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PubMed1990

Molecular basis of preferential resistance to colchicine in multidrug-resistant human cells conferred by Gly-185----Val-185 substitution in P-glycoprotein.

Expression of P-glycoprotein, encoded by the human MDR1 gene, results in cross-resistance to many lipophilic cytotoxic drugs (multidrug resistance). P-glycoprotein is believed to function as an energy-dependent efflux pump that is responsible for decreased drug accumulation in multidrug-resistant cells. Previous work showed that preferential resistance to colchicine in a colchicine-selected multidrug-resistant cell line was caused by spontaneous mutations in the MDR1 gene that resulted in a Gly-185----Val-185 substitution in P-glycoprotein. We have now compared transfectant cell lines expressing either the wild-type Gly-185 or the mutant Val-185 P-glycoprotein with regard to their levels of resistance to and accumulation and binding of different drugs. In cells expressing the mutant protein, increased resistance to colchicine and decreased resistance to vinblastine correlated with a decreased accumulation of colchicine and increased accumulation of vinblastine. Expression of the mutant P-glycoprotein also resulted in significantly increased resistance to epipodophyllotoxin and decreased resistance to vincristine and actinomycin D; smaller changes in resistance were observed for several other drugs. Unexpectedly, the mutant P-glycoprotein showed increased binding of photoactive analogs of vinblastine and verapamil and the photoactive compound azidopine and decreased binding of a photoactive colchicine analog. These results suggest that the Gly-185----Val-185 substitution affects not the initial drug-binding site of P-glycoprotein but another site, associated with the release of P-glycoprotein-bound drugs to the outside of the cell.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2002

Evaluation of commercial Ginkgo biloba dietary supplements for the presence of colchicine by high-performance liquid chromatography.

A high-performance liquid chromatographic method with photodiode array detection was developed for the detection of the presence of colchicine in commercial ginkgo products. The method is based on the baseline separation of constituents in ginkgo samples plus reference colchicine. The minimal detectable concentration of colchicine is 1.0 ng on column in the current assay. By analysis of retention time and UV profile of suspect peaks in the sample with those of reference colchicine, none of the nine commercial ginkgo products analyzed contained colchicine.

Chromatography, High Pressure Liquid↗
PubMed2005

Colchicine decreases airway hyperreactivity after phosgene exposure.

Phosgene (COCl(2)) exposure affects an influx of inflammatory cells into the lung, which can be reduced in an animal model by pretreatment with colchicine. Inflammation in the respiratory tract can be associated with an increase in airway hyperreactivity. We tested the hypotheses that (1) phosgene exposure increases airway reactivity and (2) colchicine can decrease this elevation. Sprague Dawley rats (70 d old; male) were exposed to 1 ppm COCl(2) for 1 h. Airway reactivity was tested at 0, 4, and 24 h postexposure by infusing anesthetized animals intravenously with acetylcholine and assessing expiratory resistance and dynamic compliance. Immediately and 4 h postexposure, a significant change in expiratory resistance and dynamic compliance was observed in those animals exposed to COCl(2), while at 24 h this response was greater. A second experiment was performed in rats pretreated with colchicine (1 mg/kg) or saline given intraperitoneally, exposed to 1 ppm COCl(2) for 1 h, with both expiratory resistance and dynamic compliance assessed at 24 h. After exposure, cell differentials and protein in lavage were also quantitated. The results indicate that colchicine decreased neutrophil influx, protein accumulation, and changes in both expiratory resistance and dynamic compliance after COCl(2) exposure. Colchicine may affect injury and changes in expiratory resistance and dynamic compliance by diminishing the incursion of inflammatory cells, but other properties of this medication may also be responsible for the observed results.

Acetylcholine↗
PubMed2000

Fatal cardiovascular collapse following acute colchicine ingestion.

BACKGROUND: A previously published prognostic rule predicts 100% survival after ingestion of cochicine doses less than 0.5 mg/kg and 100% mortality after ingestion of more than 0.8 mg/kg. This rule inaccurately predicted survival in a recent case. CASE REPORT: We present a case of fatal colchicine poisoning in an adult who ingested a maximum of 39.6 mg of colchicine (0.40 mg/kg). He subsequently developed hypotension which was refractory to fluid resuscitation and infusion of vasopressors. He died of cardiovascular collapse approximately 35 hours after ingestion. DISCUSSION: Fatal outcomes are possible even with colchicine doses less than 0.5 mg/kg. Physicians caring for colchicine-poisoned patients must be prepared for the possibility of acute cardiovascular collapse and ventricular dysrhythmias regardless of the reported dose of colchicine.

Adult↗
PubMed1992

Flagellar microtubule dynamics in Chlamydomonas: cytochalasin D induces periods of microtubule shortening and elongation; and colchicine induces disassembly of the distal, but not proximal, half of the flagellum.

To study the mechanisms responsible for the regulation of flagellar length, we examined the effects of colchicine and Cytochalasin D (CD) on the growth and maintenance of Chlamydomonas flagella on motile wild type cells as well as on pf 18 cells, whose flagella lack the central microtubules and are immobile. CD had no effect on the regeneration of flagella after deflagellation but it induced fully assembled flagella to shorten at an average rate of 0.03 microns-min. Cells remained fully motile in CD and even stubby flagella continued to move, indicating that flagellar shortening did not selectively disrupt machinery necessary for motility. To observe the effects of the drug on individual cells, pf 18 cells were treated with CD and flagella on cells were monitored by direct observation over a 5-hour period. Flagella on control pf 18 cells maintained their initial lengths throughout the experiment but flagella on CD-treated cells exhibited periods of elongation, shortening, and regrowth suggestive of the dynamic behavior of cytoplasmic microtubules observed in vitro and in vitro. Cells behaved individually, with no two cells exhibiting the same flagellar behavior at any given time although both flagella on any single cell behaved identically. The rate of drug-induced flagellar shortening and elongation in pf 18 cells varied from 0.08 to 0.17 microns-min-1, with each event occurring over 10-60-min periods. Addition of colchicine to wild type and pf 18 cells induced flagella to shorten at an average rate of 0.06 microns-min-1 until the flagella reached an average of 73% of their initial length, after which they exhibited no further shortening or elongation. Cells treated with colchicine and CD exhibited nearly complete flagellar resorption, with little variation in flagellar length among cells. The effects of these drugs were reversible and flagella grew to normal stable lengths after drug removal. Taken together, these results show that the distal half to one-third of the Chlamydomonas flagellum is relatively unstable in the presence of colchicine but that the proximal half to two-thirds of the flagellum is stable to this drug. In contrast to colchicine, CD can induce nearly complete flagellar microtubule disassembly as well as flagellar assembly. Flagellar microtubules must, therefore, be inherently unstable, and flagellar length is stabilized by factors that are sensitive, either directly or indirectly, to the effects of CD.

Actins↗
PubMed1972

Colchicine inhibition of nerve fiber formation in vitro.

Inhibition of nerve fiber (neurite) formation by colchicine and Colcemid was studied in monolayer cultures of dissociated spinal ganglia of the chick. Replica cultures were fixed after appropriate incubation and alkaloid treatment. Quantitative estimates of the mean total neurite length per neuron (MNL) were made by use of camera lucida tracing. MNL values plotted against time of incubation gave control curves with an initial lag period, a phase of rapid increase, and a final phase in which MNL increase was retarded. Colchicine at 0.01-0.05 microg/ml (2.4 x 10(-8)-1.2 x 10(-7)M) caused reversible, concentration dependent, inhibition of the increase in MNL when applied during the lag period or phase of rapid increase. At the highest concentration there was a net decrease in MNL. The effect of Colcemid at 0.05 microg/ml was similar to that of colchicine, but more rapidly reversible. In most experiments there was no loss of neurons during the period of inhibition of MNL increase by colchicine or Colcemid. Therefore selective destruction of neurons was not involved in the inhibition of neurite growth. Prolonged incubation after treatment with the highest concentration used resulted in a 50% loss of neurons, in part through detachment of viable cells. Quantitative radioautography of the alkaloid-treated neurons with leucine-(14)C indicated little or no inhibition of incorporation into protein during inhibition of MNL increase. The results strongly suggest that inhibition of neurite growth involves a specific effect of colchicine, presumably the disruption of microtubules. They are thus consistent with the hypothesis that the polymerization of microtubules is essential to the formation of nerve fibers.

Alkaloids↗
PubMed1975

Colchicine inhibition of plasma protein release from rat hepatocytes.

Colchicine, both in vitro and in vivo, inhibits secretion of albumin and other plasma proteins. In vitro, secretion by rat liver slices is inhibited at 10-minus 6 M with maximal effect at 10-minus 5 M. Inhibition of secretion is accompanied by a concomitant retention of nonsecreted proteins within the slices. Colchicine does not inhibit protein synthesis at these concentrations. Vinblastine also inhibits plasma protein secretion but lumicolchicine, griseofulvin, and cytochalasin B do not. Colchicine also acts in vivo at 10-25 mumol/100 g body weight. Inhibition of secretion is not due to changes in the intracellular nucleotide phosphate levels. Colchicine, administered intravenously, acts within 2 min and its inhibitory effect lasts for at least 3 h. Colchicine has no effect on transport of secretory proteins in the rough or smooth endoplasmic reticulum but it causes these proteins to accumulate in Golgi-derived secretory vesicles.

Animals↗
PubMed1978

In vivo effect of colchicine on hepatic protein synthesis and on the conversion of proalbumin to serum albumin.

Treatment of rats with 0.5-25 mumol/100 g body weight of colchicine for 1 h or more caused an inhibition of hepatic protein synthesis. This effect was not seen if animals were exposed to colchicine for less than 1 h. The delayed inhibition of protein synthesis affected both secretory and nonsecretory proteins. Treatment with colchicine (15 mumol/100 g) for 1 h or more caused the RNA content of membrane-bound polysomes to fall but did not change the polysomal profile of this fraction. By contrast, the total RNA content in the free polysome cell fraction was increased, and this was due to the presence of more ribosomal monomers and dimers. Electron microscope examination of the livers from rats treated for 3 h with colchicine showed an accumulation of secretory vesicles within the hepatocytes and a general distention of the endoplasmic reticulum. Administration of radioactive L-leucine to the rats led to an incorporation of radioactivity into two forms of intracellular albumin which were precipitable with antiserum to rat serum albumin but which were separable by diethylaminoethyl-cellulose chromatography. One form has arginine at the amino-terminal position and is proalbumin, and the other form, which more closely resembles serum albumin chromatographically, has glutamic acid at its amino terminus. Only proalbumin was found in rough and smooth endoplasmic reticulum fractions and in a Golgi cell fraction wich corresponds morphologically to mostly empty and partially filled secretory vesicles. However, in other Golgi cell fractions which were filled with secretory products, both radioactive proalbumin and serum albumin were found. This indicates that proalbumin is converted to serum albumin in these secretory vesicles just before exocytosis. Colchicine delayed the discharge of radioactive albumin from these filled secretory vesicles and caused an accumulation of both proalbumin and serum albumin within these cell fractions.

Animals↗
PubMed1983

Effect of colchicine on internalization of prolactin in female rat liver: an in vivo radioautographic study.

Binding and internalization of 125I-ovine prolactin into hepatocytes of female rats was visualized by the in vivo radioautographic method (Bergeron, J. J. M., G. Levine, R. Sikstrom, D. O'Shaughnessey, B. Kopriwa, N. J. Nadler, and B. I. Posner, 1977, Proc. Natl. Acad. Sci. USA, 745:051-5055). Receptor-mediated internalization of label was observed into lipoprotein-filled vesicles in the Golgi/bile canalicular region of the hepatocyte. Colchicine treatment had no effect on the internalization of label into the lipoprotein-filled vesicles. However, the location of the radio-labeled lipoprotein-filled vesicles was altered from the Golgi/bile canalicular region to subsinusoidal. Radioactive content of hepatocytes decreased as a function of time after injection of 125I-prolactin; however, colchicine treatment markedly retarded this loss of label. Subcellular fractionation experiments indicated that colchicine treatment led to decreased levels of 125I-prolactin accumulation in microsomes but augmented the accumulation of label in the L fraction. It is concluded that in normal female rats prolactin is internalized into lipoprotein-filled vesicles in the Golgi region before degradation of the hormone. Colchicine treatment accumulates labeled lipoprotein-containing vesicles in a subsinusoidal region and retards hormone catabolism. The labeled vesicles observed after colchicine treatment may correspond to the unique vesicles previously observed in the L fraction and found to be enriched in prolactin receptors (Khan, M. N., B. I. Posner, A. K. Verma, R. J. Khan, and J. J. M. Bergeron, 1981, Proc. Natl. Acad. Sci. USA, 78:4980-4981).

Animals↗
PubMed1999

Effect of cytochalasin B on the induction of chromosome missegregation by colchicine at low concentrations in human lymphocytes.

The aim of the present work was to investigate the possible interference of cytochalasin B (cyt B) with low concentration treatment with colchicine in the induction of chromosome/chromatid loss and micronuclei in human lymphocytes mitotically activated in vitro. Thus, cells from a single female donor were treated with colchicine (10 or 25 nM, from 24 h after PHA addition to fixation at 66 h) either in the presence or absence of cyt B. Single lagging chromosomes/chromatids were scored in bipolar ana-telophases and greater damage (disrupted and c-anaphases) was scored in cells at anaphase. Micronuclei were scored in the first 4000 nuclei observed in both cyt B-treated (in mononucleate and binucleate cells) and untreated cultures. With the same criterion, FISH analysis was performed on 2000 nuclei where chromosome 7 and 11 centromeric DNA probes were used in pairs. Our results showed that: (i) the frequency of laggards and of micronuclei increased with colchicine concentration but in the presence of cyt B there was a lower frequency of both (with a mean reduction of approximately 49%); (ii) FISH analysis showed a colchicine concentration-dependent increase in nuclei with three spots for chromosome 7; (iii) a colchicine concentration-dependent increase in tetraploid cells was observed. This increase was particularly remarkable (5-fold) in cells grown in the presence of cyt B compared with cyt B-untreated cells. The observed 'cyt B effects' can be explained if it is assumed that in cytokinesis-blocked cells there is a shorter distance between the poles. As a consequence: (i) laggards would be engulfed in the nearest daughter nucleus with a consequent lower induction of micronuclei; (ii) segregating sister chromatids in heavily impaired anaphases would not travel a sufficient distance to give rise to two daughter nuclei, leading to an increased frequency of polyploid nuclei.

Adult↗
PubMed1999

Detection of aneuploidy by multicolor FISH in mouse sperm after in vivo treatment with acrylamide, colchicine, diazepam or thiabendazole.

Multicolor fluorescence in situ hybridization (FISH) was used to investigate the induction of aneuploidy during meiosis in young adult male mice treated with chemicals chosen for the EU sponsored aneuploidy project (acrylamide, colchicine, diazepam and thiabendazole). The aim of the present study was to evaluate the frequency of aneuploid sperm induced by each of these chemicals by sperm FISH. Male (102/ElxC3H/El)F1 mice were treated with acrylamide (120 and 60 mg/kg single dose i.p.), colchicine (1.5 and 3 mg/kg single dose, i.p.), diazepam (300, 150 and 75 mg/kg single dose by oral intubation) or thiabendazole (100 and 300 mg/kg daily for 11 days by oral intubation). At 22 days after the last treatment, sperm were collected from the cauda epididymis. Three chromosome FISH was applied to determine hyperhaploid and diploid sperm with DNA probes specific for the chromosomes X, Y and 8. Five animals were treated per dose group and sperm aneuploidy was evaluated in 10,000 sperm per animal. We found significant increases in the frequency of total hyperhaploidy for the males treated with 3.0 mg/kg colchicine (0.092 versus 0.056%, P < 0.05) and with 1.5 mg/kg colchicine (0.082 versus 0.050%, P < 0.05), as well for the males treated with 300 mg/kg diazepam (0.081 versus 0.050%, P < 0.05), indicating that colchicine and diazepam each induced germ cell aneuploidy. We also found significant increases in the frequency of total diploidy for the males treated with 300 mg/kg diazepam (P < 0.05) and with 300 mg/kg thiabendazole (P < 0.05). No significant effects were found for 120 and 60 mg/kg acrylamide or for the other doses of diazepam and thiabendazole. These first results indicate that the multicolor FISH method is useful to determine aneuploidy induction in sperm of mice.

Acrylamide↗
PubMed2002

Microtubules of the mouse testis exhibit differential sensitivity to the microtubule disruptors Carbendazim and colchicine.

The testicular toxicant benomyl and its metabolite, carbendazim cause reproductive damage to the rat, an early sign of which is sloughing of germ cells with associated Sertoli cell fragments. However, the sensitivity of other mammalian species to these benzimidazole compounds is not clear. In this study, the effects of carbendazim and colchicine, a known microtubule disruptor, on the mouse seminiferous epithelium were characterized, and the amount of carbendazim reaching the mouse testis was measured. Testes were assessed for histological effects 3 h and 6 h after administration of carbendazim (2000 mg/kg, ip), and 6 h after intratesticular administration of either a low or high dose (5.3 or 117.6 micro g/g testis) of colchicine. Carbendazim caused no signs of histological damage to the mouse testis, and the microtubule cytoskeleton was intact and identical to controls based on immunostaining with tyrosinated alpha tubulin and beta tubulin antibodies. Similarly, the seminiferous epithelium of mouse testis was undamaged and the microtubule cytoskeleton was intact after a low dose of colchicine, while a comparable dose of colchicine injected into rat testis caused marked toxicity. However, mouse testes did show microtubule disruption and severe germ cell sloughing after administration of a high dose of colchicine. The amount of carbendazim measured in mouse testis was 375 nmol/g testis, which is higher than the value measured in rat testis after a toxic dose of carbendazim. Therefore, carbendazim reaches the mouse testis at or above levels measured in the rat, yet the mouse is apparently insensitive to this microtubule disrupting agent.

Animals↗
PubMed1993

Colchicine disrupts the cytoskeleton of rat testis seminiferous epithelium in a stage-dependent manner.

Sertoli cell microtubules play an important role in the process of spermatogenesis. We investigated the effects of colchicine, a microtubule-disrupting agent, on the seminiferous epithelium. Rats were injected intratesticularly with 0.004-40 micrograms colchicine/testis. Colchicine had a dose-related effect on seminiferous tubule fluid secretion and completely blocked secretion at a dose of 40 micrograms colchicine/testis. Colchicine also resulted in a dose-related decrease in testes weight 2 and 8 wk after injection. When 40 micrograms colchicine/testis was used, testis morphology showed a time-dependent increase in the incidence of sloughing over a time course of 1, 3, 6, and 16 h. Quantitative analysis demonstrated that stage IX-XIV seminiferous tubules were most sensitive to sloughing. Changes in the distribution of tubulin immunostaining within Sertoli cells occurred preferentially in stage VII-VIII seminiferous tubules, which were most resistant to sloughing. In addition, colchicine resulted in disruption of vimentin filaments in stage IX-XIV seminiferous tubules, which correlated with the stage-dependent sensitivity of sloughing. We propose that the stage dependence of colchicine-induced effects reflects the dynamic and stage-dependent role of microtubules in spermatogenesis. Furthermore, cellular structures other than microtubules, such as vimentin filaments, may be important for maintaining the structural integrity of the seminiferous epithelium.

Animals↗
PubMedDate not supplied

A cytogenic evaluation of long-term colchicine therapy in the treatment of Familial Mediterranean fever (FMF).

Thirty-eight patients suffering from Famlial Mediterranean Fever (FMF) and undergoing colchicine therapy for periods varying from one week to three years were examined cytogenetically. Preparations were derived from short-term lymphocyte cultures; mitotic rate, percent tetraploidy, and chromosome breakage rates were determined. Twenty-one patients were examined prior to treatment, 22 during treatment and 5 both before and during treatment and 5 both before and during treatment. No statistically significant differences were observed in the parameters studied between ten controls and the patient groups. An in vitro experiment indicated a direct correlation between increased colchicine concentration and mitotic rate. However, tetrapoloidy or chromosome damage showed no such association with colchicine concentration. Among the patient group, pregnancy occurred in four patients while under treatment; three pregnancies resulted in the birth of normal children while the fourth has not yet been completed. In one preganancy, cultured fetal amniotic fluid cells demonstrated no effect of colchicine on the cytogenetic parameters invetigated. These results indicate no untoward effects on long-term colchicine treatment in FMF with respect to fertility, teratogenicity and chromosomal damage.

Adolescent↗
PubMedDate not supplied

Colchicine-induced acute myopathy in a patient with concomitant use of simvastatin.

Colchicine and 3-hydroxy-3-methy-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are well known to cause myopathy. Myotoxicity is dose-dependent in both drugs; therefore, the onset of symptoms usually takes months or years. We report the case of a patient with chronic renal failure who had been taking simvastatin for 2 years and developed acute weakness 2 weeks after the start of treatment with colchicines for recurrent gout. The electromyography and elevated muscle enzymes indicated that his symptoms were caused by myopathy. When this patient stopped taking both drugs, his weakness resolved rapidly. Acute myopathy induced by combination therapy with colchicines and simvastatin is rare. In patients with chronic renal failure, co-administration of colchicine with simvastatin may accelerate the onset of myopathy because CYP3A4 (part of cytochrome P450) is crucial in the breakdown of both drugs. When adding colchicine to a medication regimen that includes a HMG-CoA reductase inhibitor for patients with renal insufficiency, drugs that are metabolized outside the CYP3A4 system (e.g., fluvastatin and pravastatin) should be selected instead.

Acute Disease↗
PubMed1975

Colchicine administration to mice: a metabolic and ultrastructural study.

A single injection of colchicine has been administered to normal albino mice, and the metabolic effects as well as the hepatic ultrastructural changes resulting from this treatment have been studied at various time intervals. A marked decrease in circulating triglyceride levels was evident 4 hours after colchicine injection and was maximum after 11 hours. It coincided with a marked increase in hepatic triglyceride content. Twenty hours after colchicine administration, plasma triglyceride levels and hepatic triglyceride content had returned to normal values. Similar changes in the levels of circulating proteins were observed although their magnitude was less than that observed for triglycerides. Ultrastructurally, colchicine treatment resulted in the virtual disappearance of the microtubules from the hepatocytes, and in the appearance of many clusters of vesicles containing very low density lipoprotein-like particles which eventually transformed into lipid droplets. These ultrastructural alterations were also completely reversible, the reversibility coinciding with the morphological reappearance of microtubules. Finally, colchicine treatment resulted in marked metabolic changes that are interpreted as representing an attempt, by the organism, to keep adequate energy sources during the period of lack of circulating triglycerides.

Amino Acids↗
PubMed1986

The effect of albendazole and triclabendazole on colchicine binding in the liver fluke Fasciola hepatica.

Albendazole (ABZ) and its sulfoxide (SX) and sulfone (SO) metabolites inhibit the binding of 3H-colchicine, a ligand with high affinity for tubulin to homogenate preparations of the liver fluke Fasciola hepatica. The relative potency of these compounds is SX greater than ABZ greater than SO. The benzimidazoles (cambendazole, parbendazole, oxibendazole and mebendazole), when tested at a concentration of 10 microM, also inhibited colchicine binding to fluke homogenates. However, a potent new benzimidazole flukacide, triclabendazole (TCB), was without effect on colchicine binding to F. hepatica homogenates. When intact flukes were exposed in vitro to 10(-5)M SX for as little as 5 min the subsequent binding of 3H-colchicine to fluke homogenates was significantly reduced. However, flukes recovered from sheep either 12 or 24 h after treatment with ABZ did not have a decreased ability to bind colchicine, although the non-specific binding was higher in flukes from treated sheep, suggesting some interaction of drug with tubulin in vivo. ABZ, SX and SO were effective in preventing embryonation of fluke eggs at doses as low as 0.01 microM, but TCB was without effect at concentrations as high as 10 microM. The results suggest that ABZ exerts at least part of its anthelmintic effect by interaction with fluke tubulin.

Albendazole↗
PubMedDate not supplied

The effects of long-term colchicine therapy on male fertility in patients with familial Mediterranean fever.

Four out of 19 male patients suffering from familial Mediterranean fever (FMF) had fertility problems while on colchicine therapy (0.5-2.0 mg daily for as long as 11 years). Three of the patients had had children while off therapy but their wives could not conceive while they were on therapy. In one patient primary sterility remained one year after cessation of colchicine. In this and two other patients the spermiogram was normal but the sperm penetration test was pathological. The fourth patient had azoospermia. Patients should be informed about this possible risk of colchicine therapy. The need for continued follow-up and the value of the sperm penetration test in the detection of fertility problems in male patients on long-term colchicine therapy are stressed. It is concluded however, that overall the benefits outweigh the danger of long-term colchicine treatment in male patients with FMF.

Adult↗