Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colchicine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,513 records · Page 84Linked to original sources
PubMed1980

CHO mutants resistant to colchicine, colcemid or griseofulvin have an altered beta-tubulin.

Single-step mutants of Chinese hamster ovary (CHO) cells have been isolated which are resistant to killing by the anti-mitotic drugs colchicine, colcemid or griseofulvin. Two-dimensional gel analysis showed that two mutants resistant to griseofulvin, one resistant to colcemid and one resistant to colchicine carry an alteration in the beta-tubulin subunit. Most of the remaining isolates are believed to be permeability mutants on the basis of their cross resistance to drugs which do not interefere with microtubular polymerization or function (Ling and Thompson, 1974; Bech-Hansen, Till and Ling, 1976). A reduced amount of the wild-type beta-tubulin protein remained in each of the beta-tubulin mutants, but a beta-tubulin protein with a more basic isoelectric point also appeared. Messenger RNAs coding for both wild-type and variant beta-tubulins were found in at least one mutant as assayed by in vitro translation in a reticulocyte lysate. This indicates that the altered tubulin does not arise as the result of a posttranslational modification.

Animals↗
PubMed1988

Inhibition, by vinca alkaloids and colchicine, of antigenic modulation induced by anti-CD19 monoclonal antibodies.

Several clinical trials have been reported in which monoclonal antibodies (McAb) were used for therapy of lymphoid malignancies. Such trials have shown that infusion of McAb recognizing lymphoid antigens, is well-tolerated, and leads to the coating of tumor cells and tumor regression in some patients. However, the tumoricidal capacity of a McAb is hampered by the presence of circulating free antigen, antigenic modulation, development of human anti-mouse antibodies, emergence of antigen-negative variants of tumor cells and the inadequacy of host-effector cell mechanisms. We have studied the antigenic modulation induced by immunoglobulin (Ig) heavy chain switch variants of anti-CD19 McAb. Modulation of CD19 molecules was not related to the IgG subclass of the McAb. Immunofluorescence studies on the Burkitt tumor cell line Daudi showed that CD19 molecules are internalized after incubation by anti-CD19 McAb. Next, the effect of cytoskeleton inhibitors on antigenic modulation was studied. We found that antigenic modulation on Daudi cells and on an Epstein-Barr virus-transformed B-cell line was completely inhibited by vinca alkaloids (VA) or by colchicine. Interestingly, antigenic modulation of tumor cells from a VA-resistant patient, was not inhibited by VA or colchicine. These findings provide information for the rational design of more effective clinical trials with McAb.

Antibodies, Monoclonal↗
PubMed1983

Thymus-dependent immune functions in chickens bursectomized with colchicine applied to the anal lips.

Thymus-dependent immune functions were investigated in chickens bursectomized neonatally with colchicine solution given per anum. Antibody responses to thymus-dependent antigens sheep red blood cells (SRBC) and human gamma-globulin (HGG) were delayed, reaching the normal level after the third antigen stimulation. Also the mitogenic responses of peripheral blood lymphocytes were preserved, and no changes in the thymic morphology were found. In contrast, antibody responses to bursa-dependent antigen Brucella abortus were low and the switch of immunoglobulin isotypes from IgM to IgA and IgG was disturbed. It can be concluded that neonatal bursectomy with cloacal administration of colchicine does not significantly affect T cell functions, whereas B cell functions are partially deficient.

Animals↗
PubMed1989

Colchicine blocks beta adrenoceptor and class I antigen-specific interactions.

Previously we have demonstrated a molecular relationship between H-2 class I antigens and beta adrenoceptors from cardiac tissue. Here we show this type of interaction taking place with beta adrenoceptors from splenic cells and their purified membranes and the participation of cytoskeletal proteins in the phenomenon. Alloimmune, as well as anti-class I but not anti-class II, antibodies were able to inhibit in a competitive manner the binding of (-)-[3H]dihydroalprenolol to splenic lymphocytes and their purified membranes, and to increase cyclic AMP levels in intact cells as a consequence of beta adrenoceptor activation. Furthermore, colchicine (a microtubule disrupting drug), but not cytochalasin B (a microfilament disrupting drug), was able to abrogate alloimmune antibody inhibition over the beta radioligand binding to its receptor on both intact splenocytes and their membranes. Alloantibody actions were significantly diminished by peripheral protein solubilization in purified spleen cell membranes. These data pointed indirectly to the participation of a colchicine binding protein in class I antigen hormone-receptor associations.

Animals↗
PubMed1989

Micronucleus test with colchicine given by intraperitoneal injection and oral gavage.

The effects of micronucleus induction in mouse bone marrow cells by intraperitoneal injection (i.p.) and oral administration (p.o.) were studied with the spindle poison colchicine in 2 strains of mice (MS/Ae and CD-1). The final micronucleus test was performed with a 24-h sampling time at doses of 0.25-2.0 mg/kg by the i.p. route and 2-16 mg/kg by the p.o. route based on a simple acute toxicity test and a pilot micronucleus experiment. Colchicine induced micronuclei in both strains and at all doses tested. Micronuclei were induced more effectively by the i.p. route.

Administration, Oral↗
PubMed1990

Evidence that bremazocine prevents urine retention induced by intraspinal cord injection of colchicine in rats.

Intra-spinal cord injection of colchicine (2.5-5 micrograms/rat) produced an inhibition of reflex micturition leading to voiding suppression, bladder hypertrophy and overflow incontinence. Intraperitoneal administration of bremazocine, a kappa-receptor agonist with antagonistic properties for mu- and delta-receptors minimized the colchicine induced effects. The selective kappa-receptors agonist, U-69593, had little effect, while eledoisin or naloxone administration worsened rather than counteracted urine retention.

Analgesics↗
PubMed1990

Continuous delivery of colchicine in the rat brain with osmotic pumps for inhibition of rabies virus transport.

Rabies virus is a neurotropic agent which spreads in the CNS via axonal transport. Previous studies had shown that this axonal transport through the brain could be inhibited by stereotaxic administration of colchicine; however, this inhibition was reversible. We describe here a method to enhance the duration of this colchicine-mediated inhibition by delivering the drug continuously in the rat brain with osmotic pumps.

Animals↗
PubMed1982

Effect of colchicine on mammalian liver nuclear envelope and on nucleo-cytoplasmic RNA transport.

The binding of colchicine to nuclear envelopes was studied in order to elucidate the mechanism whereby this compound inhibits nucleocytoplasmic RNA transport. The results suggest that a single class of colchicine-binding site (dissociation constant=approx. 0.7 mM, concentration=approx. 330 nmol colchicine/mg protein) is localised in the nuclear periphery (pore-lamina) and that binding to these sites effects a constriction of the pore-complexes with concomitant inhibition of RNA egress and disordering of the nuclear membrane phospholipid bilayers.

Animals↗
PubMed1985

Isolation and characterization of new proteins produced by the infusion of colchicine in goat mammary gland.

Three new proteins have now been isolated from goat milk obtained after colchicine is infused into the mammary gland. Two of the proteins are proline-rich, and a third is a very acidic phosphoprotein. One of the proline-rich proteins is related compositionally to a sheep colostrum proline-rich protein, which has been shown to have a regulatory effect on the immune response (Janusz, M., Stavoscik, K., Zimecki, M., Wieczorek, Z., and Lisowski, J. (1981) Biochem. J. 199, 9-15). Other aspects of colchicine-treated milks are described.

Amino Acids↗
PubMed1995

Colchicine induces the GAP-43 gene expression in rat hypothalamus.

Injection of colchicine, a mitogen inhibitor, in the dorsal third ventricle induced the expression of the growth associated protein-43 (GAP-43) mRNA in some groups of cells of the adult rat brain. These mRNAs were detected by in situ hybridization histochemistry using an alkaline phosphatase labeled oligonucleotide probe. A substantial up-regulation of GAP-43 mRNA was noticed by the increase of both the number of positive cells and the intensity of the hybridization signal. These changes were observed in the hypothalamic nuclei located near the ventral third ventricle, namely the preoptic area, the supraoptic nucleus, the peri- and the paraventricular nuclei of the hypothalamus, the dorsal subnucleus of the ventromedial nucleus, the arcuate nucleus and the posterior part of the peri-mammillary region. Such abundant GAP-43 mRNA positive cells have not been observed in control adult rat hypothalamus. Since the positive cell number and shape initially suggested that these were neurons or astrocytes, double labeling in situ hybridization using both radioactive (for the detection of GFAP mRNA as a marker of astrocyte) and non-radioactive (for the detection of GAP-43 mRNA) probes was carried out. This demonstrated that these GAP-43 mRNA positive cells were not astrocytes. In addition enhanced GAP-43 mRNA expression was also found in some neuronal component, particularly in neurosecretory magnocells of the pareaventricular and the supraoptic nuclei. This up-regulation was further confirmed by the Northern blot analysis. About five fold increase in GAP-43 mRNA in the colchicine-treated hypothalamic tissue was shown.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Cryptophycin 1 binds to tubulin at a site distinct from the colchicine binding site and at a site that may overlap the vinca binding site.

Cryptophycin 1 is a new cytotoxic antimicrotubule agent with excellent antitumor activity. The methods of Sackett (Biochemistry, 34, 7010-7019, 1995), utilizing the selective and specific proteolysis of alpha- and beta-tubulin by trypsin and chymotrypsin, was used to identify the cryptophycin 1 binding site on tubulin. Occupancy of the colchicine or vinca binding sites causes changes in the structure of tubulin that can be detected by proteolysis with trypsin and chymotrypsin. The addition of cryptophycin 1 to tubulin causes changes in both the tryptic and chymotryptic cleavage of tubulin consistent with occupation of the vinca binding site and distinct from occupation of the colchicine binding site. The effects of cryptophycin 1 on the tryptic digests are identical to the effects seen with vinblastine and differ saliently from the effects of maytansine and rhizoxin, other agents known to bind to the vinca site. The data suggest that the binding site of cryptophycin 1 may overlap the vinca binding site on tubulin.

Antineoplastic Agents↗
PubMed1980

Loss of striatal neurons after local microinjection of colchicine.

Intrastriatal injections of colchicine (4 micrograms) produced irreversible striatal damage characterized 30 days later by loss of intrinsic striatal neurons, gliosis and shrinkage but no apparent damage to myelinated bundles of the internal capsule. This neuronal loss was associated with a dramatic reduction of striatal and nigral glutamate-decarboxylase (GAD), the marker of GABA-ergic synapses and of striatal choline-acetyltransferase (CAT), the marker of cholinergic synapses. The levels of dopamine (DA) and serotonin (5HT) in the striatum as well as those of their metabolites were also reduced, indicating that colchicine exerts toxic effects also on terminals of striatal afferent neurons.

Animals↗
PubMed1981

Intraocular colchicine selectively destroys immature ganglion cells in chicken retina.

Low doses of colchicine (greater than 0.5 microgram) injected into the eyes of young chickens irreversibly inhibit axonal transport of material labelled with [3H]fucose. This is due to almost total destruction of the retinal ganglion cells, while other retinal cell types, including the displaced amacrine cells found in the same retinal layer, survive the treatment. The neurotoxic effect of colchicine on chick retinal ganglion cells decreases after hatching, and it is suggested that the decrease in sensitivity may be related to myelination of the retinal ganglion cell axons.

Animals↗
PubMed1992

Nuclear localization of estrogen receptor-immunoreactivity in the preoptic area of female rats and its reduction by intraventricular colchicine treatment.

The subcellular localization of estrogen receptor (ER) was investigated in the preoptic area of ovariectomized female rats by electron microscopic immunohistochemistry, using a monoclonal antibody to ER. ER-immunoreactivity was localized in the nuclei of neurons of the periventricular preoptic nucleus (Pe) and the medial preoptic area (MPA). ER-immunoreactivity had a speckled pattern in the nucleus, but was not observed in the nucleolus or cytoplasm. After intraventricular colchicine treatment, ER-immunoreactivity within the nucleus was reduced drastically in neurons of the Pe and the MPA. The possible mechanism by which colchicine alters ER-immunoreactivity is mentioned.

Animals↗
PubMed1986

Topical application of colchicine, vinblastine and vincristine prevents strychnine-enhanced transsynaptic degeneration in the medullary dorsal horn following transection of the inferior alveolar nerve in adult rats.

The effect of topical application of axonal transport blockers to the transected peripheral nerve was assessed by quantitating the strychnine-enhanced transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats. Systemic administration of strychnine (1 mg/kg/day) for 7 days at the postoperational interval of 23 days proved to be suitable for quantitating the transsynaptic degeneration at the light microscopic level. When the proximal stump of transected nerve was treated with 2% colchicine immediately after transection, 5.8 +/- 6.8 dark neurons in a single section of the medullary dorsal horn, ipsilateral to the nerve transection, were observed. Following similar treatment with 0.4% vinblastine and 0.2% vincristine, 24.4 +/- 10.5 and 9.4 +/- 7.0 dark neurons were seen, respectively. When compared with 43.0 +/- 9.4 dark neurons, which were seen in animals without alkaloid treatment, colchicine, vinblastine and vincristine significantly reduced the transsynaptic degeneration by 86, 43, and 78%, respectively. Possible mechanisms involved in prevention of transsynaptic degeneration by the alkaloids are discussed.

Administration, Topical↗
PubMed1978

Effect of colchicine on estrogen action. I. Inhibition of 17 beta-estradiol-induced water and potassium uptake in the immature rat uterus.

The effects of colchicine on 17 beta-estradiol-induced water and electrolyte uptake in the uterus of the immature rat have been examined 6 h after treatment with this estrogen. Estradiol stimulates an increase in total uterine Na+, K+ and water while intracellular Na+ and K+ concentrations remain relatively unchanged. Assuming the sodium space is equivalent to the extracellular space, the extracellular fluid compartment increases about 84% in response to estradiol. Similarly, the intracellular compartment increases by about 62%. The uptake of water into the cellular compartment may be a direct response to a stimulation of K+ accumulation by uterine cells. Colchicine inhibits both estradiol-induced rise in intracellular potassium and both intra- and extracellular water.

Animals↗
PubMed1989

Dissociation between changes in glutamate receptor binding sites and their coupling to phosphatidylinositol metabolism following intrahippocampal colchicine injection.

Intrahippocampal colchicine injection produces a rapid death of granule cells and pyramidal neurons in the hippocampus in the rat. Under the appropriate assay conditions, [3H]glutamate labels the N-methyl-D-aspartate type of glutamate receptors while [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate labels the quisqualate type. Unilateral injection of colchicine (15 micrograms) in the dorsal hippocampus did not produce any change in [3H]glutamate and [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate binding in membrane fractions from the dentate gyrus or CA1 field contralateral to the injection side, at least up to 12 days after the injection. However, it produced a progressive decrease in the binding of both ligands in dentate gyrus and CA1 of the injected hippocampus. In the dentate gyrus the changes in binding as a function of time after the injection were biphasic with a rapid exponential decrease (t1/2 about 8 days for both [3H]glutamate and [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate) until 12 days after the injection followed by a much slower decrease afterwards. A similar pattern was observed in CA1 although the changes in binding were smaller and delayed by about three days as compared to the dentate gyrus. Kinetic analyses of the binding at equilibrium were performed seven days after the injection and indicated that the changes in [3H]glutamate binding were due to a change in the maximum number of sites but not in affinity for the ligand.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Long-term changes in phosphoinositide hydrolysis following colchicine lesions of the nucleus basalis magnocellularis.

The effect of bilateral colchicine lesions of the nucleus basalis magnocellularis (NBM) on agonist-stimulated phosphoinositide (PI) hydrolysis was examined in cortical slices 1, 3, or 14 months after surgery. Colchicine lesions resulted in a loss of acetylcholinesterase staining in the cortex which recovered to control levels by 14 months. Choline acetyltransferase activity in the cortex was decreased by 43% one month after lesioning, but returned to control levels by 3 months. In vitro stimulation with carbachol produced a concentration-dependent increase in PI hydrolysis, which was enhanced 3 and 14 months after NBM lesions. Norepinephrine and quisqualate-stimulated PI hydrolysis was also enhanced 14 months after NBM lesions. These results suggest a slow up-regulation of postsynaptic receptor function following presynaptic loss of transmitter.

Acetylcholinesterase↗