Were also treated with UV rays at periods of 1 and 2 h and X-rays for 75 KeV at periods of 5. The seeds of the plant were treated with chemical mutagens including ethidiumīromide and colchicine in concentration of (0.05 and 0.10%) and (0.01 and 0.02%), respectively. The aim of this study was to modify the growth, reproductive and yield parameters of Praecitrullusįistulosus by mutagenesis. Hence these mutagens can be used for improving the germination behaviour and the 0.4% colchicine is effectiveįor other agronomical characters. With EMS (especially 0.7%) treatment is much more beneficial as compared to colchicine and SA. So, the effect of chemical mutagenesis on seedling and pollen sterility Sterility (61.1%) was observed under 0.7% colchicine. Pollen sterility also increased with increasing mutagenic doses. To increase germination percentage at seedling stage, but they were not survived till maturity. It was noted that increase in theĭose of EMS and SA, germination percentage and survivability were decreased whereas colchicine doses were proportional Mutagen treated pure-line seeds were sown in experimentalįield following randomized block design (RBD) layout to raise first mutant (M1) generation. Lethality, pollen sterility and other related agro-metrical traits. Three different concentrations like 0.1%, 0.4% and 0.7% were used to analyze their effect on seed germination behaviour, In this study, colchicine (Col), ethyl methane sulphonate (EMS) and sodium azide (SA) with Other chronic inflammatory diseases that invoke these molecular pathways may represent new therapeutic applications for colchicine.Ĭhemical mutagenesis is an efficient tool used in mutation breeding programme for improving various vital characteristics inįloricultural crop, like Dianthus. The multimodal mechanism of action of colchicine suggests potential efficacy of colchicine in other comorbid conditions associated with gout, such as osteoarthritis and cardiovascular disease.Ĭolchicine has multiple mechanisms of action that affect inflammatory processes and result in its utility for treating and preventing acute gout flare. Many of these cellular processes can be found in other diseases involving chronic inflammation. Colchicine prevents microtubule assembly and thereby disrupts inflammasome activation, microtubule-based inflammatory cell chemotaxis, generation of leukotrienes and cytokines, and phagocytosis.
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Colchicine modulates multiple pro- and antiinflammatory pathways associated with gouty arthritis. The molecular pathology of acute inflammation associated with gouty arthritis involves several concurrent pathways triggered by a variety of interactions between monosodium urate crystals and the surface of cells.
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Relevant articles pertaining to the mechanism of action of colchicine and the clinical applications of colchicine in gout and other inflammatory conditions were identified and reviewed. The English-language literature on PubMed was searched for articles published between 1990 and October 2013, with a cross-reference to citations across all years. The aims of this article were to systematically review the literature about the mechanism of action of colchicine in the multimodal pathology of acute inflammation associated with gout and to consider the clinical utility of colchicine in other chronic inflammatory diseases.