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PubMed1977

Enhancement of the PGE1 response of macrophages by concanavalin A and colchicine.

The effect of concanavalin A (Con A) and colchicine on the prostaglandin E1 (PGE1)-mediated cyclic AMP generation in rat peritoneal macrophages have been studied. Although Con A and colchicine by themselves did not affect cyclic AMP levels, they greatly enhanced cyclic AMP production induced by PGE1. There was not only augmentation of cyclic AMP levels at maximally active concentrations of PGE1, but also an increased sensitivity to low (inactive) concentrations of PGE1. Except for lentil lectin, none of the other lectins affected PGE1 sensitivity whereas lumicolchicine was as effective as colchicine. In addition, both Con A and colchicine raised the sensitivity to isoproterenol and choleraenterotoxin. Although details of the mechanisms by which Con A or colchicine influenced the membrane-bound adenyl cyclase and PGE1 receptors remain unclear, these observations suggest that certain alterations of the cell membrane may render macrophages more susceptible to the regulating effects of prostaglandins.

Adenylyl Cyclases↗
PubMed1978

Potentiation of lymphocyte activation by colchicine.

Proliferation of human lymphocytes induced by IO4- is potentiated by 30 min exposure to colchicine (10(-6)M), whereas the response to Con A is inhibited. Treatment with colchicine before or after IO4- modification has similar enhancing effects. Lumicolchicine does not alter proliferative responses. In addition to the proliferation of IO4--oxidized cells, irradiated IO4- modified lymphocytes induce proliferation when mixed with untreated lymphocytes. Enhancement occurs in both these conditions only when IO4--modified cells are treated with colchicine. Preliminary data indicate that proliferation in mixed lymphocyte cultures is also potentiated when either stimulating or responding cells are pretreated with colchicine. These findings suggest a selective stimulatory effect of colchicine on lymphocyte responses induced by cell-cell contact. Agents that modify microtubular assemblies might regulate the induction of immune responses that involve cellular interactions.

Adult↗
PubMed1990

[Ultrastructural studies on effects of colchicine in treating hepatic fibrosis of schistosomiasis rabbits].

8 rabbits were infected percutaneously with the cercariae of Schistosoma japonicum. After hepatic fibrosis had developed in these rabbits 4 months after infection, 4 out of the 8 infected rabbits were given colchicine orally at a dosage of 40 micrograms/kg per day for 7 weeks. Another uninfected rabbits were used as controls. The therapeutic effects of colchicine on hepatic fibrosis were studied by transmission electron microscopy and morphometry, in which the area of collagen microfibrils in the space of disse and liver cells was measured. The results showed that colchicine relieved ultrastructural injury of liver cells and reduced the number of active fibroblasts and collagen microfibrils. The area of collagen microfibrils measured in the liver of the infected rabbits and colchicine-treated rabbits accounted for 42.5% and 0.2%, respectively (P less than 0.01), suggesting that colchicine has therapeutic effect against schistosomal liver fibrosis.

Animals↗
PubMed1987

[Angiogenic effect of colchicine].

The effect of colchicine on the microcirculatory vessels of eye perilimbal area was revealed in 2 groups of experimental rabbits. Colchicine was found to promote the growth of capillaries both during intravenous injections of colchicine solution and during local colchicine application as an ointment. The proper substance of cornea was also changed under the influence of colchicine. Changes in the ultrastructure of the capillary wall and endothelial cells forming the capillaries have been noted.

Animals↗
PubMed1989

Cytoplasmic microtubules in human neutrophil degranulation: reversible inhibition by the colchicine analogue 2-methoxy-5-(2',3',4'-trimethoxyphenyl)-2,4,6-cycloheptatrien-1- one.

The colchicine analogue 2-methoxy-5-(2',3',4'-trimethoxyphenyl)-2,4,6-cycloheptatrien-1-on e (MTC) was found to inhibit concanavalin A- and formyl-methionyl-leucyl-phenylalanine-stimulated human neutrophil degranulation and to depolymerize the microtubule network at low concentrations. The inhibitory capacity of MTC for neutrophil degranulation was similar to that of nocodazole and taxol. The mechanistically distinct actions of these three drugs on microtubules support the notion that microtubules are required for neutrophil enzyme release in response to different stimuli. MTC affected both degranulation and microtubule integrity rapidly and reversibly, after only a 5-min preincubation. At these short periods of incubation, colchicine irreversibly affected neutrophil degranulation only at concentrations in the millimolar range and behaved similarly to its microtubule-inactive analogue lumicolchicine. At longer times of incubation (30-60 min), low concentrations of both MTC and colchicine induced a drastic shortening and depolymerization of microtubules, preserving the microtubule-organizing center, but only MTC was able to completely inhibit the secretory response of neutrophils. These results suggest that the colchicine effect on neutrophil degranulation is not specifically mediated by its action on the microtubule network of these cells. In contrast, the specific and reversible effects of the colchicine analogue MTC suggest that it may be a useful agent with which to study the role of microtubules in this cellular function.

Cell Degranulation↗
PubMed1989

Treatment of alcoholic hepatitis with colchicine. Results of a randomized double blind trial.

A randomized double-blind trial of colchicine vs placebo was conducted in 67 patients with histologically proven alcoholic hepatitis, 33 of whom had cirrhosis. Patients with hepatic encephalopathy, ascites, protracted prothrombin time, severe thrombocytopenia, hepatocellular carcinoma, evident lack of discipline or refusal to participate in the trial were not included. Thirty-three patients received colchicine (1 mg/day) and 34 received placebo for 6 months. Blood parameters including N-terminal peptide of type III procollagen were assessed in the serum, and a percutaneous liver biopsy was performed at the start of the trial and after 3 and 6 months. Alcoholic hepatitis and fibrosis scores were established for each biopsy specimen. Twenty-eight percent of patients were lost to follow-up at 3 months, and fifty-two percent at 6 months. One patient died of liver failure. Fifty-eight percent of patients were abstaining from alcohol at 3 months and fifty percent at 6 months. No significant effect of treatment was noted. Nevertheless, improvement in alcoholic hepatitis core at 3 months was more important in the colchicine group than in the placebo group. No side-effects were noted except transient diarrhea. Our results suggest that colchicine has no important effect on the course of alcoholic hepatitis. A trial including of at least 260 patients might be necessary for the observed alcoholic hepatitis score difference at 3 months, favoring colchicine, to be statistically significant.

Colchicine↗
PubMed1987

Characterization of osteoblast precursor cells isolated from colchicine treated rats.

The previous study showed that an unusual mineralized tissue appeared in the bone marrow of rats 5 days after colchicine injection. The bone marrow stroma cells isolated from the colchicine treated rats were cultured and characterized to elucidate the relationship between the bone marrow stroma cells and the unusual mineralized tissue. The bone marrow cells were obtained 1 to 5 days after the injection of colchicine and the attached cells (marrow stroma cells) were cultured and tested for alkaline phosphatase (ALP) activity as a marker of osteoblastic characteristics. The cultured cells isolated 2 days after the injection (Col. 2 cells) showed a low ALP activity during the initial culture period. However, the activity began to increase and showed a high level from the 14th to the 30th day of culture. The other cell populations did not show an increase of ALP activity during the culture period. The ALP of the Col. 2 cells resembled the bone type enzyme by their biochemical characteristics. The Col. 2 cells became to respond to both the parathyroid hormone and prostaglandin E2 during the late stage of culture period. These findings suggest that the bone marrow stroma cells isolated from the rats 2 days after the colchicine injection become enriched with osteoblast precursor cells. These cells might differentiate into the osteoblasts during the repair process following the severe damage after the colchicine injection and produce an unusual mineralized tissue in the bone marrow cavity.

Acid Phosphatase↗
PubMed1985

Effect of in vitro colchicine and oral theophylline on suppressor cell function of asthmatic patients.

Extrinsic asthmatic patients have been reported to have a deficiency of concanavalin A (Con A)-induced suppressor cell function. We tested whether in vitro colchicine and oral theophylline can correct this immunoregulatory abnormality. Asthmatic patients' mononuclear cells were incubated with Con A and/or colchicine and then suppression of proliferation was measured by coculture of these cells with healthy volunteers' mononuclear cells and phytohaemagglutinin. The Con A induced suppressor cell function of 29 theophylline treated patients (26 +/- 16%, mean +/- s.d.) was significantly (P less than 0.002) increased as compared to 21 untreated patients (12 +/- 10%) but significantly (P less than 0.01) decreased as compared to 45 healthy volunteers (39 +/- 17%). A pharmacological concentration (10(-8) M) of colchicine had no significant effect on Con A-induced suppressor cell function of 19 untreated patients (from 12 +/- 9% to 9 +/- 22%) but significantly (P less than 0.05) increased Con A-induced suppressor cell function of 20 theophylline treated patients (from 26 +/- 17% to 36 +/- 19%). Thus asthmatic patients have decreased Con A-induced suppressor cell function which is partially corrected by oral theophylline and almost completely corrected by oral theophylline plus in vitro colchicine. This synergistic effect raises the possibility that oral colchicine together with theophylline may be useful in treating patients with extrinsic asthma.

Adolescent↗
PubMed1986

Interaction between prostacyclin and colchicine on the gastric mucosa of rat in different experimental ulcer models.

The effect of prostacyclin and colchicine on the fundic gastric mucosa of adult female Wistar rats was investigated in stress (immobilization) and indomethacin induced ulcer models. Under prostacyclin treatment the ulcer index decreased significantly in both ulcer models. This effect was inhibited by colchicine. The nuclear volume of fundic epithelial cells increased significantly after application of either type of ulcerogenic stimulus. Prostacyclin did not influence the nuclear volume changes in stress ulcer, while it prevented this phenomenon in indomethacin-induced ulceration. Following colchicine treatment the nuclear volume decreased in both ulcer models. After combined prostacyclin and colchicine treatment the nuclear shrinkage remained unaltered in stress ulcer, while in indomethacin ulcer the nuclear volume decreasing effect of the separately administered drugs disappeared after combined treatment. The latter phenomenon was interpreted as an antagonistic interaction between prostacyclin and colchicine.

Animals↗
PubMed1987

Colchicine reverts cell shape but not collagen phenotypes in corneal endothelial cells modulated by polymorphonuclear leukocytes.

The authors have shown previously that polymorphonuclear leukocytes (PMN) modulate rabbit corneal endothelial cells (CEC) into cells that irreversibly acquire the characteristics of fibroblasts, including multilayering of spindle-shaped cells and deposition of interstitial extracellular matrix composed predominantly of type I collagen. In an attempt to determine if the changes in cell shape caused by the disruption of cytoskeleton are correlated with the alteration of collagen phenotypes in fibroblastic corneal endothelial cells (FCEC), colchicine and cytochalasin B (CB) were used. A series of dose-response studies were performed, and correlated with exposure time. When cells were exposed to the drugs (ranging from 0.01-4.0 micrograms/ml) 24 hr after plating, the majority of cells treated with colchicine dramatically changed from fibroblastic to polygonal shape: cells became flattened and cytoplasmic processes disappeared. Conversely, no apparent changes were observed in the CB-treated cells. On removal of colchicine, the cells resumed fibroblastic morphology within 24 hr; most of the cells again developed cytoplasmic processes. When collagen phenotypes were analyzed by electrophoresis, types I, III, and V collagen were present in either the colchicine or CB-treated cells, regardless of the concentration of drug used. However, synthesis of type I trimer and type III collagen was significantly increased in the cells treated with colchicine at concentrations greater than or equal to 1.0 microgram/ml; the alpha 1:alpha 2 ratio was approximately 4.5, and type III accounted for 35-40% of the total collagen. CB did not induce a similar alteration. These observations indicate that changes in cell shape are not related to the switch of collagen phenotypes in FCEC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Inverse effects of colchicine on the induction of long microvillous-like processes by cytochalasin B in cultured chick embryonic duodena.

Previously, the author reported that long microvillous-like processes (long processes) containing core actin filaments seemed to be related to the formation of previllous ridges in the chick embryonic duodenum and that similar long processes were induced by cytochalasin B (CB) treatment. The appearance of long processes by CB (polymerization of core actin filaments) seemed to be related to the ability of cell proliferation. In this study, the effect of colchicine on the induction of long processes by CB was examined in 11-day-old chick embryonic duodena in the culture system. The results were as follows: The induction of long processes by CB was inversely influenced by the concentration of colchicine; the appearance of long processes by CB was differently influenced by local parts of the epithelial cells in the presence of colchicine; and alteration of the arrangement of intracellular actin elicited by CB and colchicine was confirmed by immunohistochemistory using actin antiserum. It was also suggested that sudden intracellular alterations elicited by higher concentrations of colchicine may act as a trigger of cell division differing from normal conditions.

Actins↗
PubMed1985

Effect of colchicine on the migration of human lymphocyte subpopulations under agarose.

The effect of colchicine on the random migration of human peripheral blood mononuclear cells under agarose gel was studied. Separated T cell and non-rosetting sheep red blood cell fractions were incubated in the presence of colchicine at concentrations ranging from 10(-8)M to 10(-2)M, and then allowed to migrate for 72 hours. Significant inhibition of migration was not observed at colchicine concentrations less than 10(-3)M. At 10(-3)M, significant impairment of both T cell (p less than 0.01) and non-rosetting cell (p less than 0.001) migration was observed. At 10(-2)M colchicine, migration was completely inhibited. Enhancement of migration of any type of human mononuclear cells by colchicine was not observed at any concentration. The results are consistent with the hypothesis that microtubules are not required for the random migration of these cells.

Cell Movement↗
PubMed1985

The effect of colchicine on translocation of incorporated [3H] proline in Hymenolepis diminuta.

Portions of adult Hymenolepis diminuta were exposed to a fixed concentration of colchicine (5 X 10(-4) M) in order to determine its effect upon incorporation of [3H] L-proline. Additional studies of the effect of colchicine upon tegumental morphology were performed. Autoradiographs showed a significant decrease in amount of incorporated label in the distal tegument of colchicine tissue and a heavy accumulation of label in the parenchyma. Radioassays indicated that the effect of colchicine on proline-incorporated protein was qualitative rather than quantitative suggesting that colchicine inhibits translocation in the tegument. It was hypothesized that microtubules within the internuncial processes facilitate movement of cell products from tegumentary cytons to the body surface.

Animals↗
PubMed1979

[Electron microscopic study of the effect of colchicine on limb bud cartilage in organ culture (mouse embryos)].

Limb buds of 11-day-old mouse embryos were cultured. On day 5, 0.1 mM colchicine was added for 3, 6, 12 or 24 h in vitro. 3 or 6 h after application of colchicine, electron-dense granula appear to an increasing extent. These granula can be interpreted as collagen-containing secretion granula and as an indication of a secretion inhibition. The peripheral localization of the granula groups speaks for an effect on the actual discharge of the secretion after having passed the Golgi apparatus. Additional effects of colchicine are fragmentation of the Golgi apparatus and an increased occurrence of bundles of fine filaments. Since only few microtubuli occur in the periphery of the chondroblasts and recent studies indicate an influence of colchicine not only on the microtubule system, a site of action at the functional unity 'cell membrane-microfilaments' is discussed. 12 or 24 h after colchicine application, the contents of the congested secretion granula change. The occurrence of cross-striated structures indicates an activity of procollagen peptidase in the granula in the case of secretion inhibition. In addition, cytolysosomes (autophagic vacuoles) develop. The occurrence of polymorphism of the granula contents under these conditions is attributed to an effect of lysosomal enzymes.

Animals↗
PubMed1972

Induction of the generalized Shwartzman reaction in pregnant and nonpregnant rats by colchicine.

The intravenous injection of colchicine (2 mg/kg body weight) into pregnant rats on the last 4 to 5 days of gestation induced disseminated intravascular coagulation, occluding glomerular capillaries with fibrin thrombi, typical of the generalized Shwartzman reaction. Thrombi did not form earlier than 9 hours after the injection of colchicine, whereas in the endotoxin-induced generalized Shwartzman reaction, thrombi were already observed 2(1/2) hours after the injection of endotoxin. The colchicine-induced generalized Shwartzman reaction could also be produced in hysterectomized "pregnant" rats. A single injection of colchicine into nonpregnant rats did not induce disseminated intravascular coagulation. If, however, fibrinolysis was inhibited with epsilon-aminocaproic acid, the colchicine-induced generalized Shwartzman reaction could also be elicited in nonpregnant rats. In this regard fibrinolysis inhibition represents one mechanism by which pregnancy prepares for the generalized Shwartzman reaction.

Aminocaproates↗
PubMed1979

Microtubules and protein secretion in rat lacrimal glands. Inhibitory effect of the tubulin . colchicine complex isolated from lacrimal glands upon brain tubulin polymerization. Identification of the complex by gel electrophoresis.

The specific inhibitory effect of colchicine upon protein secretion by lacrimal glands could be related to the formation of a complex between colchicine and tubulin from the soluble fraction of the gland. By gel electrophoresis under nondissociating conditions, it is shown that this complex is similar to the colchicine . tubulin complex from brain. The complex isolated from lacrimal glands is highly inhibitory upon brain tubulin assembly since as low as 0.07 microM complex impedes the polymerization of 8 microM tubulin by 50%, compared to 3 microM for free colchicine. Therefore, a small percentage of complexed tubulin (0.9%) is enough for polymerization to be blocked. In lacrimal glands the complex might prevent the polymerization of tubulin, and colchicine shift the tubulin in equilibrium microtubules equilibrium to microtubules disassembly. The disorganization of the labile microtubular system could lead to a modification of the transport of the secretory granules and to a perturbation of secretion.

Animals↗
PubMed1979

A morphometric analysis of microtubules in relation to the inhibition of lysosome movement caused by colchicine.

Colchicine was administered intraperitoneally to rats in doses which are known to inhibit the basal migration of lysosomes in uterine epithelial cells. The fractional volume of microtubules in the cells was then measured by morphometry. Colchicine at 0.10 mg/kg reduced the microtubule content of the cells from 0.22% down to 0.15%, and 1.0 mg/kg reduced microtubule content to 0.03%. Microtubules were essentially absent from the cells after colchicine doses of 3.0 and 10.0 mg/kg. The microtubule content of uterine epithelial cells thus decreased in the colchicine dose range from about 0.10 to 1.0 mg/kg, the same dose range in which an inhibition of lysosome migration has been observed. These results support the suggestion that microtubules are necessary for the basal migration of lysosomes in uterine epithelial cells. In addition, colchicine at 1.0 mg/kg caused a redistribution of the Golgi complex and a class of electron-transparent, 130 to 450 nm vesicles. These organelles were restricted to the apical halves of the cells in untreated rats, but they were dispersed throughout the cells after drug treatment. The change in the position of the organelles may be caused by a loss of cytoskeletal function of the microtubules.

Animals↗
PubMed1977

Cytologic features of Harding-Passey melanoma following different regimes of colchicine treatment.

Ultrastructural observations were undertaken on Harding-Passey melanomas in control tumors and in tumors treated with different regimens of colchicine. The treated tumor was made up of pleomorphic cells containing tubulovesicular mitochondria, ribosomes, and rough endoplasmic reticulum. Tumor-bearing mice in Experiment A received a single regimen of colchicine, 0.5 mg/kg/day of 7 days. The treated tumor was subsequently passed through five transplantations in mice. Tumor-bearing mice in Experiment B received colchicine treatment of 0.5 mg/kg/day for 7 days followed by passage through five transplantations. In addition, the mice carrying the tumor received the same colchicine treatment during the second and fourth transplantations. Colchicine treatment resulted in tumor cells of Experiments A and B developing microfilaments, margination of melanin granules, and junctional complexes, considered to be evidence of altered morphologic differentiation in melanocytes. The effects persisted for 10 weeks throughout the five transplantations. The features were more striking in Experiment B animals receiving intermittent therapy.

Animals↗