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Showing papers on "Curcumin published in 1988"


Journal Article
TL;DR: The effects of topically applied curcumin, chlorogenic acid, caffeic acid, or ferulic acid on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal ornithine decarboxylase activity, epidersmal DNA synthesis, and the promotion of skin tumors were evaluated in female CD-1 mice.
Abstract: The effects of topically applied curcumin, chlorogenic acid, caffeic acid, and ferulic acid on 12- O -tetradecanoylphorbol-13-acetate (TPA)-induced epidermal ornithine decarboxylase activity, epidermal DNA synthesis, and the promotion of skin tumors were evaluated in female CD-1 mice. Topical application of 0.5, 1, 3, or 10 µmol of curcumin inhibited by 31, 46, 84, or 98%, respectively, the induction of epidermal ornithine decarboxylase activity by 5 nmol of TPA. In an additional study, the topical application of 10 µmol of curcumin, chlorogenic acid, caffeic acid, or ferulic acid inhibited by 91, 25, 42, or 46%, respectively, the induction of ornithine decarboxylase activity by 5 nmol of TPA. The topical application of 10 µmol of curcumin together with 2 or 5 nmol of TPA inhibited the TPA-dependent stimulation of the incorporation of [ 3 H]-thymidine into epidermal DNA by 49 or 29%, respectively, whereas lower doses of curcumin had little or no effect. Chlorogenic acid, caffeic acid, and ferulic acid were less effective than curcumin as inhibitors of the TPA-dependent stimulation of DNA synthesis. Topical application of 1, 3, or 10 µmol of curcumin together with 5 nmol of TPA twice weekly for 20 weeks to mice previously initiated with 7,12-dimethylbenz[ a ]anthracene inhibited the number of TPA-induced tumors per mouse by 39, 77, or 98%, respectively. Similar treatment of mice with 10 µmol of chlorogenic acid, caffeic acid, or ferulic acid together with 5 nmol of TPA inhibited the number of TPA-induced tumors per mouse by 60, 28, or 35%, respectively, and higher doses of the phenolic acids caused a more pronounced inhibition of tumor promotion. The possibility that curcumin could inhibit the action of arachidonic acid was evaluated by studying the effect of curcumin on arachidonic acid-induced edema of mouse ears. The topical application of 3 or 10 µmol of curcumin 30 min before the application of 1 µmol of arachidonic acid inhibited arachidonic acid-induced edema by 33 or 80%, respectively.

779 citations


Journal Article
TL;DR: A soluble curcumin derivetive wes found to be not cyotoxic in vitro end in tissue culture and inhibited ascite tumour formation in mice induced with Dalton's lymphoma ascites tumour cells.
Abstract: 1. curcumin which is the active ingredient in turmeric was found to be cytotoxic to various cell lines in vitro at concentrations 8(g/ml or more. Complete disintegration of cells could be seen upon incubation with higher concentration (50(/ml) of curcumin. 2. Due to the insolubility of curcumin. liposomally encapsulated curcumin wee prepared which showed the same acvitiy es curcumin in tissue culture. 3. Roth curcumin end liposmally encepeulsted curcumin inhibited the tritisted thymidine incorporation into DNA. Liposomally encapsulated curcumin also inhibited ascites tumour formation in mice induced with Dalton's lymphoma ascites tumour cells. 4. Sodium curcumate. a soluble curcumin derivetive wes found to be not cyotoxic in vitro end in tissue culture. Sodium curcumate inhibited thvmidine incorporation into PNA only at higher concentration.

37 citations


Journal ArticleDOI
TL;DR: The effects of turmeric extract and its pure yellow pigments curcumin I, II and III were tested on the nitrosation of methylurea by sodium nitrite at pH 3.6 and 30 degrees C andCurcumin III was the most effective nitrosations inhibitor among the compounds tested.
Abstract: The effects of turmeric extract and its pure yellow pigments curcumin I, II and III were tested on the nitrosation of methylurea by sodium nitrite at pH 3.6 and 30 degrees C. The nitrosomethylurea formed was monitored by checking the mutagenicity in S. typhimurium strains TA1535 and TA100 without metabolic activation. Turmeric extract as well as curcumins exhibit dose-dependent decreases of nitrosation. Curcumin III was the most effective nitrosation inhibitor among the compounds tested. The simultaneous treatment of inhibitor with nitrosation precursors was essential and pre- or post-treatment of inhibitor had no effect on the mutagenicity of nitrosomethylurea. The binding of nitrite with the inhibitors was studied at pH 3.6 and 30 degrees C. Curcumin I shows a dose-dependent depletion of nitrite ions thus making nitrite non-available for nitrosation. Curcumin I and III when tested also showed a time-dependent depletion of nitrite ions at pH 3.6 and 30 degrees C. Curcumin III has a higher affinity for nitrite ions than curcumin I.

21 citations



Journal ArticleDOI
TL;DR: Addition of curcumin to serum samples in clinical laboratories may improve the results of nifedipine determination, with a 6-fold increase in half-life by addition ofCurcumin.

6 citations