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Results for “Lumicolchicines”

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At least 19 recordsLinked to original sources
PubMed1986

The phagocytosis of yeast cells by monocytes: effects of colchicine, beta-lumicolchicine, and gamma-lumicolchicine.

The effect of microtubule antagonist (MA) colchicine and its two non-MA derivatives beta-lumicolchicine and gamma-lumicolchicine on the phagocytosis of yeast cells by glass-adherent monocytes were studied with a fluorescence quenching technique which allowed a distinction between the adherence and engulfment phases of phagocytosis. The engulfment of yeast cells was depressed by colchicine (p = 0.031) but not by the lumicolchicines. The adherence of yeast cells to the monocytes, on the other hand, was depressed by gamma-lumicolchicine (p = 0.028). The colchicine effect suggests that cytoplasmic microtubules play a role in the engulfment process whereas the lumicolchicine effect suggests a role of nucleoside transport over the cell membrane in the adherence process of phagocytosis.

Cell Adhesion↗
PubMed1987

Comparison of the effects of colchicine and beta-lumicolchicine on cultured adrenal chromaffin cells: lack of evidence for an action of colchicine on receptor-associated microtubules.

The involvement of microtubules in adrenomedullary secretion is presently unclear. Evidence exists for a possible role of microtubules in cholinergic nicotinic receptor-related events. We now describe the actions of the microtubule disrupter, colchicine, on primary cultures of bovine adrenal chromaffin cells and compare these with corresponding actions of beta-lumicolchicine. beta-Lumicolchicine is a structural isomer of colchicine which neither binds microtubular protein (tubulin) nor interferes with microtubule assembly. Both colchicine and beta-lumicolchicine were found to inhibit acetylcholine-induced secretion with similar potencies (half maximal inhibitory concentration 0.2-0.5 mM). The inhibitory actions of both drugs are time-dependent and reversible. However, unlike colchicine which has no inhibitory effects on secretion evoked by depolarization with excess K+, beta-lumicolchicine also inhibits K+-induced secretion. Because colchicine and beta-lumicolchicine have similar effects, the selective inhibitory actions of colchicine on nicotinic receptor-mediated secretion cannot in itself be used as evidence in support of a role of microtubules in receptor-mediated events. However, our data do not preclude such a role. Differences in the effect of colchicine and beta-lumicolchicine on K+-evoked secretion suggests different modes of action of these structural isomers on chromaffin cell function.

Acetylcholine↗
PubMedDate not supplied

Nmr studies of colchicine and its photoisomers, beta- and gamma-lumicolchicines.

Unambiguous 1H- and 13C-nmr assignments of colchicine, beta-lumicolchicine, and gamma-lumicolchicine have been obtained using a combination of 1D- and 2D-nmr spectroscopic techniques. The data indicate that gamma-lumicolchicine is a stereoisomer of beta-lumicolchicine and provide definitive evidence for their stereochemical assignments.

Colchicine↗
PubMed1994

beta-Lumicolchicine interacts with the benzodiazepine binding site to potentiate GABAA receptor-mediated currents.

An analogue of colchicine, beta-lumicolchicine, does not bind tubulin or disrupt microtubules. However, this compound is not pharmacologically completely inactive. beta-Lumicolchicine was found to competitively inhibit [3H]flunitrazepam binding and to enhance muscimol-stimulated 36Cl- uptake in mouse cerebral cortical microsacs. It also markedly potentiated GABA responses in Xenopus oocytes expressing human alpha 1 beta 2 gamma 2S, but not alpha 1 beta 2, GABAA receptor subunits; this potentiation was reversed by the benzodiazepine receptor antagonist flumazenil. These results strongly suggest a direct effect of beta-lumicolchicine on the GABAA receptor/chloride channel complex and caution that it possesses pharmacological effects, despite its inability to disrupt microtubules. Furthermore, beta-lumicolchicine is structurally unrelated to benzodiazepines or quinolines and may provide a novel approach to the synthesis of ligands for this receptor.

Animals↗
PubMed1978

The effects of lumicolchicine, colchicine and vinblastine on pigment migration in fish chromatophores.

The effects of lumicolchicine, colchicine, vinblastine and cold temperature on the pigment migration in melanophores and xanthophores of Fundulus heteroclitus and Oryzias latipes were examined by light and electron microscopy. Xanthophores of both species which contain numerous microfilaments and a poorly developed microtubule system were extremely sensitive to the alkaloids. Lumicolchicine and colchicine induced irreversible dispersion while vinblastine caused permanent aggregation of the pigments. Treatment in lumicolchicine or colchicine at 5 mM for 60 minutes did not disrupt microtubules of melanophores to an appreciable degree, however, melanosome aggregation was partially inhibited by these drug in Oryzias. When melanophores were kept in the cold in the presence of colchicine at 1 mM, almost all microtubules were disrupted and their repolymerization at room temperature was nearly completely inhibited by colchicine. These melanophores lacking in microtubules responded to epinephrine with slow aggregation. Vinblastine at 0.1 mM induced partial aggregation of melanosomes and disruption of microtubules but most melanophores were still able to respond with pigment migration. Vinblastine at 1 mM made all melanophores punctate and immobile. Large vinblastine-induced crystals were frequently seen in the dendritic processes. The results of the present investigation suggest that cytoplasmic microtubules in fish melanophores facilitate melanosome migration only in directional orientation and appear not be responsible for the motive force.

Animals↗
PubMed1976

[Effect of colchicine and lumicolchicine on the ultrastructure of non-myelinated axons in autonomic nerves in cat in vitro].

The effects of colchicine and lumicolchicine on the ultrastructure of non-myelinated axons in cat autonomic nerves were studied using in vitro preparations of inferior mesenteric ganglion/hypogastric nerves. After 24 hrs of in vitro incubation with colchicine added to the medium (10 microng/ml) a significant decrease in number of neurotubules per 1 axon was observed. In the presence of a solution of alpha-beta and gamma-lumicolchicine (10 microng/ml) severe degenerative changes occured in axons and Schwann cells. At a lower dose of lumicolchicine (3 microng/ml) these changes were less frequent and the number of neurotubules per 1 axon did not differ from that in control nerves.

Animals↗
PubMed2001

Does the photochemical conversion of colchicine into lumicolchicines involve triplet transients? A solvent dependence study.

beta- and gamma-lumicolchicines are photoproducts formed by the cycloisomerization of the tropolone ring of colchicine (COL) alkaloids. The mechanism of the photoconversion, suggested to involve the triplet state, is examined here by studying the effect of the solvent polarity on the lumicolchicine photoisomer ratio. Triplet COL, detected by laser flash photolysis, is quenched by oxygen, but not by transtilbene or 1-methylnaphtalene. Neither the quantum yield of conversion of COL nor the photoproduct ratio was altered by the presence of oxygen. Likewise, energy transfer to COL from triplet acetone produced by either isobutanal/horseradish peroxidase system or tetramethyldioxetane thermolysis failed to provoke photoreaction of COL. Our data argue against the intermediacy of a COL triplet state in the photoisomerization and stress on the role of specific solvent-solute interactions in determining the partitioning of excited singlet state into the beta- and gamma-isomer formation.

Colchicine↗
PubMed1981

Behavioral investigation of neurotoxicity: the effects of colchicine, lumicolchicine and vincristine sulfate on goldfish optic nerve regeneration.

Experiments were carried out to investigate a behavioral method of assessing neurotoxicity. The proposition is that developing or regenerating neurons. The regenerating optic nerve in goldfish was examined as a preparation for investigating the effects of chemicals on neuronal development. Restoration of optic nerve connections following crushing of the optic nerve, as detected by a noninvasive behavioral technique permitting sequential testing of individual fish, occurred within 17 days. The effect on regeneration of biweekly, intraperitoneal administration of alkaloid neurotoxins was investigated. Regeneration was inhibited by colchicine and vincristine sulfate but not by lumicolchicine. The potency of vincristine was approximately twice that of colchicine. Neither drug had a detectable effect on the maintenance of optic nerve function in sham-operated fish. The results suggest that the behavioral protocol can be used to identify chemical agents which impair neuronal development in vivo, and to estimate their relative neurotoxicity.

Animals↗
PubMed1983

Factors involved in the sensitivity of Stentor to colchicine, lumicolchicine, and vinblastine sulfate.

Oral regeneration by the ciliate Stentor coeruleus is inhibited by colchicine (Cc), but only at a relatively high concentration (0.9 mM); moreover, regeneration is inhibited by an even lower concentration of lumicolchicine (LCc) (0.2 mM). Together these results suggest that Cc may not be acting via tubulin binding. To evaluate this possibility we: (1) tested the effect of both drugs, and vinblastine sulfate (Vb) for comparison, on a population of labile cytoplasmic microtubules; and (2) measured the kinetics of association of all three drugs with regenerating cells. We found that Cc and Vb reduced the number of microtubules only at concentrations that blocked regeneration, whereas LCc blocked regeneration without reducing microtubule number. In addition, LCc associated with the cells much more readily than Cc, such that the cell-associated concentration of Cc that blocked regeneration was actually several fold lower than the effective concentration of LCc. We propose that common effects of Cc and LCc unrelated to tubulin binding play no more than a minor role in Cc effects on regeneration and conclude that Cc acts primarily if not exclusively via its antimicrotubule activity.

Animals↗
PubMed1975

Comparison between the effect of colchicine and lumicolchicine on axonal transport in rat motor neurons.

The mitotic inhibitor colchicine (COL) and its isomer lumi-colchicine (lumi-COL) were tested on the axonal transport of acetylcholine (ACh), cholineacetyltransferase (CAT) and ACh-esterase (AChE) in rat motor nerves in vivo. COL was found to be far more effective in blocking axonal transport of all 3 substances than was an equimolar concentration (0.1 M) of lumi-COL, when injected into the sciatic nerve. Since COL and lumi-COL have similar properties as regards binding to cellular membranes, but differ markedly in their binding capacity to microtubule protein, the results give strong support for the theory that microtubules are essential for intra-axonal transport in mammalian nerves.

Acetylcholine↗
PubMedDate not supplied

Reduced transport of bilirubin and asialoorosomucoid in regenerating rat liver is a microtubule-independent event.

In previous studies, we found that uptake of bilirubin and asialoorosomucoid is depressed in regenerating rat liver. To determine what role the hepatic cytoskeleton plays in this modulation of uptake, animals were treated with colchicine, an inhibitor of microtubular polymerization. Normal unoperated rats or rats following two-thirds hepatectomy or sham surgery were injected with colchicine, lumicolchicine (50 micrograms per 100 gm of body weight, i.p.) or normal saline. Lumicolchicine, an analog of colchicine, has no effect on microtubules and was used as a control. At 12 hr after surgery, sham-operated and unoperated animals received a second equal dose. Partially hepatectomized animals received one-third the initial dose. At 24 hr after surgery, livers were perfused in situ and single-pass multiple indicator dilution studies were performed. Colchicine as compared to lumicolchicine pretreatment reduced apparent influx of bilirubin and asialoorosomucoid in regenerating liver by 50% but had no effect in liver from normal or sham-operated rats. Analysis of indicator dilution curves revealed that reduced influx in colchicine-treated liver was attributable to an increased vascular volume of distribution. These results suggest that microtubules may play a role in maintenance of normal hepatic vascular architecture during regeneration. Lack of effect of colchicine on modulation of bilirubin and asialoorosomucoid uptake during regeneration suggests that other, as yet unknown, factors result in down-regulation of the specific hepatocellular transport systems for these two ligands.

Animals↗
PubMed1984

The effect of colchicine on the pigmentation of the enamel surface in rat incisors.

The effect of colchicine and lumicolchicine on the secretion of an iron-containing pigment vesicle onto the enamel surface in the rat maxillary incisors has been studied histologically and by line scan analysis of the iron with an X-ray microanalyzer. Rats were killed at intervals of 12 and 24 hours and 3, 6 and 10 days after the subcutaneous injection of colchicine or lumicolchicine at a dose of 1.3 mg/kg. At 10 days after the colchicine injection, two pigmentation-free bands were observed on the enamel surface in each pair of incisors. By the line scan analysis of the iron with an X-ray microanalyzer, the pigmentation-free bands corresponded to the decrease of the iron concentration profile. By the histological observation at 12 and 24 hours after the injection, no remarkable changes were observed from the late pigmentation stage to the regression stage. However, at 3 and 6 days after the injection, the pigmentation-free bands appeared on the enamel surface. A large number of pigment vesicles was observed in the ameloblasts and in the papillary cells facing the pigmentation-free bands. These phenomena were not observed in the rats injected with lumicolchicine. The present study suggests that the secretion of an iron-containing pigment vesicle in the ameloblasts onto the enamel surface is mediated by the microtubules.

Animals↗