-cycloaddition of an in situ generated carbonyl ylide, and (d) regioselective conversion of the cycloadduct into a tropolone derivative. The new synthetic strategy opens an efficient enantioselective access to colchicine and structural analogues.

Colchicine↗
PubMed1977

Effect of colchicine injection prior to the initiating phase of two-stage skin carcinogenesis in mice.

Colchicine injected 5, 9 and 24 h respectively before initiation (using s.c. injection of urethane for initiating action and TPA skin applications for promoting action, in female ICR mice) led to a significant increase in skin tumour incidence in the --9-h group, and an increase in percentage malignancy in both the --5- and --9-h groups. These times corresponded to the peak of metaphase arrest by the colchicine. The results are discussed in relation in those of Pound and Withers (1963) and others, who found that mitotic stimulation at the time of urethane initiating action raised the ultimate tumour incidence; and the inference is drawn that initiating action in mouse skin may occur during the M phase, rather than during the G1, S, or G2 phases, as suggested by others.

Animals↗
PubMed1984

Effect of colchicine and calcitonin on calcemic response to metabolic acidosis.

To examine the mechanism responsible for enhanced calcium mobilization from bone in metabolic acidosis, we evaluated the effect of colchicine and calcitonin, two blockers of cell-mediated bone resorption, on the calcemic response to acute metabolic acidosis in thyroparathyroidectomized rats. Metabolic acidosis lasting 16 hr and induced by the feeding of NH4Cl led to a significant rise in serum calcium of 1.2 to 1.9 mg/dl. The administration of colchicine or calcitonin led to a decrement in serum calcium of 1.1 +/- 0.2 (P less than 0.01) and 0.7 +/- 0.2 mg/dl (P less than 0.05), respectively. Cyclic AMP levels in calvaria from rats with metabolic acidosis and from control rats were not different. These data suggest that mobilization of calcium from bone which occurs in metabolic acidosis is due, in part, to increased bone resorption, which is mediated by a cAMP-independent mechanism.

Acidosis↗
PubMed1975

Colchicine inhibition of the heparin-stimulated release of clearing-factor lipase from isolated fat-cells.

When isolated fat-cells are incubated at 25 degrees C in serum-based media containing glucose, insulin and heparin, the rise that occurs in the clearing-factor lipase activity of the incubation medium is inhibited by colchicine. The rise in the fat-cell clearing-factor lipase activity that occurs during similar incubations in the absence of heparin is not affected by colchicine.

Adipose Tissue↗
PubMed1983

Abnormal secretion of proteins into bile from colchicine-treated isolated perfused rat livers.

The microtubule poison, colchicine, caused an abnormal output of a variety of proteins into rat bile. After 3 h of exposure to the drug, livers were isolated and perfused with media of defined protein composition. There was no essential change in permeability of the hepatobiliary system to proteins (e.g. bovine serum albumin) entering bile from the perfusion fluid. The rat (serum) albumin and fibrinogen that were secreted into bile from colchicine-treated livers were probably derived from the hepatocytes. Disruption of the microtubular system reduces the secretion of proteins at the sinusoidal face of the hepatocyte and results in an accumulation of secretory vesicles in the cytoplasm. It is suggested that under these conditions some of the vesicles discharge their contents into the bile canaliculus.

Animals↗
PubMed1985

Transcytosis and paracellular movements of horseradish peroxidase across liver parenchymal tissue from blood to bile. Effects of alpha-naphthylisothiocyanate and colchicine.

The pathways for the entry of horseradish peroxidase (HRP) into bile have been investigated using the isolated perfused rat liver operating under one-pass conditions. Following a 1 min one-pass infusion of HRP, two peaks of HRP activity were noted in the bile. The first, at 5-7 min post-infusion, correlated with the biliary secretion of the [3H]methoxyinulin which was infused simultaneously with the HRP. The second peak of HRP activity occurred at 20-25 min, and correlated with the biliary secretion of 125I-IgA, which was also infused simultaneously with the HRP. If the isolated livers were perfused with a medium containing 2.5 microM-colchicine, the biliary secretion of IgA and the second secretion peak of HRP were inhibited by 60%. If rats were pretreated for 12h with alpha-naphthylisothiocyanate (25mg/100g body wt.) prior to liver isolation, the biliary secretion of [3H]methoxyinulin and the first secretion peak of HRP were increased. Taken together, these results suggest that HRP enters the bile via two routes. The faster route, which was increased by alpha-naphthylisothiocyanate and correlated with [3H]methoxyinulin entry into bile, was probably paracellular, involving diffusion across tight junctions. The slower route, which was inhibited by colchicine and correlated with the secretion of IgA, was probably due to transcytosis, possibly within IgA and other transport vesicles.

1-Naphthylisothiocyanate↗
PubMed1979

Effects of diphosphonate and colchicine administration upon acid-base changes induced in rats by bilateral nephrectomy.

1. The effects of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) and colchicine on acid--base balance were examined in intact and nephrectomized rats. 2. Both drugs increased extracellular hydrogen ion concentrations and depressed extracellular bicarbonate concentrations in nephrectomized rats compared with controls but did not alter these parameters in intact animals. 3. Intracellular hydrogen ion concentrations in the skeletal muscle of nephrectomized rats given EHDP were higher than those of control animals. 4. It is postulated that colchicine and EHDP inhibit skeletal buffering of non-volatile acids produced endogenously in nephrectomized rats.

Acid-Base Equilibrium↗
PubMed2002

Colchicine-induced apoptosis and anti-Fas localization in rat-incisor ameloblasts.

Apoptosis of ameloblasts were examined by the TdT-mediated dUTP-biotin nick end-labelling method and electron microscopy 8 h after injection of colchicine. The results showed that extensive apoptosis occurred in ameloblasts of secretion to maturation zones. To determine the possible involvement of stimulators in ameloblast apoptosis, Fas, Fas ligand, tumor-necrosis-factor alpha, and tumor-necrosis-factor receptor 1 were examined utilizing immunohistochemistry and Western blotting analysis. Only Fas was consistently detected in the secretion, transition and maturation ameloblasts and overlying enamel organ epithelia. These results suggest that ameloblasts could undergo apoptosis by colchicine and that one of the ameloblast apoptosis mediators would be the Fas receptor.

Ameloblasts↗
PubMedDate not supplied

Treatment of linear IgA bullous dermatosis of childhood with colchicine.

Linear IgA bullous dermatosis of childhood is the most common immunobullous disorder of childhood. First-line treatment includes dapsone or sulfapyridine. We report a child with linear IgA dermatosis who was treated successfully with colchicine after developing hemolytic anemia from dapsone. We recommend colchicine as an alternative therapy for linear IgA dermatosis of childhood in patients in whom first-line treatment is contraindicated or who fail first-line treatment or develop side effects from it.

Anemia, Hemolytic↗
PubMed1972

Inhibition of release of dopamine- -hydroxylase and norepinephrine from sympathetic nerves by colchicine, vinblastine, or cytochalasin-B (hypogastric nerve stimulation-exocytosis-microtubules-microfilaments-guinea pig).

Stimulation of the hypogastric nerve to the guinea pig vas deferens in the presence of phenoxybenzamine produced an enhanced release of both dopamine-beta-hydroxylase (EC 1.14.2.1) and norepinephrine. Addition of colchicine, vinblastine, or cytochalasin-B to the incubation medium caused an almost complete inhibition of release of both the amine and the enzyme. Colchicine and cytochalasin-B produced a blocking effect but did not, however, modify the ratio of dopamine-beta-hydroxylase to norepinephrine recovered in the bath fluid. The findings indicate that norepinephrine and dopamine-beta-hydroxylase are released from sympathetic nerve terminals by exocytosis and that this process is dependent upon the integrity of both microtubules and microfilaments.

Animals↗
PubMed1974

Effect of nerve growth factor on the expression of colchicine-binding activity and 14-3-2 protein in an established line of human neuroblastoma.

Purified nerve growth factor induced the outgrowth of neurites from cultured human neuroblastoma cells (NJB line) and a concomitant increase in colchicine-binding activity in extracts from these cultures. The parallel stimulation of neurite outgrowth from the cells and colchicine-binding activity of the extracts is interpreted to represent de novo synthesis of microtubular subunit protein in response to the challenge by nerve growth factor. The regulation of the expression of 14-3-2 protein, a protein characteristic of differentiated neuronal cells, was not affected in NJB cells by the addition of nerve growth factor to the culture medium. 14-3-2 protein is present in NJB cells at a concentration equal to that present in human brain from subculture to the stationary phase of growth of the tumor cells. It was concluded that these two gene products, characteristic of differentiated neural cells, are not coordinately regulated in NJB human neuroblastoma cells.

Cell Division↗
PubMed1974

Effects of phagocytosis and colchicine on the distribution of lectin-binding sites on cell surfaces.

The effect of phagocytosis on lectin binding to plasma membranes of polymorphonuclear leukocytes was examined. The specific activities of binding sites of concanavalin A and Ricinus communis agglutinin (defined as mug of lectin bound per 100 mug of membrane protein) were measured on isolated membranes; they decreased in parallel with phagocytosis. Our data suggest that this removal occurs by concentration of binding sites into internalized membrane. Colchicine and vinblastine, which did not inhibit phagocytosis, prevented the selective removal of lectin-binding sites from the surface. It was also shown that at 37 degrees lectins induce their own internalization. This property was used to define operationally three classes of lectin receptors, one of which is most extensively removed from plasma membrane during phagocytosis. Based on other morphological studies in which it is shown that before phagocytosis the surface distribution of concanavalin-binding sites is random, it is inferred that phagocytosis alters surface topography by inducing the selective movement of binding sites into membrane undergoing internalization and that colchicine-sensitive proteins are essential for this imposed topographical reorganization.

Animals↗
PubMed1975

Colchicine permeation is required for inhibition of concanavalin A capping in Chinese hamster ovary cells.

Several antimitotic, tubulin-binding agents, such as colchicine, colcemid, and podophyllotoxin, inhibit the capping of fluorescent-labeled concanavalin A in Chinese hamster ovary cells. By comparing the effects of these agents on parental cell lines on several independently selected colchicine-resistant mutants with decreased drug permeability, we have demonstrated that permeation of these drugs in required for inhibition of capping. These data support the hypothesis that these antimitotic agents interact with an intracellular component, probably microtubules, to prevent the directional movement of concanavalin A receptors on the surface membranes of Chinese hamster ovary cells.

Binding Sites↗
PubMed1975

Colchicine affects kinetics of concanavalin a-mediated agglutination of hepatoma cells and plasma membranes from liver and hepatoma cells.

Concanavalin A-mediated agglutination reactions of hepatoma cells [AH-130F(N)] and isolated liver cells, as well as of plasma membranes prepared from the liver and hepatoma, were investigated kinetically together with the effect of colchicine upon them. Concanavalin A-mediated agglutination of hepatoma cells at 25 degrees proceeded with biphasic kinetics (first and second stages of agglutination), while no appreciable agglutination of liver cells was observed in the presence of concanavalin A. The plasma membranes from the liver and hepatoma cells were similarly agglutinated with concanavalin A at 25 degrees but not at 0 degrees. The concanavalin A-mediated membrane agglutination proceeded with monophasic kinetics and was incomplete. Colchicine inhibited preferentially the second stage of concanavalin A-mediated agglutination of hepatoma cells, but it did not affect the concanavalin A-mediated agglutination of plasma membranes of both types of cells.

Agglutination↗
PubMed1976

Antisera against electrophoretically purified tubulin stimulate colchicine-binding activity.

Several rabbit antisera have been prepared against reduced and alkylated, electrophoretically purified tubulin isolated from chick brain. These antisera give a single precipitin line in Ouchterlony double diffusion plates when tested against partially purified tubulin, and label specifically microtubule- and tubulin-containing structures, such as mitotic spindles, cilia, and vinblastine-induced crystals, in a variety of cells. The same antisera also display the unique ability to stimulate the colchicine-binding activity of tubulin preparations from chick brain and Chinese hamster ovary tissue culture cells. This specific stimulation of colchicine binding activity is also obtained with the gamma globulin fractions purified by ammonium sulfate precipitation of these antisera.

Animals↗
PubMed1977

Changes in membrane microviscosity associated with phagocytosis: effects of colchicine.

The effects of phagocytosis on plasma membrane microviscosity were studied by fluorescence depolarization techniques. It was shown that lipophilic probes are accumulated in intracellular vesicles to a significant degree in fibroblasts and neutrophils. Microviscosity was thus determined from the behavior of probes in isolated membranes. Phagocytosis of oil emulsions or polystyrene beads by rabbit polymorphonuclear leukocytes induces a marked decrease in plasma membrane microviscosity that parallels the extent of phagocytosis. Liposomes made from extracts of membrane lipid show qualitatively the same changes, indicating that the alteration of microviscosity results at least in part from changes in lipid composition. The decrease in microviscosity is abolished when colchicine is present during phagocytosis. Addition of colchicine to membranes previously isolated from control or phagocytic cells has no effect on their microviscosity. The results suggest that phagocytosis is accompanied by a microtubule-dependent reorganization of membrane lipids.

Animals↗
PubMed1989

Colchicine analogues that bind reversibly to tubulin define microtubular requirements for newly synthesized protein secretion in rat lacrimal gland.

The role of microtubules in 3H-labeled protein secretion in rat lacrimal glands was probed by the use of colchicine and two of its analogues that reversibly bind to tubulin. These analogues were 2-methoxy-5-(2,3,4,4'-trimethoxyphenyl)-2,4,6-cycloheptatriene-1-o ne and 2,3,4,4'-tetramethoxy-1,1'-biphenyl, the latter having been synthesized for these studies. Immunofluorescence revealed that untreated exocrine acinar cells contained an intact microtubule network, which was totally abolished by drug addition. Subsequent drug removal restored the network for the two reversibly binding drugs--more rapidly so for the biphenyl, but this was not the case with colchicine. The protein-secretory process was examined by adding the three drugs at various stages--prepulse incubation, pulse, maturation, apical storage of granules, and discharge under cholinergic stimulation. Comparison with the kinetics of microtubular network restoration, which differed for the two reversibly binding drugs, led to the conclusion that the microtubular system is critical to the maturation phase of secretion.

Animals↗