Chin J Physiol. 2003 Mar 31;46(1):15-8.
Differential effects of colchicine on central dopaminergic neuronal activity and prolactin secretion in estrogen-primed ovariectomized rats.

Yang SC, Pan JT.

Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.

Colchicine is a potent chemical that disrupts the assembly of microtubulin and affects the integrity of cytoskeleton. It is commonly used to block the axonal transport in neurons. Central administration of colchicine (48 microg/3 microl/rat) two days earlier significantly lowered 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the striatum and nucleus accumbens, both in the morning and in the afternoon. Median eminence DOPAC levels exhibit a diurnal change between morning and afternoon as previously shown. Colchicine treatment lowered and elevated median eminence DOPAC levels in the morning and afternoon, respectively. The estrogen-induced prolactin surge was also blocked. The findings indicate that neuronal inputs are necessary for maintaining basal activities in all dopaminergic neurons, while an inhibitory one predominates in the afternoon for TIDA neurons.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12817700&dopt=Abstract colchicine



J Nephrol. 2003 May-Jun;16(3):421-5.
Multiple organ failure in a kidney transplant patient receiving both colchicine and cyclosporine.

Minetti EE, Minetti L.

Nephrology, Dialysis and Medical Therapy of Renal Transplant Section, Niguarda Ca Granda Hospital, Milan, Italy. e.minettatamail.com

Colchicine is a relatively safe and effective medication when given at appropriate doses to patients with normal kidney and liver function. A clinical picture of multiple organ failure has been described in cases of colchicine poisoning and in kidney graft recipients treated with usual doses of colchicine during cyclosporine therapy. We report a case of multiple organ failure in a renal transplant patient who received appropriate doses of colchicine in combination with cyclosporine therapy. Interaction between colchicine and cyclosporine is postulated but boosting of CSA toxicity was excluded because of the low CSA blood through levels before and throughout the episode, in the presence of relatively stable renal function and for the prompt CSA withdrawal. Mechanism of toxicity and modulation of the P-glycoprotein by cyclosporine are reviewed. Although the proscription of the drug in cyclosporine-treated patients is not justified, caution is recommended in prescribing colchicine to patients receiving cyclosporine therapy, particularly in the presence of suboptimal kidney graft function.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12832745&dopt=Abstract colchicine



Farm Hosp. 2003 May-Jun;27(3):188-90.
[Suicidal attempt with colchicine]

[Article in Spanish]

Larrubia Marfil Y, Villamanan Bueno E, Jimenez-Caballero E, Diazaraque Marin R, Lucendo Villarin A, Fernandez-Capitan C, Arnalich Fernandez F.

Servicio de Farmacia. Hospital Universitario La Paz, Madrid. Spain.

Colchicine is an alkaloid that has been successfully used for a long time in the treatment of acute gout episodes. It's efficacy lies in its inhibition of inflammation cell migration and in the action of specific cytokines, as well as of the production of lactic acid and deposition of uric acid in affected tissues. Colchicine toxicity is rare but may entail highly negative consequences for health unless a rapid gastric decontamination with stomach lavage and active carbon is carried out, and adequate support measures are taken as wellas appropriate hydration and electrolyte replacement. We present the case of a patient who was admitted to hospital after ingesting colchicine with suicidal intention. Colchicine inhibits cell division, which explains its distinct toxicity stages. The lack of proportion existing between ingested dose and clinical impact may result from concomitant treatment with other drugs or from peculiarities in its metabolism.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12835821&dopt=Abstract colchicine [PubMed - in process]



Chembiochem. 2003 Jul 7;4(7):633-9.
Improvement of hepatocyte-specific gene expression by a targeted colchicine prodrug.

Van Rossenberg SM, Sliedregt-Bol KM, Koning G, Van Den Elst H, Van Berkel TJ, Van Boom JH, Van Der Marel GA, Biessen EA.

Division of Biopharmaceutics Leiden/Amsterdam Center for Drug Research Gorlaeus Laboratories, Leiden University P.O. Box 9502, 2300 RA Leiden, The Netherlands, Fax: (+31) 71-527-6032.

Colchicine, an established tubulin inhibitor, interferes with the trafficking of endocytotic vesicles and thereby promotes the escape of lysosome-entrapped compounds. To improve its potency and cell specificity, a targeted prodrug of colchicine was synthesized by conjugation to a high-affinity ligand (di-N(alpha),N( varepsilon )-(5-(2-acetamido-2-deoxy-beta-D-galactopyranosyloxy)pentanomido)lysine, K(GalNAc)(2)) for the asialoglycoprotein receptor on parenchymal liver cells. The resulting colchicine-K(GalNAc)(2) conjugate bound to this receptor with an affinity of 4.5 nM. Confocal microscopy studies confirmed rapid uptake and receptor dependency of a prodrug conjugated with fluorescein isothiocyanate. Colchicine-K(GalNAc)(2) substantially increased the transfection efficiency of polyplexed DNA in parenchymal liver cells in a concentration- and receptor-dependent fashion. Colchicine-K(GalNAc)(2) was found to enhance the transfection efficiency by 50-fold at 1 nM, whereas the parental colchicine was ineffective. In conclusion, this nontoxic colchicine-K(GalNAc)(2) conjugate can be a useful tool to improve the transfection efficiency of hepatic nonviral gene transfer vehicles.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12851933&dopt=Abstract colchicine [PubMed - in process]