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PubMed1997

Effect of colchicine on nuclear presence of two lysosomal enzymes in rat implantation sites.

The purpose of the study was to demonstrate that the effect of colchicine on the implantation and embryo development in rat is caused in part by its action on lysosome translocation to the perinuclear region. The subcellular enzymatic distribution of two lysosomal enzymes, acid phosphatase (E.C.3.1.3.2.) and beta-glucuronidase (E.C.3.2.1.3.1.), were measured. The right uterine horn was treated during preimplantation with colchicine (2 micrograms/kg of body weight on day 4) and the left with lumicolchicine (control). In the control horn, the nuclear activity of lysosomal enzymes was significantly higher in the implantation site tissue than the treated horn (colchicine) (p < 0.01). There were no modifications on the undecidualized endometrium under colchicine treatment. Simultaneously to this result, implantation and embryonic development were abolished. From the results presented herein, it is proposed that the inhibitory effect of colchicine is due to an inadequate biochemical differentiation at the implantation site, related to both arrest of cell division (mitosis is arrested in methaphase) and inhibition of the lysosomal movement toward the nucleus.

Acid Phosphatase↗
PubMed1981

Suppression of spermatogenesis in patients with Behçet's disease treated with cyclophosphamide and colchicine.

Reproductive function was studied in 31 adult male patients with Behçet's disease during treatment with cyclophosphamide and/or colchicine for 1 to 64 months. Semen was obtained from 27 patients. Azoospermia or severe oligospermia was found in 13 of 17 patients receiving cyclophosphamide with or without colchicine, whereas the sperm count was almost normal in six patients treated with colchicine alone and in four patients receiving neither drug (control patients). Blood samples were available for 31 patients. The mean follicle-stimulating hormone level among 12 cyclophosphamide-treated patients was significantly higher than that of 6 colchicine-treated patients and 6 control patients. These results indicate that cyclophosphamide impairs spermatogenesis in adult men, whereas colchicine does not.

Adult↗
PubMed1983

Reduction of peritoneal adhesion formation by colchicine: a comparative study in the rat.

Colchicine inhibits processes known to be involved in the pathogenesis of peritoneal adhesions. Daily administration of 50 micrograms of colchicine to 22 rats significantly diminished adhesion formation, as compared with dexamethasone-treated and untreated rats. Rats that developed at least three adhesions of grade 3 (scale 0 to 4) were strikingly less prevalent among the colchicine-treated animals than the untreated group (9.1% versus 40.9%, P less than 0.001). The double product of the number and grading of adhesions was significantly lower (P less than 0.05) in the colchicine group. Colchicine is more effective than dexamethasone in inhibiting adhesion formation in the rat.

Animals↗
PubMed1984

Separation of colchicine and related hydrolysis and photodecomposition products by high-performance liquid chromatography, using copper ion complexation.

The high-performance liquid chromatographic separation of colchicine and its hydrolysis and photodecomposition products has been investigated. Separation of colchicine, N-desacetyl-colchicine, beta- and gamma-lumicolchicine can be accomplished by modification of existing methods; however, under these conditions the tropolone derivatives, colchicine and trimethylcolchicinic acid, do not elute. Based on the observed complexation of tropolone with metal ions, copper(II) ions were incorporated in the eluent enabling the direct detection and quantitation of the tropolone derivatives. Separation of colchicine, isocolchicine and their respective derivatives has been optimised for both phosphate buffer and aq. copper solutions.

Chemical Phenomena↗
PubMed1983

Effect of colchicine on rat small intestinal absorptive cells. II. Distribution of label after incorporation of [3H]fucose into plasma membrane glycoproteins.

By means of radioautography the influence was tested of various periods (5, 15, 30, 40 min, 2 hr) of pretreatment with colchicine, administered intraperitoneally to rats at a dosage of 0.5 mg/100 g of body weight, on the intracellular pathway of [3H]fucose in absorptive cells of the small intestine. Administration of colchicine for 30 min and longer time intervals causes delay in the insertion of [3H]fucose into the oligosaccharide chains of glycoconjugates in the Golgi apparatus, and results in redistribution of the label apparent over the different portions of the plasma membrane. In controls, at 2 and 4 hr after administration of [3H]fucose the apical plasma membrane is strongly labeled; 53.7 +/- 3.2% of the silver grains are recorded over apical regions of the plasma membrane that contrast to basolateral portions comprising 25.4 +/- 3.2% of the label. Colchicine causes equalization of the reaction of apical and basolateral regions of the plasma membrane: the number of silver grains attributable to the apical plasma membrane is reduced; following treatment with colchicine, apical portions of the plasma membrane comprise 31.6 +/- 1.8% of the silver grains, 38.6 +/- 3.8% are attributable to basolateral membrane regions. The colchicine-induced equalization of the density of label of apical and basolateral regions of the plasma membrane, in addition to the occurrence of basolateral microvillus borders (demonstrated in the companion paper), suggests microtubules to be important in the maintenance of the polar organization of small intestinal absorptive cells.

Animals↗
PubMed1999

Colchicine causes excessive ocular growth and myopia in chicks.

Colchicine has been reported to destroy ganglion cells (GCs) in the retina of hatchling chicks. We tested whether colchicine influences normal ocular growth and form-deprivation myopia, and whether it affects cells other than GCs. Colchicine greatly increased axial length, equatorial diameter, eye weight, and myopic refractive error, while reducing corneal curvature. Colchicine caused DNA fragmentation in many GCs and some amacrine cells and photoreceptors, ultimately leading to the destruction of most GCs and particular sub-sets of amacrine cells. Colchicine-induced ocular growth may result from the destruction of amacrine cells that normally suppress ocular growth, and corneal flattening may result from the destruction of GCs whose central pathway normally plays a role in shaping the cornea.

Animals↗
PubMed2002

Intracerebroventricular administration of colchicine produces cognitive impairment associated with oxidative stress in rats.

Oxidative stress has been implicated in neurodegenerative disorders including the Alzheimer's disease (AD). Central administration of colchicine is known to cause cognitive impairment in rats and is likened to sporadic AD in humans. However, it is not known whether this cognitive impairment is associated with free radical generation. Therefore, in the present study, the effect of intracerebroventricular colchicine was studied on paradigms of learning and memory behavior and the markers of oxidative stress in rats. Adult male Wistar rats (200-250 g) were injected with colchicine (intracerebroventricular) bilaterally (15 microg/rat; 7.5 microg/site) on the first day. The learning and memory behavior was assessed using passive avoidance paradigm, elevated plus maze and closed field activity test on Days 13, 14 and 21. The parameters of oxidative stress were assessed by measuring the malondialdehyde (MDA), glutathione, superoxide dismutase (SOD) and catalase levels in brain tissue on Day 21 of the colchicine injection. The rats developed significant learning and memory impairment as indicated by deficit in behavioral paradigms. There was a significant elevation in MDA levels and decrease in levels of glutathione. No significant difference was observed in SOD and catalase levels. Thus, the study demonstrates that central administration of colchicine causes impairment in learning and memory with associated increase in oxidative stress.

Animals↗
PubMed1997

Increased frequency of P-glycoprotein gene amplification in colchicine-resistant Rat-1 clones transformed by v-src.

A rat fibroblast cell line (Rat-1) carrying a temperature-sensitive mutation of v-src was used to determine whether inducible cellular transformation altered the ability of cells to amplify the p-glycoprotein gene in response to colchicine selection. Transformed and nontransformed Rat-1 fibroblasts selected under 4 times the LD50 generated the same number of colchicine-resistant colonies. We next examined colchicine-resistant colonies derived from transformed cells and compared them to colchicine-resistant colonies derived from nontransformed cells. When Rat-1 cells were selected at 35 degrees C (transforming temperature), 7 out of 7 clones exhibited a 3- to 5-fold p-glycoprotein gene amplification. These results contrasted to those found at the nontransforming temperature (40 degrees C); none of the 8 colchicine-resistant clones examined had amplified the p-glycoprotein gene. Thus in Rat-1 cells carrying a temperature-sensitive v-src gene, p-glycoprotein gene amplification was observed at a high frequency only in transformed clones selected at the temperature permissive for v-src activity.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2001

Colchicine inhibits taurodeoxycholate transport in pericentral but not in periportal hepatocytes.

Indirect evidence for a microtubule-dependent vesicular hepatocellular transport of bile acids has accumulated. Since inhibition of this transport by colchicine can be achieved only at high but not at low bile acid infusion rates we were wondering whether this transport pathway shows a hepatic zonation or not. To answer this question we perfused isolated rat livers antegradely or retrogradely, respectively, with unlabeled and labeled taurocholate or taurodeoxycholate. Inhibition of microtubule-dependent bile acid transport was aimed at co-infusion of colchicine. Periportal cells eliminated the likewise hydrophobic taurodeoxycholate as fast as the more hydrophilic taurocholate. In contrast, pericentral cells excreted taurodeoxycholate much slower than taurocholate. Colchicine did not change the biliary taurocholate excretion profile in periportal and pericentral cells. However, colchicine reduced significantly taurodeoxycholate excretion in pericentral but not in periportal cells. It is concluded that a microtubule-dependent vesicular, colchicine-sensitive transport pathway seems to be involved in the translocation of taurodeoxycholate in pericentral but not in periportal cells. Since such a vesicular bile acid transport is regarded to be much slower than transcellular transport by diffusion, this observation may explain the much slower excretion of hydrophobic bile acids like taurodeoxycholate in pericentral than in periportal cells under physiological conditions.

Animals↗
PubMed1987

A controlled trial of colchicine in primary biliary cirrhosis. Trial design and preliminary report.

Colchicine (1 mg/day), or an identical placebo, was given to 64 patients with primary biliary cirrhosis in a double-blind controlled trial. Due to a novel, pair-matched trial design, the two groups were exceptionally well matched at entry. In comparison with placebo, colchicine produced a beneficial effect on serum albumin and bilirubin levels at 3 months in patients who had abnormal liver function (bilirubin greater than 20 mumol/l) at entry: (albumin, P = 0.047; bilirubin, P = 0.022). In patients with normal liver function at entry (bilirubin less than 20 mumol/l), beneficial effects were noted on total globulin levels at 3 months (P = 0.013) and on immunoglobulin G levels at 3 and 6 months (P = 0.044 and 0.001, respectively). At 18 months, survival estimate in the colchicine and placebo groups were 84% and 69%, respectively. The difference did not reach significance. Colchicine produced an early improvement in liver function and immunoglobulin levels. Few serious side effects were encountered, and colchicine clearly merits long-term study in the treatment of primary biliary cirrhosis.

Bilirubin↗
PubMed1994

Prevention of recurrent aphthous stomatitis with colchicine: an open trial.

BACKGROUND: Recurrent aphthous stomatitis (RAS) is a common disorder with hitherto unsatisfactory drug therapy. OBJECTIVE: Our purpose was to evaluate the prophylactic effect of colchicine in the treatment of RAS. METHODS: An open, prospective, 4-month study was conducted in 20 patients with RAS who served as their own controls. During the first 2 months of the study no medications were given and in the last 2 months colchicine, 1.5 mg/day, was prescribed. RESULTS: The mean number of aphthae per week and the subjective daily pain scores were reduced by 71% and 77%, respectively, during colchicine treatment as compared with the previous period (p < 0.001 for both). No serious side effects of colchicine were noted. CONCLUSION: These findings suggest a role for continuous colchicine therapy in the prevention of RAS.

Adolescent↗
PubMed1999

Effect of colchicine in the subcorneal pustular dermatosis type of IgA pemphigus.

BACKGROUND: IgA pemphigus of the subcorneal pustular dermatosis (SPD) type is characterized by subcorneal acantholysis and by an abundance of neutrophils, making colchicine a reasonable pharmacologic option for treatment. OBJECTIVE: We attempted to determine the efficacy of colchicine in the treatment of SPD-type IgA pemphigus. METHODS: Two patients with SPD-type IgA pemphigus were treated with colchicine 1.5 mg/day as monotherapy. RESULTS: A sustained clinical response was achieved within 2 to 3 weeks of therapy. Relapses were noted each time colchicine was stopped. CONCLUSION: Colchicine should be considered in the treatment of SPD-type IgA pemphigus.

Colchicine↗
PubMed2003

Colchicine-induced myopathy with myotonia in a patient with chronic renal failure.

Although colchicine induced myopathy has been described in patients with chronic renal failure, colchicine induced myopathy with myotonia has been reported very rarely. A 49-year-old man with chronic renal failure was hospitalised for investigation of fatigue, malaise and severe pain in all extremities. He was on colchicine therapy for 5 months. Neurological examination showed mildly decreased sensation in a distal symmetric pattern in lower extremities, moderate proximal limb weakness, hyporeflexia and severe myalgia on palpation. No clinical evidence of myotonia was present. Laboratory studies showed elevated creatine phosphokinase (CK), lactic dehydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Electromyographic (EMG) findings were compatible with myopathy and abundant, widespread myotonic discharges were determined. Muscle biopsy was consistent with vacuolar myopathy. After withdrawal of colchicine, CK, LDH, AST and ALT levels were normalised and the symptoms were disappeared gradually. In conclusion, the detection of myopathic motor unit potentials with myotonic discharges on EMG in patients on colchicine therapy is an important finding and it is possible to suggest that this clue may lead to the invasive procedure of muscle biopsy unnecessary.

Biopsy↗
PubMed1999

Effect of colchicine on neuropeptide Y expression in rat dorsal root ganglia and spinal cord.

Neuropeptide Y (NPY) expression in the spinal cord and dorsal root ganglia (DRG) was examined after application of colchicine, an axonal transport blocker, on the intact sciatic nerve or prior to axotomy or chronic constriction injury (CCI). Rats that underwent topical application of colchicine on the sciatic nerve showed decreased responsiveness to heat stimulation, ipsilaterally. CCI-induced hyperalgesia was prevented by prior application of colchicine. However, colchicine did not block axotomy-induced NPY increase when applied proximally to the injury. In fact, colchicine induced the expression of NPY in the DRG and spinal cord in an identical manner to axotomy. The present data indicates that the increase in NPY observed after nerve injury could be initiated by the suppression of retrograde transport of factors, possibly neurotrophins, rather than by the production of an active factor at the site of injury.

Animals↗
PubMed1999

Metabotropic glutamate receptor agonists protect from oxygen-glucose deprivation- and colchicine-induced apoptosis in primary cultures of cerebellar granule cells.

The effects of the metabotropic glutamate receptor agonists against apoptosis induced by oxygen-glucose deprivation or colchicine were studied in the primary cultures of mature cerebellar granule cells. Oxygen-glucose deprivation (90 min) or addition of colchicine (1 microM) resulted in neuronal damage as revealed by Trypan Blue assay 12 h later. Further analysis demonstrated that the cells exposed to oxygen-glucose deprivation or colchicine exhibit typical features of apoptosis: internucleosomal DNA fragmentation, condensation and fragmentation of chromatin and typical DNA ladder on agarose gel electrophoresis. Metabotropic glutamate receptor agonist, (1S,3R)-1-aminocycloheptane-trans-1,3-dicarboxylic acid, acting at group I and II receptors, and selective agonist, (2S,1'R,2R',3R')-2(2,3-dicarboxycyclopropyl)glycine, acting at group II receptors, added to cells recovering from oxygen-glucose deprivation exerted neuroprotective action against oxygen-glucose deprivation-induced apoptosis. Similar neuroprotective effects of metabotropic glutamate receptor agonists were observed against colchicine-induced apoptosis. The results thereby provide evidence that metabotropic glutamate receptor agonists have therapeutic potential in the treatment of pathologies associated with increased neuronal apoptosis. The selective protein kinase C inhibitor bisindolylmaleimide (100 nM) abolished the neuroprotective action of (1S,3R)-1-aminocycloheptane-trans-1,3-dicarboxylic acid, whereas the activator of adenylyl cyclase forskolin (10 microM) abolished the neuroprotective action of (2S,1'R,2R',3R')-2(2,3-dicarboxycyclopropyl)glycine (30 microM) against colchicine-induced apoptosis. It is concluded that both phosphoinositide hydrolysis with consequent activation of protein kinase C and inhibition of adenylyl cyclase seem to contribute to the neuroprotective action of metabotropic glutamate receptor agonists against neuronal apoptosis in the primary culture of cerebellar granule cells.

Animals↗
PubMed1998

Does the lack of the P-glycoprotein efflux pump in neutrophils explain the efficacy of colchicine in familial Mediterranean fever and other inflammatory diseases?

Colchicine is an alkaloid drug commonly used in familial Mediterranean fever (FMF), gout, Behcet's syndrome, psoriasis and Sweet's syndrome. The exact mechanism of its action in these diseases is not entirely known. However, it has been shown that colchicine may inhibit neutrophil chemotaxis, thereby decreasing the inflammatory process. Recently, it was shown that colchicine accumulates in neutrophils in higher concentrations than in lymphomonocytes. Studies dealing with the multiple drug resistance (MDR) issue disclosed that neutrophils lack the P-glycoprotein (P-gly) membranal pump (encoded by the MDR1 gene). We propose that the preferential accumulation of colchicine in neutrophils compared with lymphomonocytes is due to the absence of the P-gly efflux pump in the former. This may explain the effectiveness of colchicine in diseases where increased chemotaxis is evident. The hypothesis may also provide an explanation for FMF patients who do not respond to the drug.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1990

Determination of the antimitotic agents N-desacetylcolchicine, demecolcine and colchicine in serum and urine.

In an effort to characterize the pharmacokinetic behavior of the antimitotic agent N-desacetylcolchicine a selective, sensitive high-performance liquid chromatographic method was developed for the determination of N-desacetylcolchicine, demecolcine and colchicine in serum or urine. To 0.5 ml of serum or 0.1 ml of urine diluted to 0.5 ml were added 50 microliters demecolcine (2 micrograms/ml) which serves as the internal standard. The sample was extracted using a C2 reversed-phase solid extraction column. N-Desacetyl-colchicine, colchicine and the internal standard were eluted from the column with methanol. The combined eluates were evaporated to dryness and the residue was reconstituted with water. The reconstituted sample was injected into a C18 reversed-phase column and eluted using a mobile phase consisting of 0.1 M potassium dihydrogenphosphate, 5 mM 1-pentanesulfonic acid in methanol and acetonitrile with a final pH of 6.0, at a flow rate of 1.5 ml/min. N-Desacetylcolchicine, colchicine and the internal standard were detected using a variable-wavelength ultraviolet detector at 254 nm. The limit of detection was 0.4 ng/ml for desacetylcolchicine and 4.0 ng/ml for colchicine. The method is linear over a concentration range of 1.0-200 ng/ml. The method has been shown to be a rapid, reliable method to monitor N-desacetylcolchicine levels in clinical trials in cancer patients.

Chromatography, High Pressure Liquid↗
PubMed2002

Epithelial cell mitotic arrest--a useful postmortem histologic marker in cases of possible colchicine toxicity.

Following ingestion of 30 mg of presumed benztropine (Cogentin) a 39-year-old male developed nausea, vomiting and diarrhea. His admission to hospital was soon followed by collapse and death. Histological examination, however, revealed increased numbers of mitotic figures in otherwise normal epithelial cells of the esophagus and bronchioles, a feature characteristic of colchicine toxicity. Subsequent toxicological analyses confirmed the presence of colchicine in the urine, but not in the blood. A dispensing error had resulted in substitution of colchicine for Cogentin. Histological findings had, therefore, provided evidence of colchicine toxicity and had guided subsequent toxicological evaluation. In suspected cases of colchicine toxicity, histological samples should, therefore, be taken from multiple sites along the gastrointestinal and respiratory tract in addition to other organs and tissues so that diagnostic morphological changes can be looked for.

Adult↗