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 991 records · Page 55Linked to original sources
PubMed2000

Exogenous administration of L-arginine protects cholinergic neurons from colchicine neurotoxicity.

The effect of L-arginine administration on susceptibility/resistance of NO-producing neurons was investigated in non-ischemic neurodegenerative conditions. ChAT mRNA level was measured by in situ hybridization in the basal forebrain after i.c.v. colchicine administration. Colchicine induced down-regulation of ChAT mRNA level followed by degeneration of cholinergic neurons. L-Arginine treatment increased ChAT mRNA level and prevented/delayed ChAT mRNA decrease by colchicine. These data suggest that L-arginine treatment may protect cholinergic neurons from colchicine-induced degeneration.

Animals↗
PubMedDate not supplied

Effect of colchicine on angiotensin receptors in rabbit aorta.

Colchicine (10(-5) M) significantly depressed the dose-response curve for angiotensin in isolated rabbit aortic strips. A lower maximal response was observed without apparent change in receptor affinity for angiotensin, as can be judged by unchanged ED50 values. Colchicine also diminished the dose-response curve for norepinephrine. The angiotensinase activity in cell membrane fraction and high-speed supernate was significantly inhibited. Colchicine did not change the specific receptor binding of radioactive angiotensin to either cell membrane fraction or supernate. It is concluded that colchicine possibly depresses the response to angiotensin through a mechanism involving a site beyond membrane receptors.

Angiotensin II↗
PubMed1990

Intravenous colchicine for low-back pain: a double-blind study.

Colchicine, a drug used for centuries in the treatment of gout, has been reported to be effective for low-back pain due to disc disorders. A prospective, randomized, double-blind study evaluating the therapeutic effect of intravenous colchicine was conducted in a group of patients with low-back pain with symptoms originating less than 6 months previously. Each patient completed a questionnaire and a pain drawing. Laboratory studies including uric acid and sedimentation rate were performed, as was a detailed physical examination and lumbar thermography. All treatment parameters (including physical therapy, anti-inflammatory medications, and instructions) were constant except that each patient received either intravenous colchicine or intravenous saline. Results indicate a significant difference between the two groups, the intravenous colchicine group showing improvement in symptoms for a few hours or days over a 3-week course of treatment. However, the relief was often of short duration.

Adult↗
PubMed2006

Colchicine intoxication diagnosed in a skin biopsy: a case report.

Colchicine toxicity is a rare, but well-described clinical entity. The histopathologic findings in various organ systems have been delineated in colchicine intoxication; however, skin findings have only been described in rare cases. We present a case of colchicine toxicity diagnosed on skin biopsy in a patient presenting with mental status changes. Her cutaneous manifestation consisted of a diffuse, blanchable, violaceous, morbilliform rash involving the trunk and proximal extremities. The histopathologic findings included metaphase-arrested keratinocytes with underlying basal vacuolization. These features, considered in the setting of multiorgan dysfunction and a known exposure of colchicine, led to the diagnosis.

Biopsy↗
PubMed1981

Suppression of active Arthus reaction by colchicine.

An effect of colchicine on the active Arthus reaction in rabbits was investigated in vivo with simultaneous evaluation of in vitro chemotactic activity of polymorphonuclear leukocytes. Arthus reactions were induced by intracutaneous injection of ovalbumin into rabbits preimmunized with ovalbumin. Colchicine, 1 mg/kg or 2 mg/kg, injected intraperitoneally one hour prior to the induction of the Arthus reaction, suppressed erythema and induration at 12 h, when histology showed decreased numbers of C3, suggestive of the presence of immune complexes, persisted to 24 h. In vitro chemotaxis of polymorphonuclear leukocytes using Boyden chamber techniques revealed suppression of the activity in the colchicine-treated animals at 6 and 12 h. These findings suggest that colchicine inhibits vascular injury by interfering with directional chemotaxis of polymorphonuclear leukocytes to the lesional sites.

Animals↗
PubMed2004

Toxic epidermal necrolysis-like reaction secondary to colchicine overdose.

Colchicine is a microtubule-inhibiting drug used to treat gout, familial Mediterranean fever and many other skin diseases. Intoxication with colchicine affects multiple organs, often fatally. Cutaneous sequelae of colchicine toxicity are rare. We describe the clinical and histological features of a toxic epidermal necrolysis-like exanthem in a patient who lethally overdosed on colchicine.

Apoptosis↗
PubMed1986

Effect of oral colchicine on T cell subsets, monocytes and concanavalin A-induced suppressor cell function in asthmatic patients.

Asthmatic patients have a deficiency of concanavalin A-(Con A) induced suppressor cell function. We tested whether oral colchicine 0.5 mg twice daily for 7 days could correct this immunoregulatory abnormality. Peripheral blood mononuclear cells were incubated with Con A and then suppression of proliferation was measured by coculture of these cells with healthy volunteers' mononuclear cells and phytohaemagglutinin. Sixteen asthmatic patients had significantly (P less than 0.002) decreased Con A-induced suppressor cell function (17.0 +/- 17.2%, mean +/- s.d.) as compared to 13 healthy volunteers (37.9 +/- 14.9%). Oral colchicine significantly (P less than 0.05) increased, though only partially corrected, these 16 asthmatic patients' Con A-induced suppressor cell function (28.1 +/- 14.3%). Asthmatic patients had an increased number of monocytes (691 +/- 289 vs 388 +/- 271/mm3 for normals, P less than 0.01) and a normal number of lymphocytes, Leu 4+ total T cells, Leu 3+ helper/inducer T cells, and Leu 2+ suppressor/cytotoxic T cells as well as a normal Leu 3/Leu 2 ratio. Oral colchicine significantly (P less than 0.005) decreased the number of monocytes (451 +/- 255/mm3) without significantly affecting the number of lymphocytes, Leu 4+, Leu 3+, or Leu 2+ T cells, or the Leu 3/Leu 2 ratio. These results are consistent with the hypothesis that the deficiency of Con A-induced suppressor cell function in asthmatic patients may be due, in part, to an increased number and/or abnormal activity of monocytes. If so, then oral colchicine may have partially corrected the deficiency of Con A-induced suppressor cell function by decreasing the number and/or modulating the activity of monocytes.

Adult↗
PubMedDate not supplied

Combination therapy with ursodeoxycholic acid and colchicine for primary biliary cirrhosis.

Twelve patients with primary biliary cirrhosis (PBC), stages I to III, received long-term therapy with a combination of 600 mg ursodeoxycholic acid (UDCA) and 1 mg colchicine given daily for more than 2 years. Drug toxicity was mild; one patient experienced diarrhoea that was probably due to colchicine. Serum levels of bilirubin, alkaline phosphatase (ALPase), gamma-glutamyl transpeptidase and alanine aminotransferase decreased by more than 50% of the initial values. Serum albumin and cholesterol levels also improved, but immunoglobulins and anti-mitochondrial antibody titre did not change. Histologic features in the eight patients who received serial liver biopsies before and 2 years after the beginning of treatment were evaluated. Piecemeal necrosis and portal inflammation were improved, but there was no change in portal fibrosis. Patients were divided into two groups; the first received both drugs from the outset, and the second group were started on UDCA for 3 months followed by the addition of colchicine. After 3 months, the improvement in serum bilirubin and ALPase in the first group was greater than in the second. However, in the second group, the ALPase levels had decreased significantly when measured at 6 and 9 months after the treatment compared with the levels at 3 months. These findings suggest that UDCA and colchicine may have a synergistic effect. This combination therapy appears to be safe and effective, both clinically and histologically, for treating PBC.

Colchicine↗
PubMed1980

An improved DEAE-cellulose filter assay for colchicine binding protein (during mouse brain development).

A DEAE-cellulose filter assay for colchicine binding protein (CBP) has been modified to include 1 M-sucrose in the incubation medium (single-point assay). Due to the much greater stability of colchicine binding capacity under the conditions described, multiple time-point assays (time-decay method) were not necessary for accurate determination of CBP in brain samples, as shown by the agreement of results obtained using the two methods to measure CBP in C129F1 hybrid mouse brains at different stages of development. In this study, the highest concentrations of CBP (millimoles of colchicine bound per milligram of total protein) were observed in the 160,000 g supernatant and pellet of newborn-brain homogenate. The CBP concentrations in these two fractions were approximately twice those observed in the earliest stage measured (13.5 days gestation) and in the 11-month-old adult. However, CBP concentration, in terms of millimoles of colchicine bound per gram of brain wet weight, reached a maximum at the end of the 1st week after birth. Between 17.5 days gestation and the end of the 1st postnatal week, more CBP accumulated in the pellet fraction than in the supernatant.

Animals↗
PubMed1984

Effects of monensin and colchicine on myelin galactolipids.

Monensin and colchicine have been used in a variety of systems to disrupt functioning of the Golgi apparatus and transport of Golgi-derived vesicles to the plasma membrane. In this study the effects of monensin and colchicine on the synthesis of cerebroside and sulfatide and their appearance in myelin were examined to determine whether these myelin components are processed through the Golgi apparatus. Brain slices from rats 17 days old were incubated with [3H]galactose and [35S]-sulfate to label cerebroside and sulfatide. Myelin was isolated on sucrose density gradients. Fractions highly enriched in cerebroside and sulfatide were prepared from homogenates and myelin fractions by lipid extraction, alkaline methanolysis, and in some cases TLC. Monensin at 0.1 microM had no significant effect on synthesis of these galactolipids as measured by incorporation of [3H]-galactose into cerebroside or [35S]sulfate into sulfatide in homogenates. However, appearance of [35S]sulfatide in the myelin fraction was reduced to 49% of control, while appearance of [3H]cerebroside was not significantly reduced. Colchicine from 1 mM to 0.1 microM had effects similar to monensin, that is, appearance of [35S]sulfatide in myelin was depressed, but again [3H]cerebroside was not affected. Incorporation of [35S]sulfate into sulfatide in homogenate was 93% of control, while appearance of [35S]sulfatide in the myelin fraction was depressed to 58% of control. The inhibition of appearance of sulfatide in myelin by colchicine and monensin is consistent with the view that sulfation of cerebroside occurs in the Golgi and that sulfatide is transported via Golgi-derived vesicles to the forming myelin membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Decreased metabolism of cerebrosides and sulfatides in rat sciatic nerve after intraneural injection of colchicine.

To obtain an understanding of the importance of the neuronal cytoskeleton in Schwann cell metabolism, an antimicrotubular agent (colchicine) was injected into the rat sciatic nerve 24 or 48 h before incubation of the nerve with labeled precursor: [35S]sulfate, [14C]galactose, or [3H]-galactose. Colchicine inhibited the incorporation of 35S radioactivity into sulfatides and, to a lesser extent, into proteins. With galactose as the radioactive precursor, synthesis of cerebrosides was reduced by colchicine injection, whereas incorporation of radioactivity into phosphatidylserine and phosphatidylcholine increased. Intraneural injection of lumicolchicine had no effect. The effects of colchicine on the metabolism of the Schwann cell are discussed in relation to its action on microtubules.

Animals↗
PubMed1989

Model-independent pharmacokinetics of colchicine after oral administration to healthy volunteers.

The pharmacokinetics of colchicine were studied after oral administration of three doses (0.5, 1.0 and 1.5 mg) to nine healthy male volunteers according to randomized cross-over design. Plasma and urine samples were collected during 48 h after ingestion, and assayed for colchicine levels by a specific and highly sensitive radio-immunoassay. Pharmacokinetic parameters t1/2 beta, AUC, MRT, CIT/F, CIR, Vd area/F) were calculated by model-independent methods and compared across doses by multiway analysis of variance. Terminal half-life (15.5-19.2 h), mean residence time (15.7-20.3 h), oral systemic (32.2-40.3 l/h) and renal (3.9-4.7 l/h) clearances, and oral volume of distribution (11.4-14.9 l/kg) did not differ significantly between doses, whereas the area under the concentration-time curve was proportional to dose. Our results show that: 1. within the dose range studied (0.5-1.5 mg), the pharmacokinetics of colchicine are linear; 2. monitoring colchicine levels up to 48 hours yields much larger estimates of terminal half-life and volume of distribution than previously reported from considerably shorter studies.

Administration, Oral↗
PubMed1996

Effect of colchicine and trimethylcolchicinic acid on CCl4-induced cirrhosis in the rat.

Colchicine is one of the most promising drugs for the treatment of cirrhosis. However, due to its toxicity, other drugs are being evaluated and colchicine-like molecules may be good alternatives. The aim of this work was to compare the beneficial effects of colchicine and trimethylcolchicinic acid (a colchicinoid less toxic than colchicine) on CCl4-cirrhosis. The drugs were administered either through CCl4 administration (8 weeks) or after CCl4 intoxication for 4 weeks at a dose of 10 micrograms/rat/day, orally. Liver plasma membranes were isolated for high affinity Ca(2+)-ATPase, gamma-glutamyl transpeptidase and alkaline phosphatase activities. The activities of gamma-glutamyl transpeptidase and alkaline phosphatase were also measured in serum. Liver glycogen content and a marker for lipid peroxidation were determined in liver samples. We found that both compounds preserved and significantly reversed high affinity Ca(2+)-ATPase, gamma-glutamyl transpeptidase and alkaline phosphatase plasma membrane and serum enzyme activities as well as the hepatic glycogen content.

Alanine Transaminase↗
PubMed2005

Resolution of liver fibrosis in chronic CCl4 administration in the rat after discontinuation of treatment: effect of silymarin, silibinin, colchicine and trimethylcolchicinic acid.

The purpose of this work was to obtain a suitable model of fibrosis, in which spontaneous reversion was minimal, to study the ability of silymarin, silibinin, colchicine and trimethylcolchicinic acid (TMCA) to reverse it. Reversal of liver fibrosis was studied in male Wistar rats after one, two or three months of CCl(4) administration (0.4 g/kg intraperitoneally, three times per week), by discontinuation of the toxin for 2 months. Silymarin (50 mg/kg), silibinin (50 mg/kg), colchicine (10 microg/rat) and trimethylcolchicinic acid (100 microg/rat) were administered daily, by gavage, after 3 months of CCl(4) administration. Collagen content was determined by measuring hydroxyproline in liver samples; glycogen, was determined utilizing the anthrone reagent; Mallory's trichromic stains of liver sections were performed. The best scheme of treatment was obtained when CCl(4) was administered during three months (collagen increased 6 times). Discontinuation of the toxin for two months produced a significant but relative small reduction of fibrosis (collagen was still 4.5 times over control). Colchicine, TMCA, silymarin or silibinin treatment showed no significant fibrolitic effect. This scheme of treatment may be an excellent tool to study the ability of drugs to reverse fibrosis. The hepatoprotective properties of silymarin, silibinin, colchicine and trimethylcolchinic acid may be irrelevant to reverse established cirrhosis.

Alanine Transaminase↗
PubMed1995

Colchicine induces enhanced intestinal permeability in the rat.

Intestinal permeability was determined in rats receiving colchicine 0.5 +/- 0.15 mg day-1 in drinking water (30 mg L-1) for periods up to 23 days. The lactulose/mannitol method was used to determine whole gut permeability before and on days 2, 4, 8, 18 and 23 of colchicine administration. The 8-h urinary lactulose excretion following the test meal increased significantly in rats receiving colchicine, compared with the pretreatment value. Increased lactulose permeability was present after 2 days and remained stable throughout the experimental period. Mannitol urinary excretion was not changed. Colchicine increases intestinal tight junction permeability by an as yet undetermined mechanism.

Animals↗
PubMed1975

A reexamination of the reaction between colchicine and tubulin.

The rate of reversible dissociation of the colchicine-tubulin complex has been determined for purified porcine brain tubulin and for sea urchin tubulin from 100,000 times g supernatant. The rate constant, which is essentially the same for both species, is extremely slow; it corresponds to a half-life of approximately 36 hours for the reaction. This rate was the same whether or not sucrose was present, and was not influenced by low concentrations of vinblastine or by millimolar concentrations of colchicine. The association rate constant was determined for porcine brain tubulin with and without CaCl2. The sample without CaCl2 had been maximally polymerized prior to the addition of colchicine. A 4.7-fold difference was observed between the association rate constants under these two conditions. Equilibrium constants calculated from the measured rate constants are 5 to 20 times greater than directly measured values; this suggests that the interaction of microtubules and colchicine is more complex than was previously thought.

Animals↗
PubMed1986

Colchicine-induced tubular, vesicular and cisternal organelle aggregates in absorptive cells of the small intestine of the rat. II.--Endocytosis studies.

Administration of the antimicrotubular agent colchicine to adult rats (0.5 mg/100 g of body weight for 6 hr) induces formation of extended aggregates of tubular, vesicular, and cisternal organelles in the absorptive cells of the small intestine. The phosphatase reaction pattern (thiamine pyrophosphatase, acid phosphatase, acid trimetaphosphatase) suggests that the majority of them belongs to the lysosomal system (Ellinger and Pavelka, 1984). The present study extends these findings and examines the uptake and fate of intravenously injected horseradish peroxidase (HRP) at the basal and lateral cell surfaces and of intraluminally applied HRP at the apical cell surface. HRP, applied to control animals and animals pretreated with colchicine, was internalized at both apical and basolateral cell surfaces of the absorptive cells, and delivered into endosome-like vesicles, multivesiculated bodies (mvbs), dense bodies (dbs), and in several instances into Golgi cisternae. Following intraluminal application, evidence was obtained for the transport of HRP across the cell; in contrast, intravenously applied HRP was never detected at the apical cell surface. Colchicine pretreatment did not stop the uptake of HRP, which was rapidly sequestered to the clustered tubules, vesicles, and cisternae, as well as to the mvbs and dbs. After longer intervals, the portion of HRP-reactive tubules, vesicles, and cisternae within the clusters increased: 60 min after HRP-administration all of them contained HRP-activity. These results indicate that the colchicine-induced clustered organelles are recipients of endocytic materials internalized at the apical as well as at the basolateral cell surface.

Animals↗
PubMed1989

In vitro effects of colchicine and nocodazole on ciliogenesis in quail oviduct.

Oviduct implants from quails which were primarily stimulated in vivo by estrogen so as to induce ciliogenesis in some epithelial cells were cultured in vitro in the presence or absence of colchicine or nocodazole. After 24 or 48 hr of culture, implants were examined by transmission and scanning electron microscopy to determine drug-induced alterations in ciliogenesis. After 24 hr of 10(-5) M colchicine treatment, the formation of basal bodies was totally inhibited, though the precursor material of generative complexes was unchanged. The inhibitory effect was not reversed when colchicine was removed in a 24 hr recovery culture. Treatment with 10(-6) M nocodazole for 24 hr, partially inhibited the assembly of basal bodies, which exhibited altered morphology. The assembly of basal bodies was restored during the 24 hr recovery period, after removal of nocodazole. Colchicine and nocodazole did not prevent polarized migration towards the apical surface of basal bodies formed prior to drug treatment. They anchored to the plasma membrane, but the formation of cilia was strongly disturbed in the presence of the drug. Numerous cells possessed anchored basal bodies which failed to induce the formation of cilia. The elongation of cilia was inhibited, as seen by their abnormal capping structure. In the enlarged tip, microtubules diverged. In contrast, these very short cilia possessed a mature ciliary necklace which was constructed during drug treatment. Differentiation of this membrane ciliary structure appeared to be unrelated to axoneme growth.

Animals↗