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PubMed1978

The reversible effect of colchicine on the taste bud cells of the central circumvallate papilla in the rat.

It is believed that differentiation and maintenance of taste buds in vertebrates is dependent on the trophic function of their sensory nerve supply. In the present work, colchicine was injected into the circumvallate papilla of the rat. This produced a reversible blockade of neuroplasmic transport and disappearance of taste buds. Colchicine inhibited the further differentiation of bud cells, but apparently did not change the life cycle of the cells present already at the time of injection. It is speculated that the neurotrophic factors in this particular cell system are effective to induce cell differentiation only.

Acetylcholinesterase↗
PubMed1988

Colchicine treatment in a case of pachydermoperiostosis with acroosteolysis.

We report a case of pachydermoperiostosis with arthralgia, acroosteolysis, and recurrent staphylococcal folliculitis of the face, treated with colchicine (0.5 mg once daily for the 1st week and 0.5 mg twice daily for the next 3 weeks). The evaluation of arthralgia, hyponchial angle, folliculitis, and pachyderma, performed at basal time and once weekly, showed improvement of symptoms and signs after 7-15 days of treatment. Neutrophilic chemotaxis, evaluated before starting the treatment and after 15 and 30 days of therapy, showed a progressive decrease of the initial very high index. Colchicine provided a beneficial therapeutic response in both inhibiting increased chemotactic activity and in reducing tissular oedema in our patient.

Adult↗
PubMed1982

Colchicine resistance in human cell lines. Pleiotropic phenotype and decreased membrane permeability.

Colchicine-resistant human cells were initially observed in patients exhibiting C-anaphases or tetraploidy in lymphocyte cultures. Cell lines established from these patients displayed cross-resistances to daunomycin, emetine, vinblastine, and vincristine and collateral sensitivity to Xylocaine, showing a pleiotropic phenotype similar to that described in permeability mutants in CHO cells. 3H colchicine uptake and binding assays confirmed a decreased permeability to the drug.

Cell Line↗
PubMed1985

Regular pattern of karyotypic alterations accompanying gene amplification in Djungarian hamster cells: study of colchicine, adriablastin, and methotrexate resistance.

Chromosomal analysis of 26 Djungarian hamster cell lines obtained from 11 independent clones and possessing different levels of resistance to colchicine or adriablastin as a consequence of gene amplification revealed regular patterns in the karyotypic changes that accompanied the development of drug resistance. Usually the sequence of karyotypic changes was as follows: first an additional chromosome 4 appeared: then single unpaired small chromatin bodies (SCBs) arose; later in the middle part of the long arm of one of three chromosomes 4 long homogeneously staining regions (HSRs) and double minute chromosomes (DMs) were formed; and finally in the most resistant variants large clusters of SCBs appeared. The emergence of the clusters of the SCBs correlated well with the occurrence of autonomously replicating, amplified DNA sequences. In contrast to DNA of the HSRs the DNA of the SCBs could replicate outside the S-phase of the cell cycle. When kept in a non-selective medium, the cells gradually lost their resistance to colchicine: 1%-4% of the cells lost the capacity to form colonies in the selective medium independently of the pattern of location in them of amplified genes (in chromosomal HSRs. SCBs, or DMs). Loss of drug resistance was accompanied by disappearance of the chromosomal HSRs, SCBs, and DMs. Chromosomal analysis of the set of methotrexate-resistant Djungarian hamster cell lines indicated the following karyotypic evolution: first the additional material on the distal part of one of two chromosomes 3 appeared; then the light HSRs were formed on the distal part of one of two chromosomes 4; later clusters of SCBs and HSRs arose on the distal part of the short arm of chromosome 3. Probably the amplification of different genes is characterized by specific patterns of karyotypic alterations.

Animals↗
PubMed1982

Colchicine in generalized pustular psoriasis: clinical response and antibody-dependent cytotoxicity by monocytes and neutrophils.

Four patients with generalized pustular psoriasis were treated with oral colchicine in an open study. Three of the four patients went into total remission within two weeks while receiving colchicine. The monocyte- and neutrophil function was assessed by studying antibody-dependent cytotoxicity. Increased values observed before treatment decreased during treatment. The patient who responded poorest clinically also showed less changes in monocyte- and neutrophil antibody-dependent cytotoxicity.

Administration, Oral↗
PubMed1979

Effects of dimethyl sulfoxide and colchicine on the resorption of experimental amyloid.

The induction of amyloid in C3H mice by either casein solution or complete Freund's adjuvant emulsion with Mycobacterium butyricum was confirmed by partial splenectomy. The animals were autopsied after treatment with dimethyl sulfoxide (550 mg/kg, 50 times), colchicine (0.02 mg/kg, 15--37 times), or saline solution as a control. Detailed histological comparisons of biopsy and autopsy spleens provided evidence that dimethyl sulfoxide was significantly effective in the resorption of amyloid, while in the animals treated with colchicine amyloid deposition was increased. The effect of dimethyl sulfoxide was discussed with reference to the modification of amyloid fibrils.

Amyloid↗
PubMed1985

Modulation of pig epidermal adenylate-cyclase responses by protein-synthesis inhibitors: its relation to glucocorticoid and colchicine effects.

The effects of protein-synthesis inhibitors (actinomycin D, puromycin, and cycloheximide) on epidermal adenylate-cyclase responses were investigated. When pig skin (epidermis) was incubated in RPMI-1640 medium, the beta-adrenergic adenylate-cyclase response (epinephrine-induced cyclic-AMP accumulations) decreased, whereas the adenosine and histamine responses increased after long-term (up to 48 h) incubation. The addition of actinomycin D or puromycin to the incubation medium resulted in a marked increase in epinephrine-induced cyclic-AMP accumulations and a decrease in adenosine- and histamine-induced cyclic-AMP accumulations. Cycloheximide had a weak effect on the epinephrine response, and had apparently stronger effects on the adenosine and histamine responses than actinomycin D or puromycin. Histologically, various degenerative changes of keratinocytes (with or without acantholytic changes) were observed after long-term incubation with these protein-synthesis inhibitors. Both low- and high-Km cyclic-AMP phosphodiesterase activities were moderately decreased by the protein-synthesis inhibitors. However, augmentation effects on the beta-adrenergic response were also observed in the presence of the cyclic-AMP phosphodiesterase inhibitor, theophylline. We have described previously similar augmentation effects on the beta-adrenergic response caused by glucocorticoids and colchicine. Comparison of the effects of these chemicals with those of protein-synthesis inhibitors revealed that the most marked effects on the beta-adrenergic response were produced by actinomycin D, puromycin and colchicine; glucocorticoid had a moderate effect (hydrocortisone), while cycloheximide had only a weak effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1979

[The influence of cytochalasin B, colchicine, and vinblastine on the attachment of Entamoeba histolytica to glass surfaces (author's transl)].

The attachment of E. histolytica trophozoites from monoxenic TPS-medium to glass surfaces was studied at different temperatures and pH values and in the presence of cytochalasin B, colchicine, and vinblastine. At pH 7.0 and at 36 degrees C optimal adhesion rates of the amebae were observed in the range from 80% to 95%. Marked inhibition of adhesion was noted at higher concentrations of cytochalasin B. The adhesion rate was reduced to 50% by 50 micrograms/ml CB. Higher dosages successively prevented nearly all adhesion. Colchicine was without any effect. Vinblastine had a certain low effect but only at very high dosage. The observations are consistent with the assumption that the adhesion process is at least partially mediated by cytochalasin-sensitive contractile microfilaments, whereas microtubuli are obviously not involved in the cell-substrate adhesion.

Adhesiveness↗
PubMed1982

Differential effect of colchicine upon the entry of proteins into myelin and myelin related membranes.

Brain slices from 20 day old rats were incubated with radioactive aminoacids in the presence and absence of 500 microM colchicine and the appearance of labeled proteins in myelin and in a myelin-like fraction (SN4 fraction) was measured. In the presence of the inhibitor, the entry of proteolipid proteins was decreased to 55% in myelin and to 45% in SN4 fraction with reference to control values while the entry of basic proteins and other minor protein components was unaffected in both fractions. The synthesis of proteolipid proteins was not affected by the presence of colchicine; moreover, a slight accumulation of these proteins was observed in microsomes. The results suggest that the microtubular system is involved in the transport of proteolipid proteins from their site of synthesis to their site of deposition and that the various types of myelin proteins follow different transport routes to enter into this special type of membrane.

Animals↗
PubMedDate not supplied

Elimination of granular cells after intrahippocampal colchicine injection causing disappearance of evoked potentials and deterioration of development of the conditioned avoidance reflex in rats.

The aim of our work was to study the involvement, in the process of learning, of synapses between the perforant path and granular cells of the hippocampal dentate fascia for formation of a conditioned reflex (CR) of active avoidance elaborated in response to electrostimulation of the perforant path. To achieve this we used the property of the neurotoxin colchicine at a certain concentration of eliminating selectively the fascia cells. One month after colchicine injection we observed destruction of granular cells, disappearance of the dentate fascia focally evoked potentials, and considerable deterioration in the elaboration of active avoidance CR. Administration of saline solution in control experiments did not bring about such changes. The results obtained show the important role of the entorhinal input into the hippocampus in the learning model used.

Action Potentials↗
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↗
PubMed1996

Dexamethasone and colchicine reduce inflammation and delayed oedema following experimental brain contusion.

The effect of anti-inflammatory treatment on monocyte/macrophage infiltration, major histocompatibility complex molecules (MHC) class II expression and delayed oedema following experimental brain contusion was studied by immunohistochemistry and tissue-specific gravity measurement in 44 rats. Colchicine, chloroquine and dexamethasone administered once daily for five days after the trauma reduced inflammation and oedema. The difference was statistically significant with colchicine and dexamethasone. The findings comprise further evidence of a pathogenetically important inflammation after experimental contusion. It is probable that anti-inflammatory agents may prevent secondary neurological damage due to elevated intracranial pressure and cell to cell- or cytokine-mediated neuronal degeneration and demyelination.

Animals↗
PubMedDate not supplied

Effects of colchicine on the gallbladder of the mouse.

The effects of colchicine on the mouse gallbladder followed a course depending on the dosage given (0.4-4 mg/100 g body weight). Following 0.5 mg/100 g, by 16 h there was a marked cholestasis with dilatation of the gallbladder and steatosis. There were progressive alterations in the Golgi apparatus and accumulation of vesicles. The apical mucous droplets decreased in number and became pleomorphic and dispersed throughout the cytoplasm. Lipid droplets appeared in numbers on the epithelial cytoplasm. By 48 h the tissues had reverted to normal appearances. When cholecystokinin, pilocarpine or ceruletide were given to animals which had received colchicine 18 h previously, the excess bile from the dilated gallbladder was discharged into the duodenum, remaining apical mucous droplets secreted and electron dense material accumulated in the lateral intercellular space. This formed a quasi-regular array between the epithelial bases and the basement membrane. Biochemically there was a significant decrease in alkaline phosphatase activity and a significant increase in acid phosphatase activity.

Acid Phosphatase↗
PubMed1976

Melatonin antagonizes colchicine-induced mitotic arrest.

Melatonin, in concentrations up to 10(-3) M, showed no effect on mitosis in cultures of HeLa or KB cells. However, when melatonin at 10(-4) M was preincubated with HeLa cells prior to addition of 10(-7) M colchicine, a reduction in the mitotic index, in comparison to colchicine alone, was observed.

Animals↗
PubMed1989

Effects of adenosine on neutrophil polarization induced by N-formyl-methionyl-leucyl-phenylalanine, sodium propionate and colchicine.

Polarization of human neutrophils (a characteristic bipolar shape change) can be induced by the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP); sodium propionate, which causes a rapid acidification of the cytosol; or colchicine, which disrupts microtubules. We have previously reported that adenosine, endogenously produced in human neutrophil suspensions, inhibits FMLP-induced polarization. We report here that endogenously produced adenosine also inhibits sodium propionate-induced polarization but has no effect on colchicine-induced polarization. These results suggest that neutrophil polarization may be a multistep process inducible by compounds that trigger different biochemical events.

Adenosine↗
PubMed1991

A comparison of the anti-inflammatory activity of selective 5-lipoxygenase inhibitors with dexamethasone and colchicine in a model of zymosan induced inflammation in the rat knee joint and peritoneal cavity.

Intraperitoneal and intra-articular (knee joint) injection of zymosan in the rat caused two phases of increased vascular permeability, a rapid increase (0.25-0.5 h) and a secondary increase (2-3 h) which was temporally associated with the onset of leukocyte infiltration. Intraperitoneal injection of zymosan led to a single peak of eicosanoid production (LTB4, C4, D4, E4 and 6-oxo-PGF1 alpha) which was maximal at 0.125-0.25 h. Intra-articular injection led to an initial peak of LTB4 production (maximal at 0.25 h) and a secondary peak of LTB4 and PGE2 production (maximal at 3 h). Oral administration of the 5-lipoxygenase (5-LO) inhibitors phenidone, BW A4C (N-hydroxy-N-[3-(3-phenoxyphenyl)-2-propenyl] acetamide), A63162 (N-hydroxy-N-[1-(4-(phenylmethoxy) phenyl)ethyl] acetamide and ICI 207 968 (2-[3-pyridylmethyl]-indazolinone inhibited LTB4 production in A23187 stimulation blood ex vivo. The glucocorticosteroid dexamethasone had no effect in this model. The initial phase of increased vascular permeability in the peritoneal cavity and LTB4 production was dose dependently inhibited by the 5-LO inhibitors phenidone, BW A4C, A63162, and ICI 207 968 but not by dexamethasone or colchicine. The initial phase of increased permeability in the joint was unaffected by phenidone, BW A4C, dexamethasone or colchicine. However the latter two drugs inhibited the later phase of increased permeability and leukocyte infiltration in the joint and peritoneal cavity. These results demonstrate that zymosan induces eicosanoid production in vivo but the relative importance of these mediators varies depending on the inflammatory site.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗