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PubMedDate not supplied

Marrow aplasia following colchicine treatment for gouty arthritis.

A 69-year-old man was given 8 mg of colchicine intravenously to treat an acute attack of gout. A maintenance dose of 2 mg/day of oral colchicine was then used to prevent recurrence. Three months later, the patient developed thrombocytopenia, followed by leukopenia and then by anemia at three and four months distance, respectively. The patient had shown no signs of acute toxicity with intravenous colchicine, but liver enzymes were raised after two months of oral treatment. The sequential involvement of the three blood precursor lines, in the order to their physiological half-lives, suggests direct toxicity, rather than idiosyncrasy, due to slow accumulation of the drug within target cells. The prophylactic use of colchicine, especially in the elderly, is questioned.

Aged↗
PubMed1978

[Effect of colchicine on virus-induced interferon synthesis in chick embryo cells].

Colchicine, at a concentration of 5 X 10(-4) M (0.2 microgram/ml), inhibits interferon synthesis induced by theLee strain of influenza B virus in chick embryo cells, but it does not influence the release of preformed interferon from cells. The same drug concentration does not affect the overall synthesis of cellular RNA and protein. The inhibition of interferon synthesis by colchicine is a temperature-dependent process and is not manifested at 0 degrees C. Colchicine is found to be most effective when it is introduced into the medium at early stages of infection. It is suggested that colchicine inhibits the formation of messenger RNA for interferonogenesis.

Animals↗
PubMed1984

[Genetic characteristics of Chinese hamster cell resistance to colchicine, actinomycin D and ethidium bromide].

We have tried to study genetics of Chinese hamster cellular drug resistance to colchicine, actinomycin D and ethidium bromide. Resistant variants arising at a frequency 10(-5) to 10(-7) were selected from a sensitive population. Pretreatment with MNNG increased this frequency 106, 9-15, 12-26 times for colchicine, actinomycin D and ethidium bromide, respectively. Fluctuation test analysis allows to suppose that phenotypic expression of drug resistance is genetically determined and resulted from random genetical events. Significant values of particular correlation coefficients for selecting resistant variants in a set of independently originated subpopulations suggest the genetical identity of the majority of variants selected by colchicine and actinomycin D. At the same time, the significant portion of colchicine-resistant cells may be selected using ethidium bromide. It is not unlikely that under above experimental conditions, each selective agent reveals genetically different resistant variants. The possible genetic mechanisms of resistance to the drugs used are discussed.

Animals↗
PubMed1983

Decreased sensitivity to colchicine-mediated inhibition of metabolite uptake in isolated hepatoma cells.

The effects of colchicine on the incorporation of [3H]-leucine and [3H]thymidine were studied in inbred BUF rats bearing Morris hepatomas and in isolated hepatoma cells and hepatocytes. The results confirmed previous work by other investigators that uptake of amino acids in hepatomas can be inhibited by colchicine (250 micrograms/100 body wt) under conditions in which uptake is not impeded in host liver. Uptake and incorporation of [3H]thymidine in hepatomas were also more sensitive to inhibition by colchicine. Evidence was obtained that these inhibitory effects on incorporation were diminished in isolated cells and were similar for isolated hepatoma cells and hepatocytes. The data did not exclude alternative mechanisms, but they were compatible with a previous suggestion that an effect of colchicine on circulation in hepatomas may be a factor in the inhibitory action on metabolite uptake.

Animals↗
PubMed1978

The effect of colchicine and dibucaine on the morphogenesis of Semliki Forest virus.

The effect of colchicine, Nocodazole, and dibucaine on the assembly of Semliki Forest virus was investigated. Colchicine, Nocodazole, and dibucaine reduced the production of extracellular virus by 75 to 90%. Lumicolchicine had no effect on virus growth. Other control experiments showed no effect by these drugs on the incorporation of [3H]leucine into material precipitated by trichloroacetic acid. Colchicine (100 micron) disrupted the microtubles of the baby hamster kidney cells (BHK-21), whereas dibucaine did not alter microtubule polymerization. The stage of virus assembly inhibited by colchicine and dibucaine was studied by experiments with [3H]-leucine or [35S]methionine. At various times after addition of one of these drugs, the incorporation of the labeled precursors into viral proteins associated with fractions enriched for endoplasmic reticulum or plasma membrane from the cell was evaluated. The results clearly show that the envelope and nucleocapsid proteins of the virus move to the plasma membrane of the cell where they accumulate. The studies strongly suggest that the cytoskeletal system is involved in the final stages of morphogenesis of Semliki Forest virus from the plasma membrane.

Cell Membrane↗
PubMed1983

Concanavalin A-mediated agglutination and distribution of concanavalin A-binding sites in Acanthamoeba following treatment with colchicine and cytochalasin B.

Incubation of Acanthamoeba castellanii (Neff strain) with FITC-ConA (15 micrograms/ml) resulted in the appearance of patches of fluorescence on the amoebae within 2 min of incubation. These patches disappeared following treatment of the amoebae with alpha-MeMan. Pretreatment of the amoebae with colchicine or cytochalasin B or with colchicine and cytochalasin B in combination did not significantly alter the distribution pattern of fluorescence in the amoebae. 2,4-Dinitrophenol and incubation at 4 degrees C on the other hand decreased the degree of patching of the amoebae. Pretreatment with 2,4-dinitrophenol and incubation at 4 degrees C also decreased the ConA-mediated agglutination of the amoebae. No effect on the ConA-mediated agglutination was, however, observed following pretreatment of the amoebae with colchicine and cytochalasin B neither alone nor in combination. Our results indicate that ConA-mediated agglutination and long-range ConA-receptor mobility in the Acanthamoeba are not under the control of structures sensitive to cytochalasin B or colchicine.

Agglutination↗
PubMed1982

Modification of the cytoprotective effect of prostacyclin on gastric epithelial cells of rats by colchicine.

The effect of prostacyclin (PGI2) and colchicine on fundic gastric mucosa of sexually mature female Wistar rats was investigated histochemically after restraint stress. Under PGI2 treatment the ulcer index decreased significantly; this effect was moderately inhibited by colchicine. The mucus content of epithelial cells was decreased during restraint and was increased by PGI2 treatment. This protective action was also inhibited by colchicine. The nuclear volume of fundic epithelial cells increased significantly in restraint and decreased following colchicine application. These phenomena were not influenced by PGI2. According to our results the cytoprotective effect of PGI2 is not accompanied by nuclear volume changes.

Animals↗
PubMed1980

Chemical bursectomy of chickens with colchicine applied to the anal lips.

To induce chemical bursectomy, 30 microliter colchicine dissolved in saline solution (1 mg/ml) was applied on the anal lips of White Leghorn chickens once daily for four consecutive days after hatching. Histologic characteristics of the bursa of Fabricius, spleen, thymus, cecal tonsils, and rectal wall were studied 1-7 days after hatching. Total necrosis of the lymphoid cells and the follicle-associated epithelium in the bursa was observed during the four days of colchicine application. The bursal stroma remained unchanged, and only minor changes were found in the interfollicular surface epithelium. After colchicine application ceased, some regeneration of the epithelium, as evidenced by small epithelial buds, was found. At the end of the observation period the epithelial buds were often covered by the follicle-associated epithelium, which was capable of phagocytizing carbon. However, practically no lymphoid repopulation was seen in the buds. Since this method of colchicine application had no direct effect on other lymphoid organs or on the survival or weight of the chickens, this bursectomy model seems to be a new tool for use in studies of bursal function.

Anal Sacs↗
PubMedDate not supplied

[Effect of colchicine on the in vitro maturation of frog oocytes as affected by a suspension of hypophysis and progesterone].

The influence of colchicine (250 micrograms/ml) on in vitro oocyte maturation in the frog Rana temporaria was studied. The maturation of oocytes was induced by treatment of the follicles with pituitary suspension or progesterone. The gonadotropin-dependent period upon oocyte maturation in all studied females was shortened under the effect of colchicine. The dose of progesterone required for 50% GVBD in the colchicine-treated follicles of 4 out of 11 females was lower than in the intact follicles, in the other cases the dose was the same. Colchicine did not influence the time of 50% GVBD.

Animals↗
PubMed1982

Effects of colchicine, Colcemid and vincristine on ethyl methanesulfonate-induced sister chromatid exchanges and chromosomal aberrations in Chinese hamster cells.

The effect of colchicine, Colcemid and vincristine on ethyl methanesulfonate-induced sister chromatid exchanges and chromosomal aberrations was studied in Chinese hamster cells. The number of ethyl methanesulfonate-induced sister chromatid exchanges was markedly decreased with increasing doses of colchicine and vincristine. In the presence of colchicine, ethyl methanesulfonate-induced chromosomal aberrations increased; these were mainly breaks and fragmentations. The effects were most prominent at the earlier stage of the cell cycle. Colchicine, Colcemid and vincristine had no effect on spontaneous sister chromatid exchanges or chromosomal aberrations.

Animals↗
PubMed1981

Thymidine transport in human lymphocytes stimulated with concanavalin A: effect of colchicine.

Concanavalin A (Con A) was found to induce the appearance of time-dependent and saturable thymidine transport in human peripheral lymphocytes with a Km that ranged from 200 to 500 microM and a Vmax of between 5 to 8 pmols/cell/sec; transport of thymidine could not be demonstrated in resting cultures. Colchicine was found to cause the disappearance of microtubular networks in the majority of cells in the population, whereas lumicolchicine as expected had no significant effect on the presence of microtubules. Lumicolchicine caused 50% inhibition of thymidine transport and of DNA synthesis at a concentration of about 10(-4) M; the effect of this agent on the transport of thymidine could account for its ability to inhibit DNA synthesis. Colchicine also inhibited the transport of thymidine by 50% at about 10(-4) M. However, half-maximal DNA synthesis occurred at a colchicine concentration of 5.0 X 10(-8) M; thus, the effect of this drug on transport cannot account for its effect on DNA synthesis, since the latter process is some 3 orders of magnitude more sensitive than the former. The ability of colchicine to inhibit DNA synthesis in Con A-stimulated human lymphocytes would appear to be an indirect consequence of disassembly of microtubules.

Colchicine↗
PubMed1980

Intracellular processing of procollagen induced by the action of colchicine.

Corium fragments incubated in vitro with colchicine or obtained from chick embryos 11 days old after in vivo injection of this alkaloid were studied with the electron microscope. The well known effect of colchicine in producing an accumulation of procollagen was demonstrated by electrophoretic separation of the collagenous products in polyacrylamide gels after incubation of corium fragments in vitro with labelled amino acids. Electron microscopical studies showed various types of cytoplasmic vacuoles containing collagenous fibrillar structures. Some of these vacuoles contained non-striated filaments, fibres with the periodicity of native collagen, and segment long spacing (SLS) crystallites, embedded in an electrondense substance. The central aspect of this communication is the finding of intracellular SLS in cytoplasmic vacuoles. These crystallites were morphologically intact, and had no additional bands at the NH2 or COOH ends, suggesting that they were formed by the aggregation of tropocollagen molecules. Since the presence of intact SLS in cytoplasmic vacuoles suggests that these are secretory, we believe that inhibition of the transcellular transport system by colchicine permitted the visualization of vacuoles containing the products of tropocollagen interconversions. We interpret these findings as an example of autophagocytosis, with intracellular processing of procollagen, occurring in chick embryo fibroblasts when the secretion of procollagen is inhibited by colchicine.

Animals↗
PubMed1980

The action of antimitotic herbicides on flagellar regeneration in Chlamydomonas reinhardtii: a comparison with the action of colchicine.

The effect of the antimitotic herbicides amiprophosmethyl, trifluralin, and oryzalin upon flagellar regeneration in Chlamydomonas reinhardtii has been studied. After flagellar amputation colchicine completely blocks its regeneration at 2.5 mM whereas the herbicides do so at 5 microM. When applied to regenerating flagella, one hour after amputation, the action of the herbicides is different of that of colchicine. Colchicine stops further regeneration, whereas the herbicides induce a gradual shortening of the partly regenerated flagella. Fully developed flagella also shorten after herbicide application. The induction of shortening is concentration and temperature dependent. A 30 to 50% inhibition of photosynthesis and respiration as well as calcium uptake was caused by the herbicides, whereas colchicine did not affect these metabolic processes.

Calcium Radioisotopes↗
PubMed1994

Misoprostol stimulates leukocyte cyclic adenosine 3',5' monophosphate production and synergizes with colchicine: novel combination of established drugs may boost anti-inflammatory potential.

Elevation of intracellular cyclic adenosine 3',5' monophosphate (cAMP) inhibits various proinflammatory and immune responses of leukocytes. Among agents known to stimulate cAMP production in these cells, prostaglandins E (PGEs) have received particular attention as potential immunosuppressive and/or anti-inflammatory drugs. Their clinical use, however, is limited by poor oral absorption and extreme metabolic instability. Misoprostol, a synthetic analog of PGE1 that can be given orally and that has a significantly longer biological half-life, is now used to prevent or treat nonsteroidal anti-inflammatory drug (NSAID)-induced gastric injury. Because it might also exert anti-inflammatory effects on leukocytes, we have characterized the effects of misoprostol on cAMP production in these cells. We have found that misoprostol does stimulate cAMP production, although with some-what less potency and maximal effect than PGE1; this stimulation is synergistically increased by pretreatment of cells with colchicine; a clinically relevant dose of colchicine is effective given sufficient pretreatment time, and preexposure of cells to colchicine enables a clinically relevant dose of misoprostol to stimulate cAMP generation. We conclude that colchicine and misoprostol represent a drug combination that might prove clinically useful for therapy of inflammatory disease.

1-Methyl-3-isobutylxanthine↗
PubMed1979

Effect of colchicine on guinea pig intrinsic factor-vitamin B12 receptor.

Colchicine can induce the malabsorption of vitamin B12 and other nutrients. Previous investigations have suggested but not proved that this malabsorption was due to a lesion in the ileal mucosa. Employing the receptor assay of M. Katz and B. A. Cooper (J Clin Invest 54:733-739, 1974), the authors have observed a dose-related, reversible reduction in the quantity of intrinsic factor-vitamin B12 (IF-B12) receptor (from 5.78 ng to 1.3 ng of B12 binding) in the intestinal mucosa of guinea pigs fed 0.05-0.25 mg/100 g colchicine/day for 3 days. Malabsorption of vitamin B12 was also demonstrated in vivo in similarly treated animals. Increasing intestinal motility with cascara sagrada had no effect on the IF-B12 receptor. The quantity of IF-B12 receptor and the amount of vitamin B12 absorbed increased markedly to greater than normal levels during recovery from a 3-day course of colchicine. The total number of intestinal cells decreased after colchicine administration and increased during recovery; however, the fluctuations observed were not sufficient to explain the changes in the quantity of receptor. Histologic examination of the ileal mucosa showed a decrease in the population of villus cells after colchicine. The correlation between the changes in receptor quantity and in vivo B12-absorption prove that the IF-B12 receptor is a critical limiting factor in B12 absorption.

Animals↗
PubMed1995

Synthesis of interleukin-1 beta in primary biliary cirrhosis: relationship to treatment with methotrexate or colchicine and disease progression.

Primary biliary cirrhosis (PBC) is a chronic, progressive, cholestatic liver disease. Interleukin-1 beta (IL-1 beta) may play a role in the pathogenesis of PBC by contributing to altered immune function and fibrosis. Colchicine or methotrexate has some beneficial effects in the treatment of PBC, and also affects interleukin-1 (IL-1). Therefore, we prospectively studied the synthesis of IL-1 beta by peripheral blood mononuclear cells (PBMC) from 42 patients with PBC entered into a randomized, double-blind, double-dummy controlled trial of colchicine and methotrexate. PBMC obtained at entry, 6, 12, 18, and 24 months were stimulated to produce IL-1 beta with phytohemagglutinin (PHA), lipopolysaccharide (LPS), Staphylococcus epidermidis, recombinant IL-2, or mitochondrial antigen. Patients in the two treatment groups did not differ at entry in biochemical measures or liver histological stage. Over 24 months in both groups, serum bilirubin and histologic stage remained stable and alkaline phosphatase decreased significantly. For all patients, synthesis of IL-1 beta increased constitutively and in response to immune-mediated stimulants (PHA, IL-2, and mitochondrial antigen) but not the bacterial stimulants LPS or S epidermidis. Compared with levels of IL-1 beta at entry, PHA induced increases for patients treated with methotrexate (12, 18, and 24 months) or colchicine (18 and 24 months). At 24 months, IL-2-induced IL-1 beta synthesis was increased in patients treated with methotrexate, whereas S epidermidis-induced IL-1 beta was enhanced in colchicine-treated patients. Before treatment, IL-1 beta production did not relate to severity of disease except in response to S epidermidis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Serum cholestanol, cholesterol precursors, and plant sterols during placebo-controlled treatment of primary biliary cirrhosis with ursodeoxycholic acid or colchicine.

A randomized placebo-controlled 2-year study was performed in 69 patients with primary biliary cirrhosis (PBC) on serum lipids during ursodeoxycholic acid (URSO) and colchicine treatments. In addition to serum bilirubin and alkaline phosphatase (AFOS), two variables considered to reflect liver function, serum lipoproteins, cholesterol precursors (squalene, delta 8-cholestenol, lathosterol and desmosterol), markers of cholesterol synthesis, cholestanol and plant sterols (campesterol and sitosterol), markers of liver function and cholesterol absorption, were studied before and during the treatments. Serum bilirubin was inconsistently improved by URSO, whereas improvement of AFOS values was better by URSO than colchicine, especially in patients with initially more advanced PBC. Serum total cholesterol was reduced by both drugs, very low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) cholesterol by URSO. Cholesterol precursor sterols were increased by both URSO and colchicine mainly in patients with initially less severe PBC. On the other hand, the cholestanol values were markedly increased initially, and the values were related to bilirubin during the 2-year period, were further increased in the placebo group, and reduced in the URSO and colchicine groups, so that the improvement was highest in the URSO-treated patients with the severe form of PBC. The increase of the serum plant sterols, particularly that of sitosterol, was retarded by the two drugs so that the campesterol/sitosterol ratio, which was related to serum bilirubin, was increased especially in the cases with initially more advanced PBC.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1995

Effect of colchicine on hepatic glycosaminoglycan metabolism in mice infected with Schistosoma japonicum.

AIM: To study the effect of colchicine on hepatic glycosaminoglycan (GAG) metabolism in mice infected with Schistosoma japonicum. METHODS: The amount of GAG was measured in the liver of mice infected with Schistosoma japonicum for 6-16 wk and treated with colchicine. RESULTS: Six weeks after infection, the GAG content of infected mice's livers and uninfected control was 14 +/- 2 micrograms/g liver and 4 +/- 1 microgram/g liver, respectively. The GAG content reached a peak about 6 times of the normal level in the 10th wk after infection, being 56 +/- 9 micrograms/g and 10 +/- 1 microgram/g for infected and uninfected mice respectively, and then declined. Treatment of infected mice with colchicine reduced the total GAG content to 22 +/- 3 micrograms/g liver, but not suppress the GAG content below the normal level in the 10th wk. Microscopic hepatic egg granuloma. CONCLUSION: Colchicine may exerts its GAG reduction effect through the suppression of granuloma formation.

Animals↗