Curcumin-induced inhibition of cellular reactive oxygen species generation: novel therapeutic implications.

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dc.contributor.authorBalasubramanyam, Men_US
dc.contributor.authorKoteswari, A Adaikalaen_US
dc.contributor.authorKumar, R Sampathen_US
dc.contributor.authorMonickaraj, S Finnyen_US
dc.contributor.authorMaheswari, J Umaen_US
dc.contributor.authorMohan, Ven_US
dc.date.accessioned2003-12-09en_US
dc.date.accessioned2009-06-01T14:56:58Z
dc.date.available2003-12-09en_US
dc.date.available2009-06-01T14:56:58Z
dc.date.issued2003-12-09en_US
dc.description.abstractThere is evidence for increased levels of circulating reactive oxygen species (ROS) in diabetics, as indirectly inferred by the findings of increased lipid peroxidation and decreased antioxidant status. Direct measurements of intracellular generation of ROS using fluorescent dyes also demonstrate an association of oxidative stress with diabetes. Although phenolic compounds attenuate oxidative stress-related tissue damage, there are concerns over toxicity of synthetic phenolic antioxidants and this has considerably stimulated interest in investigating the role of natural phenolics in medicinal applications. Curcumin (the primary active principle in turmeric, Curcuma longa Linn.) has been claimed to represent a potential antioxidant and antiinflammatory agent with phytonutrient and bioprotective properties. However there are lack of molecular studies to demonstrate its cellular action and potential molecular targets. In this study the antioxidant effect of curcumin as a function of changes in cellular ROS generation was tested. Our results clearly demonstrate that curcumin abolished both phorbol-12 myristate-13 acetate (PMA) and thapsigargin-induced ROS generation in cells from control and diabetic subjects. The pattern of these ROS inhibitory effects as a function of dose-dependency suggests that curcumin mechanistically interferes with protein kinase C (PKC) and calcium regulation. Simultaneous measurements of ROS and Ca2+ influx suggest that a rise in cytosolic Ca2+ may be a trigger for increased ROS generation. We suggest that the antioxidant and antiangeogenic actions of curcumin, as a mechanism of inhibition of Ca2+ entry and PKC activity, should be further exploited to develop suitable and novel drugs for the treatment of diabetic retinopathy and other diabetic complications.en_US
dc.description.affiliationDivision of Cell and Molecular Biology, Madras Diabetes Research Foundation, 4 Conran Smith Road, Gopalapuram, Chennai 600 086, India. drbalu@mdrf.orgen_US
dc.identifier.citationBalasubramanyam M, Koteswari AA, Kumar RS, Monickaraj SF, Maheswari JU, Mohan V. Curcumin-induced inhibition of cellular reactive oxygen species generation: novel therapeutic implications. Journal of Biosciences. 2003 Dec; 28(6): 715-21en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/111193
dc.language.isoengen_US
dc.source.urihttps://www.ias.ac.in/jbiosci/index.htmlen_US
dc.subject.meshCalcium --metabolismen_US
dc.subject.meshCase-Control Studiesen_US
dc.subject.meshCurcumin --pharmacologyen_US
dc.subject.meshDiabetes Mellitus --metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshProtein Kinase C --metabolismen_US
dc.subject.meshReactive Oxygen Speciesen_US
dc.subject.meshTetradecanoylphorbol Acetate --pharmacologyen_US
dc.titleCurcumin-induced inhibition of cellular reactive oxygen species generation: novel therapeutic implications.en_US
dc.typeComparative Studyen_US
dc.typeJournal Articleen_US
dc.typeResearch Support, Non-U.S. Gov'ten_US
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