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A Review on Pharmacological Properties of Colchicum luteum – A Himalayan Herb

Rayeesa Ali Shayaib Ahmad Kamil Muneeb U Rehman Masood Saleem Mir Umar Amin
Vol 8(6), 14-23

Nature has blessed us with colossal wealth of herbal plants widely distributed all over the world. They act as parcels of human society to combat diseases. As per WHO reports around 80% of world’s population relies on herbal medicines for their primary health care. Colchicum luteum is a traditional medicinal plant, having some active ingredients used for the treatment of numerous diseases. Various ingredients like colchicine, β-Lumicolchicine, Chlorogenic acid and 3’, 4’, 5, 7-Tetrahydroxyflavone has been obtained from Colchicum luteum during the recent research. Colchicine is the principle active ingredient of Colchicum luteum. The plant has potent anti-inflammatory, anti-oxidant, anti-cancer and many other properties. This review is written to put light on pharmacological properties of Colchicum luteum and its role alleviating diseases of humans and animals.

Keywords : Anticancer Antigout Colchicum luteum Herbal Plants


Plants have shown an immense importance in human affairs. The plants which possess therapeutic properties or exert pharmacological effects on body are designated as “Medicinal plants” and they serve as rich source of Alkaloids, Glycosides, volatile oils, tannins and vitamins. As per WHO, about 80% of human population relies on plant based medicine systems (Martin et al., 2013). One of the important medicinal plants is Colchicum luteum.

Botanical classification of Colchicum luteum

Kingdom——- Plantae

Division——- magnoliophyta

Class——- magnoliosida

Family ——- Liliaceae

Genus —— Colchicum

Species——- luteum

Colchicum luteum is known by many names like Yellow colchicum in English, Suranjan shirin or Suranjan talkh in Urdu, Suranjan in Hindi and Virkim-posh in Kashmiri. The plant is a perennial herb found in Himalayas and is widely distributed in China, India, Pakistan and Afghanistan. It has also been reported in hilly areas of Kashmir valley like Bandipora (Lone et al., 2013), Tragbal, Tangmarg and other areas. Yellow flowers of Colchicum luteum are earliest to blossom in Kashmir during spring season. Practitioners of traditional medicine have used corms and seeds of the plant for treatment of gout, rheumatism and diseases of liver and spleen (Singh and Aswal, 1994; Kapur and Singh, 1996). Corms are ovoid, oblong and flattened at base with longitudinal groove on one side as shown in Fig.1.






Fig.1: Colchicum luteum corms

About 31 different alkaloids have been isolated from Colchicum luteum (Capraro and Brossi, 1984). Phytochemical investigation of  ethanolic  extract obtained from corms of  the Colchicum luteum Baker (Liliaceae) have shown the presence of Lumicolchicine, Chlorogenic acid,  Colchicines,  and  3’, 4’, 5, 7-Tetrahydroxyflavone, on  the  basis  of  different  modern  spectroscopic  techniques (Bashir, 2010). However, colchicines were the main alkaloids reported (Ondra et al., 1995). The isolation of colchicines from Colchicum luteum for the first time was credited to P.S. Pelletier and J. Caventox in the year 1820 (Kokate et al., 2003; Evans, 2006). Approximately 0.25% and 0.45% colchicine has been reported in corms and seeds respectively as given in Table 1 (Chopra et al., 1986).


Table 1: Percentage of Colchicine in different parts of Colchicum luteum

Plant Parts Percentage of colchicines
Seed 0.41- 0.43 %
Colchicum luteum Corms 0.21- 0.25%
Flower 0.1- 0.8 %

Chemically colchicine is described as N-[(7S)-1, 2, 3, 10-tetramethoxy-9-oxo-6, 7-dihydro-5H-benzo[a]heptalen-7-yl] acetamide with molecular formula C22H25NO6 and molecular weight is 399.443 g/mol as given in Fig. 2.






Fig.2: Chemically structure of Colchicine is N-[(7S)-1, 2, 3, 10-tetramethoxy-9-oxo-6, 7-dihydro-5H-benzo[a]heptalen-7-yl] acetamide

Pharmacokinetics of colchicines has revealed that the route of administration should be oral but not intravenous due to certain risks associated with intravenous administration (Terkeltaub, 2008). Adverse events associated with intravenous colchicine administration include thrombocytopenia, neutropenia, pancytopenia, acute renal failure and congestive heart failure. Also dose of colchicines should be low. High doses are associated with diarrhea, vomiting and nausea (Colcrys, 2008). Hepatic metabolism of colchicine is altered by inhibitors of CYP3A4 isoenzymes or P-gp inhibitors such as ketoconazole, verapamil, cyclosporine, resulting in colchicine toxicity.

Therapeutic Properties of Colchicum luteum

Anti-oxidant Action of Colchicum luteum

Promising antioxidant activity offered by the crude ethanolic extract Colchicum luteum and its subsequent fractions have been reported (Bashir, 2010). Also, the free radicals are responsible for oxidative damage, characterized by increased lipid peroxidation. However, the inhibition activity of the crude methanolic extract and its fractions against Lipoxygenase has been reported which might be responsible for its antioxidant activity (Bashir et al., 2006). The antioxidant potential of Colchicum luteum has also been reported by Sevim et al., 2010).

Fig. 3: Therapeutic potential of Colchicum luteum

Anti-Fungal Action of Colchicum luteum

Mycotoxins like aflatoxins, ochratoxins and others cause damage to proximal convoluted tubule (PCT) of kidney or basement membrane of glomeruli, resulting in kidney dysfunction which ultimately leads to hyperuricemia. Also, long term feeding of yeast has resulted in hyperuricemia in rats (Nikolenko et al., 1989). Hyperuricemia has also been induced in humans by cyclosporine (Lin et al., 1989; West et al., 1987; Gores et al., 1988). Anti-fungal activity of colchicines was documented by Shankla and Sharma, 1969. Brian et al., in 1946 reported a metabolite from fungus “Penicilium janczewskii” and named it as “curling factor” on basis of its ability to causes shrinkage and stunting of fungal hyphae. The Curling factor was then subsequently found to be griseofulvin (Brain, 1949). Colchicum luteum shares the antifungal mode of action with griseofulvin. It disrupts the mitotic spindle and causes inhibition of fungal mitosis by binding with microtubule associated proteins, which are responsible for movement of chromatids towards poles.

Anti-Cancer Action of Colchicum luteum

As we know that the cytoskeleton of cell is composed of microtubules and these microtubules are involved in a number of vital processes like cell division, cell migration and polarization. In-vitro assay have shown binding capacity of Colchicum luteum to tubulin, which is main component of microtubule, thereby prevents its polymerization and thus functions as “mitotic poison” (Niel and Scherrmann, 2006). One of the characteristic features of cancer cells is the increased rate of mitosis and thus they are more vulnerable to colchicine toxicity. Colchicine toxicity however also affects non-target cell (normal cells). Keeping this in view, certain carriers like microspheres, immunoglobulin, erythrocytes, serum-proteins and synthetic polymers, have been used for targeting drug at certain specific sites (Molad, 2002). In-vitro studies on controlled drug delivery modes of Colchicum luteum showed very low toxicity (Balasubramanian and Gajendran, 2013).

Anti-Gout Action of Colchicum luteum

Gout is an inflammatory metabolic disease characterized by hyperuricemia and deposition of monosodium urate crystals. There are multiple etiological factors associated with gout like high dietary protein (Li et al., 1998), high dietary calcium (Guo et al., 2005), mycotoxins (Pegram and Wyatt, 1981) and others. Uric acid crystallization depends on sodium and urate concentration and when plasma concentration of monosodium urate exceeds 7mg/dl, crystallization takes place (Fiddis et al., 1983). MSU are recognized by body’s innate immune system (neutrophils and macrophages) and there occurs signal dependent release of cytokines like interleukin-1β via NLRP3 inflammasome activation (Ng et al., 2008; Di Giovine et al., 1987). Also, both classical and alternate pathway of complement system gets activated by monosodium urate crystals and results in inflammation (Fields et al., 1983). Colchicum luteum exert the anti-gout effect in a number of ways like by causing inhibition of NLRP3 inflammasome activation and suppression of regulatory genes of cell (Misawa et al., 2013; Ding et al., 1990).

Moreover, it results in modulation of adhesion protein expression on endothelial cells; inhibition of IL-1 induced L- selectin expression, cytokine maturation and neutrophil chemotaxis to cytokines (Cronstein et al., 1995; Kuijpers et al., 1994). Also, reduction of uric acid levels has been reported after Colchicum luteum administration (Mohammad et al., 2014).

Colchicum luteum as Treatment for Cardiovascular Diseases

Hyperuricemia, which being the major cause of inflammatory metabolic diseases has shown its association with hypertension, coronary diseases and pericarditis (Feig et al., 2008; Gaffo et al., 2009). The possible mechanism of cardiovascular diseases by excess urate is as a result of reduction in Nitric Oxide levels (Cook et al., 2004). Nitric Oxide is a relaxing factor derived from vascular endothelial cells. Increased plasma uric acid levels lead to decrease in plasma concentration of nitrates and nitrates by formation of unstable nitrosated uric acid after reacting with NO. Also there is reduction of VEGF stimulated NO production after direct exposure of vascular endothelial cells to uric acid (Khosla et al., 2005). Moreover, it has been reported that uric acid stimulates MCP-1 production following activation of NF-κB, MAPKs and cyclooxygenase-2 (Kanellis et al., 2003). Uric acid also mediates activation of NADPH-oxidase which causes the production of highly reactive superoxide anions by neutrophils and contributes to vascular damage (Martin-Ventura et al., 2012). Non-steroidal anti-inflammatory drugs, corticosteroids, immunosuppressive agents, and pericardiectomy were accepted modalities for cardiovascular diseases. However, colchicine which is the main alkaloid present in Colchicum luteum also reduces the risk of cardiovascular diseases in many ways. Colchicines cause inhibition of the NADPH-oxidase complex by disruption of microtubule polymerization which results in reduced superoxide production (Chia et al., 2008). Also, results from a study have shown that the administration of colchicines resulted in decrease in C-reactive protein levels in patients with stable coronary artery disease (Nidorf and Thompson, 2007). Further, the colchicine has successfully prevented recurrence of acute pericarditis after failure of conventional treatment with NSAIDS and others.

Anti-Inflammatory and Anti-Arthritic Action of Colchicum luteum

Inflammation is a defense mechanism of body which sets up in response to tissue injury, thereby up regulating the healing processes. Damage to cell membranes cause release of inflammatory mediators like prostaglandins, leukotrienes, lysosomal enzymes etc which produce a variety of effects on blood vessels, nerve endings and on cells involved in inflammation (Katzung, 2009). Inflammation also results in granuloma formation with proliferation of macrophages, neutrophils and fibroblast. Rheumatoid arthritis which is an example of inflammatory autoimmune disease condition of joints is characterized by swelling, pain, stiffness and increased cellularity of synovial tissue (Lipsky et al., 2005). As per WHO reports rheumatoid arthritis affects about 0.3-1% of the world’s population and females being more susceptible compared to males. By-products of cellular metabolism such as nitrous oxide and superoxide radicals may induce the production of interleukins (IL) and tumor necrosis factor (TNF-α) which contribute to inflammation (Fields et al., 2005). Natural product “Colchicine” obtained from plants of the genus Colchicum (Colchicum luteum and other species) has been used to treat gouty arthritis for centuries (Roberts et al., 1987). Administration of colchicines in patients with inflammatory diseases has shown increase in levels of anti-inflammatory substances like TGF-β1 (Darshna et al., 2004; Topal et al., 2006).The anti-inflammatory mechanism of action of colchicines is attributed to diminished number of TNF-α receptor on the surface of macrophages and endothelial cells and prevention of TNF-α–induced activation of macrophages (Ding et al., 1990). Also, the anti-arthritic activity of Colchicum luteum because of its modulatory effect on the pro-inflammatory cytokine expression in the synovial of joints and reduction in serum TNF-α level in a dose dependent manner has been reported (Nair et al., 2011:  Nair et al., 2013).


Colchicum luteum as Treatment for Familial Mediterranean Fever

Colchicum luteum has been found effective in preventing relapses of systemic inflammatory processes in familial Mediterranean fever (recurrent-polyserositis). FMF is an auto-inflammatory disease which is caused by mutation of a gene located on short arm of chromosome 16 known as “MEFV”, which encodes protein Pyrin. Pyrin regulates the inflammatory cascade and is known to cause suppression of caspase-1 activity (Chae et al., 2008; Sahin et al., 2011). However, inadequate Pyrin production as a consequence of gene mutation results in inflammatory bouts. Also, colchicines have shown to provide protection against oxidative stress in patients with remission of familial Mediterranean fever (FMF). The other possible disease protective modes of colchicines are its effects on pyrin and its interacting proteins (Taskiran et al., 2012), reduction of ASC speck rates in transfected cells and down regulation of MEFV gene expression. Pharmacologic action of colchicine has been potentially explained by its capability to induce reorganization of the actin cytoskeleton and alter expression of the MEFV gene.


People throughout the world prefer natural products over synthetic ones because of fewer side effects associated with them. Colchicum luteum is a strong antioxidant with almost insignificant side effects. Colchicum luteum targets the basic cytoskeleton of cell that is microtubule; thereby altering different cellular processes like it prevents release of inflammatory mediators and inhibits chemotaxis of inflammatory cells. It also scavenges free radicals. Colchicum luteum thus can be effectively used against many diseases like arthritis, hepatitis, cancer and heart failure. Keeping the above properties in view there is future requirement for further evaluation of phytochemical properties of this medicinal plant and its clinical efficacy for treating ailments.


  1. Balasubramanian E and Gajendran T. 2013. Comparative studies on the anticancer activity of colchicine by various controlled drug delivery modes. International journal of pharma and bio sciences, 4(1): (p) 9 – 26.
  2. Bashir A. 2010. Antioxidant activity and phenolic compounds from Colchicum luteum Baker (Liliaceae). African Journal of Biotechnology, 9 (35): 5762-5766.
  3. Bashir A, Haroon K, Shumaila B, Nisar, M and Muhammad H. 2006. Inhibition activities of Colchicum luteum baker on lipoxygenase and other enzymes. Journal of Enzyme Inhibition and Medicinal Chemistry, 21(4): 449-452.
  4. Brain, PW. 1949. Studies on the biological activity of griseofulvin , annals of botany 13 (40): 9-77.
  5. Brian PW, Curtis PJ, Hemming HG. 1946: A substance causing abnormal development of fungal hyphae produced by Penicillium janczewskii ZAL. I. Biological assay, production and isolation of “curling factor”. Transactions of the British Mycological Society. 29: 173.
  6. Calixto JB. 2005. Twenty five years of research on medicinal plants in Latin America: a personal review. Journal of Ethno pharmacology, 100(1-2): 131–134.
  7. Capraro HG and Brossi A. 1984. In Brossi A (editor), The Alkaloids, Vol. 23, Acedamics Press, New York, p.1
  8. Chae JJ, Wood G, Richard K, Park G, Smith BJ, Kastner DL , Masters SL . 2008. The familial Mediterranean fever protein, pyrin, is cleaved by caspase-1 and activates NF-kappaB through its N-terminal fragment. Blood , 112 (5): 1794–1803.
  9. Chia EW, Grainger R, Harper JL. 2008. Colchicine suppresses neutrophil superoxide production in a murine model of gouty arthritis: a rationale for use of low-dose colchicine. British Journal of Pharmacology, 153 (6): 1288–1295.
  10. Chopra RN, Nayar SL and Chopra IC. 1986. Glossary of Indian medicinal plant. Council of Scientific and Industrial  Research, New Delhi. 330 pp
  11. Colcrys (package insert). Philadelphia, PA: Mutual Pharmaceutical Company, INC.; 2009. Federal Register 2008; 73(27): 7565-7567.
  12. Cook S, Hugli O, Egli M, Czernichow S, Greenfield JR, Galan P, Bastard JP, Charnaux N, Samaras, K. 2004. Partial gene deletion of endothelial nitric oxide synthase predisposes to exaggerated high-fat diet-induced insulin resistance and arte-rial hypertension. Diabetes, 53(8): 2067–2072.
  13. Cronstein BN, Molad Y, Reibman J, Balakhane E, Levin RI, Weissmann G. Colchicine alters the quantitative and qualitative display of selectins on endothelial cells and neutrophils. Journal of Clinical Investigation, 96 (2): 994–1002.
  14. Darshna R. Yagnik, BJ, Evans, Oliver F, Justin C, Mason R. Clive L and Dorian OH. 2004. Macrophage release of transforminggrowth factor beta1 during resolution of monosodium urate monohydrate crystal-induced inflammation. Arthritis & Rheumatism, 50(7) :2273–2280.
  15. Di Giovine FS, Malawista SE, Nuki G, Duff GW. 1987. Interleukin 1 (IL 1) as a mediator of crystal arthritis. Stimulation of T cell and synovial fibroblast mitogenesis by uratecrystal-induced IL 1. Journal of Immunology, 138: 3213–3218.
  16. Ding AH, Porteu F, Sanchez E, Nathan CF. 1990. Down regulation of tumor necrosis factor receptors on macrophages and endothelial cells by microtubule depolymerizing agents. Journal of Experimental Medicine, 171 (3): 715–727.
  17. Evans, W. C. 15th ed. Elsevier; 2006.Trease and Evans Pharmacognosy; p-369-370.
  18. Feig DI, Kang DH, Johnson RJ. 2008. Uric acid and cardio-vascular risk. New England Journal of Medicine, 359(17):1811–1821.
  19. Fiddis RW, Vlachos N and Calvert PD. 1983. Studies of urate crystallisation inrelation to gout. Annals of Rheumatic Diseases, 42(1):12–15.
  20. Fields HL, Martin JB. Pain: pathophysiology and management. In: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL, eds. 2005. Harrison’s Principles of Internal Medicine. 16th ed. NewYork, NY: McGraw-Hill, pp. 71-73.
  21. Fields TR, Abramson SB, Weissmann G, Kaplan AP. Activation of the alternative pathway of complement by monosodium urate crystals. Clinical Immunology and Immunopathology, 26(2) : 249–257.
  22. Gaffo AL, Edwards NL, Saag KG. 2009. Gout. Hyper-uricemia and cardiovascular disease: how strong is the evidence for a causal link? Arthritis Research and Therapy, 11(4): 240.
  23. Gores PF, Fryd DS, Sutherland DE, Najarian JS, Simmons RL. 1988: Hyperuricemia after renal transplantation. American Journal of Surgery, 156(5): 397-400.
  24. Guo X, Huang K and Tang J. Clinicopathology of gout in growing layers induced by high calcium and high protein diets. Poultry Science, 46(5): 641-676.
  25. Howland RD, Mycek MJ. Lippincott’s Pharamacolgy, 3rd Ed; Lipincott Williams and Wilkins, a wolters Kluwer business, New Delhi pp 495.
  26. Kanellis J, Watanabe S, Li JH, Kang DH, Li P, Nakagawa T, Wamsley A, Sheikh-Hamad D, Lan HY, Feng L, Johnson RJ. Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2. Hypertension. Journal of clinical investigation, 41(6): 1287–1293.
  27. Kapur SK and Singh P. 1996. Traditionally important medicinal plants of Udhampur district (Jammu province) part-I. Journal of Economic Taxonomic Botany, 12: 75–81.
  28. Katzung BG. 2009. Lange’s Basic and clinical Pharmacology, 9th international Ed,Mc Graw Hill, Boston, pp 576.
  29. Khosla UM, Zharikov S, Finch JL, Nakagawa T, Roncal C, Mu W. Hyperuricemia induces  endothel ial   dys function.  Kidney International, 67(5): 1739–1742.
  30. Kokate CK, Purohit AP, Gokhale SB. 2003. Textbook of Pharmacognosy (24th ed.) Pune: Nirali Publication; p. 215
  31. Kuijpers TW, Raleigh M, Kavanagh T, Janssen H, Calafat J, Roos D, Harlan JM. 1994. Cytokine-activated endothelial cells internalize E-selectin into a lysosomal compartment of vesiculotubular shape. A tubulin-driven process. Journal of Immunology, 152(10): 5060–5069.
  32. Li XM, Deng MX, Li QY, Jia RY and Wang J. 1998. Experimental study on the clinical pathology of urate deposition in chickens. Chinese Journal of Veterinary Science, 18(1): 49-51.
  33. Lin HY, Rocher LL, McQuillan MA, Schmaltz S,  Palella TD and Fox, IH. 1989. Cyclosporine-induced hyperuricemia and gout. New  England Journal of Medicine, 321(5): 287-92
  34. Lipsky PE. Rheumatoid arthritis. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, eds. 2005. Harrison’s principles of internal medicine. 16th ed. New York: McGraw-Hill,1968-77.
  35. Lone PA, Bhardwaj AK and Bahar FA. 2013. Traditional knowledge on healing properties of plants in bandipora district of Jammu and Kashmir, India. International Journal of Recent Scientific Research, 4(11): 1755-1765.
  36. Martins E. 2013. The growing use of herbal medicines: issues relating to adverse reactions and challenges in monitoring safety. Front Pharmacol. 4: 177
  37. Martin-Ventura JL, Madrigal-Matute J, Martinez-Pinna R, Ramos-Mozo P, Blanco-Colio LM. 2012. Erythrocytes, leukocytes and platelets as a source of oxidative stress in chronic vascular diseases: detoxifying mechanisms and potential therapeutic options. Journal of Thrombosis and Haemostasis, 108(3):435–44.
  38. Misawa T, Takahama M, Kozaki T. 2013. Microtubule-driven spatial arrangement of mitochondria pro-motes activation of the NLRP3 inflammasome. Nature Immunology, 14 (5): 454–460.
  39. Mohammad IS, Latif S,  Yar M , Nasar  F, Ahmad I and Naeem M. 2014. Comparatve uric acid lowering studies of allopurinols with an indigenous medicinal plant in rabbits, Acta Poloniae Pharmaceutica с Drug Research, 71 (5) : 855-859.
  40. Molad, Y. 2002. Update on colchicine and its mechanism of action. Current Rheumatology Reports, 4(3): 252–256.
  41. Nair V, Singh S,  Gupta 2011. Evaluation of the disease modifying activity of Colchicum luteum Baker in experimental arthritis. Journal of Ethnopharmacology, 133(2):  303–307.
  42. Nair V, Kumar R, Singh S, Gupta YK. 2012. Investigation into the anti-inflammatory and antigranuloma activity of Colchicum luteum Baker in experimental models. Inflammation, 35(3):881-8.
  43. Ng G, Sharma K, Ward SM, Desrosiers MD, Stephens LA, Ling CC, Amrein MW. 2008. Receptor-independent, direct mem-brane binding leads to cell-surfacelipid sorting and Syk kinase activation in dendritic cells. Immunity, 29: 807–818.
  44. Nidorf M, Thompson PL. 2007. Effect of colchicine (0.5 mg twice daily) on high-sensitivity C-reactive protein independent of aspirin and atorvastatin in patients with stab coronary artery disease. American Journal of Cardiology,  99: 80.
  45. Niel, E and Scherrmann JM. 2006 colchicine today. Joint bone spine, 73(6): 672-678.
  46. Nikolenko L, Siniachenko OV and Diadyk Al. 1989 : Anti- deoxyribo nucleic acid antibodies in podagra. Revmatologiia Moskva, 92: 30-35.
  47. Ondra P, Valka I, Vicar J, Sutlupinar N, and Simanek V. 1995. Chromatographic determination of constituents of the genus Colchicum (Liliaceae), Journal of Chromatography A. 704 (6):  351-356.
  48. Pegram RA and Wyatt RD. 1981. Avain gout caused by Oosporein, a mycotoxin produced by Caetomium trilaterale. Poultry science, 60(11): 2429-2440.
  49. Roberts WN, Liang MH, Stern SH. 1987. Colchicine in acute gout. Reassessment of risks and benefits. Journal of the American Medical Association, 257(14):1920–1922.
  50. Sahin M, Cihangir UA, Demirkan H, Nazirolglu M. 2011. Colchicine Modulates Oxidative Stress in Se-rum and Leucocytes from Remission Patients with Family Mediterranean Fever through Regulation of Ca2+ Release and the Antioxidant System. Journal of membrane biology, 240: 55–62.
  51. Sevim D, Senol FS, Budakoglu E, Orhan IE, Sener B, Kaya E. 2010. Studies on Anticholinesterase and Antioxidant Effects of Samples from Colchicum Genus of Turkish Origin. Journal of Pharmaceutical Science, 35: 195-201.
  52. Shankhla HC, Sharma LC. 1969: Utilization of growth regulators by Aspergillus niger van Teighem. Laboratory Development Journal of Science and Technology, 7-B (4): 334-50.
  53. Singh PB and Aswal BS. 1994. Conservation and cultivation of medicinal plants in Himachal Pradesh. Indian Journal of Economic Taxonomic Botany, 18(3): 715–722.
  54. Taskiran EZ, Cetinkaya A, Balci-Peynircioglu B, Akkaya YZ, Yilmaz E. The effect ofcolchicine on pyrin and pyrin interacting proteins. Journal of Cellular Biochemistry, 113 (11): 3536-3546.
  55. Terkeltaub R. 2008. Colchicine update. Seminars in Arthritis and Rheumatism, 38(6): 411-419.
  56. Topal C, Erkoc R, Sayarlioglu H, Dogan E, Beyenik H. The effect of colchicine on the peritoneal membrane. Renal Failure, 28 (1):69–75.
  57. West C, Carpenter BJ, Hakala TR. 1987: The incidence of gout in renal transplant recipients. American Journal of Kidney Diseases, 10(5): 369-72.
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