Showing papers on "Curcumin published in 1994"
Journal Article•
TL;DR: Results indicate that not only did curcumin inhibit the number of tumors per mouse and the percentage of mice with tumors but it also reduced tumor size.
Abstract: Curcumin (diferuloylmethane), a yellow pigment that is obtained from the rhizomes of Curcuma longa Linn., is a major component of turmeric and is commonly used as a spice and food-coloring agent. The inhibitory effects of feeding commercial grade curcumin (77% curcumin, 17% demethoxycurcumin, and 3% bisdemethoxycurcumin) in AIN 76A diet on carcinogen-induced tumorigenesis in the forestomach, duodenum, and colon of mice were evaluated. Administration p.o. of commercial grade curcumin in the diet inhibited benzo(a)pyrene-induced forestomach tumorigenesis in A/J mice, N-ethyl-N'-nitro-N-nitrosoguanidine-induced duodenal tumorigenesis in C57BL/6 mice, and azoxymethane (AOM)-induced colon tumorigenesis in CF-1 mice. Dietary commercial grade curcumin was given to mice at: (a) 2 weeks before, during, and for 1 week after carcinogen administration (during the initiation period); (b) 1 week after carcinogen treatment until the end of the experiment (during the postinitiation period); or (c) during both the initiation and postinitiation periods. Feeding 0.5-2.0% commercial grade curcumin in the diet decreased the number of benzo(a)pyrene-induced forestomach tumors per mouse by 51-53% when administered during the initiation period and 47-67% when administered during the postinitiation period. Feeding 0.5-2.0% commercial grade curcumin in the diet decreased the number of N-ethyl-N'-nitro-N-nitrosoguanidine-induced duodenal tumors per mouse by 47-77% when administered during the postinitiation period. Administration of 0.5-4.0% commercial grade curcumin in the diet both during the initiation and postinitation periods decreased the number of AOM-induced colon tumors per mouse by 51-62%. Administration of 2% commercial grade curcumin in the diet inhibited the number of AOM-induced colon tumors per mouse by 66% when fed during the initiation period and 25% when fed during the postinitiation period. The ability of commercial grade curcumin to inhibit AOM-induced colon tumorigenesis is comparable to that of pure curcumin (purity greater than 98%). Administration of pure or commercial grade curcumin in the diet to AOM-treated mice resulted in development of colon tumors which were generally smaller in number and size as compared to the control group of AOM-treated mice. These results indicate that not only did curcumin inhibit the number of tumors per mouse and the percentage of mice with tumors but it also reduced tumor size. Histopathological examination of the tumors showed that dietary curcumin inhibited the number of papillomas and squamous cell carcinomas of the forestomach as well as the number of adenomas and adenocarcinomas of the duodenum and colon.
584 citations
TL;DR: Findings indicate that the spectral and photochemical properties of curcumin are strongly influenced by solvent and in biological systems, singlet oxygen, superoxide and products of photodegradation may all participate inCurcumin phototoxicity depending on the environment of the dye.
Abstract: Curcumin, bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione, is a natural yellow-orange dye derived from the rhizome of Curcuma longa, an East Indian plant. In order to understand the photobiology of curcumin better we have studied the spectral and photochemical properties of both curcumin and 4-(4-hydroxy-3-methoxy-phenyl)-3-buten-2-one (hC, half curcumin) in different solvents. In toluene, the absorption spectrum of curcumin contains some structure, which disappears in more polar solvents, e.g. ethanol, acetonitrile. Curcumin fluorescence is a broad band in acetonitrile (lambda max = 524 nm), ethanol (lambda max = 549 nm) or micellar solution (lambda max = 557 nm) but has some structure in toluene (lambda max = 460, 488 nm). The fluorescence quantum yield of curcumin is low in sodium dodecyl sulfate (SDS) solution (phi = 0.011) but higher in acetonitrile (phi = 0.104). Curcumin produced singlet oxygen upon irradiation (lambda > 400 nm) in toluene or acetonitrile (phi = 0.11 for 50 microM curcumin); in acetonitrile curcumin also quenched 1O2 (kq = 7 x 10(6) M-1 s-1). Singlet oxygen production was about 10 times lower in alcohols and was hardly detectable when curcumin was solubilized in a D2O micellar solution of Triton X-100. In SDS micelles containing curcumin no singlet oxygen phosphorescence could be observed. Curcumin photogenerates superoxide in toluene and ethanol, which was detected using the electron paramagnetic resonance/spin-trapping technique with 5,5-dimethyl-pyrroline-N-oxide as a trapping agent. Unidentified carbon-centered radicals were also detected.(ABSTRACT TRUNCATED AT 250 WORDS)
378 citations
TL;DR: Curcumin and eugenol prevented the oxidation of Fe2+ in Fentons reaction which generates.OH radicals and inhibited the generation of hydroxyl radicals.
Abstract: The spice principles curcumin (from turmeric) and eugenol (from cloves) are good inhibitors of lipid peroxidation. Lipid peroxidation is known to be initiated by reactive oxygen species. The effect of curcumin and eugenol on the generation of reactive oxygen species in model systems were investigated. Both curcumin and eugenol inhibited superoxide anion generation in xanthine-xanthine oxidase system to an extent of 40% and 50% at concentrations of 75 microM and 250 microM respectively. Curcumin and eugenol also inhibited the generation of hydroxyl radicals (.OH) to an extent of 76% and 70% as measured by deoxyribose degradation. The .OH-radical formation measured by the hydroxylation of salicylate to 2,3-dihydroxy benzoate was inhibited to an extent of 66% and 46%, respectively, by curcumin and eugenol at 50 microM and 250 microM. These spice principles also prevented the oxidation of Fe2+ in Fentons reaction which generates .OH radicals.
303 citations
TL;DR: Overall, the results indicate that curcumin is a potent and selective inhibitor of phosphorylase kinase, a key regulatory enzyme involved in the metabolism of glycogen, which has important implications for the anti‐proliferative effects ofCurcumin.
226 citations
TL;DR: The ability of curcumin and its derivatives to protect DNA against 1O2 seems to be related to their structures and may at least partly explain the therapeutic and other beneficial effects of these compounds including anticarcinogenic and antimutagenic properties.
Abstract: Curcumin, the natural antioxidant from turmeric, an Indian spice, and its derivatives have significant abilities to protect plasmid pBR322 DNA against single-strand breaks induced by singlet oxygen (1O2), a reactive oxygen species with potential genotoxic/mutagenic properties. 1O2 was generated at 37 degrees C in an aqueous buffer system by the thermal dissociation of the endoperoxide of 3,3'-(1,4-naphthylene)dipropionate (NDPO2). Among the compounds tested, curcumin was the most effective inhibitor of DNA damage followed by desmethoxycurcumin, bisdesmethoxycurcumin and other derivatives. The observed antioxidant activity was both time- and concentration-dependent. The protective ability of curcumin was higher than that of the well-known biological antioxidants lipoate, alpha-tocopherol and beta-carotene. However, the highest protective ability with saturating concentrations of curcumin did not exceed 50%. The ability of curcumin and its derivatives to protect DNA against 1O2 seems to be related to their structures and may at least partly explain the therapeutic and other beneficial effects of these compounds including anticarcinogenic and antimutagenic properties.
199 citations
TL;DR: It is found that curcumin is also phototoxic to mammalian cells, using a rat basophilic leukemia cell model, and that this phototoxicity again requires the presence of oxygen.
Abstract: Curcumin, bis(4-hydroxy-3-methoxyphenyl)-1,6-diene-3,5-dione, is a yellow-orange dye derived from the rhizome of the plant Curcuma longa. Curcumin has demonstrated phototoxicity to several species of bacteria under aerobic conditions (Dahl, T. A., et al., 1989, Arch. Microbiol. 151 183), denoting photodynamic inactivation. We have now found that curcumin is also phototoxic to mammalian cells, using a rat basophilic leukemia cell model, and that this phototoxicity again requires the presence of oxygen. The spectral and photochemical properties of curcumin vary with environment, resulting in the potential for multiple or alternate pathways for the exertion of photodynamic effects. For example, curcumin photogenerates singlet oxygen and reduced forms of molecular oxygen under several conditions relevant to cellular environments. In addition, we detected carbon-centered radicals, which may lead to oxidation products (see accompanying paper). Such products may be important reactants in curcumin's phototoxicity since singlet oxygen and reduced oxygen species alone could not explain the biological results, such as the relatively long lifetime (t1/2 = 27 s) of the toxicant responsible for decreased cell viability.
132 citations
TL;DR: Data suggest that curcumin may inhibit skin cancer through the modulation of expression of these proto-oncogenes in TPA-treated mouse skin in CD-1 mice.
116 citations
TL;DR: In this paper, Assay-guided isolation gave three new compounds, cassumunins A, B, and C, having both antioxidant and anti-inflammatory activities, from the rhizomes of a tropical ginger, Zingiber cassummunar.
Abstract: Assay-guided isolation gave three new compounds, cassumunins A, B, and C, having both antioxidant and antiinflammatory activities, from the rhizomes of a tropical ginger, Zingiber cassumunar. Antioxidant activity and antiinflammatory activity were measured using a thiocyanate method and a 12-O-tetradecanoylphorbol 13-acetate-induced method on mouse ear, respectively. The antioxidant activity of cassumunins A-C is stronger than that of curcumin, and their antiflammatory activity is also stronger than that of curcumin. Spectroscopic analysis of cassumunins A-C revealed them to be a new the of complex curcumin. Antioxidant and antiinflammatory activities of cassumunins suggested that the substituted group at the 5'-position of curcumin increased both activities
96 citations
TL;DR: Induction of XO activity is deemed to be one of the major causative elements in PMA-mediated tumor promotion, and the major inhibitory mechanism of curcumin on PMa-induced increases in XD/XO enzyme activities is through direct inactivation at the protein level.
Abstract: Treatment of NIH3T3 cells with the tumor promoter phorbol-12-myristate-13-acetate (PMA) results within 30 min in a 1.8-fold elevation of xanthine oxidase (XO) activity, an enzyme capable of generating reactive oxygen species such as superoxide and hydrogen peroxide. Simultaneous administration of 2 and 10 microM curcumin with 100 ng/ml PMA inhibits PMA-induced increases in XO activity measured 30 min later by 22.7% and 36.5%, respectively. The PMA-induced conversion of xanthine dehydrogenase (XD) to XO is reduced by curcumin to the basal level noted in untreated cells. Activity of XO is remarkably inhibited by curcumin in vitro, but not by its structurally related compounds caffeic acid, chlorogenic acid and ferulic acid. Based on these findings, induction of XO activity is deemed to be one of the major causative elements in PMA-mediated tumor promotion, and the major inhibitory mechanism of curcumin on PMA-induced increases in XD/XO enzyme activities is through direct inactivation at the protein level.
89 citations
TL;DR: The study demonstrated that chemopreventive agent curcumin strongly activates AMPK in a p38-dependent manner in CaOV3 ovarian cancer cells and observed that curcuming induces p53 phosphorylation and both compound C and SB203580 pretreatment inhibit p53osphorylation.
Abstract: AMP-activated protein kinase (AMPK), an evolutionarily conserved serine/threonine protein kinase, serves as an energy sensor in all eukaryotic cells. Recent findings suggest that AMPK activation strongly suppresses cell proliferation and induces cell apoptosis in a variety of cancer cells. Our study demonstrated that chemopreventive agent curcumin strongly activates AMPK in a p38-dependent manner in CaOV3 ovarian cancer cells. Pretreatment of cells with compound C (AMPK inhibitor) and SB203580 (p38 inhibitor) attenuates curcumin-induced cell death. We also observed that curcumin induces p53 phosphorylation (Ser 15) and both compound C and SB203580 pretreatment inhibit p53 phosphorylation. Collectively, our data suggest that AMPK is a new molecular target of curcumin and AMPK activation partially contributes to the cytotoxic effect of curcumin in ovarian cancer cells.
78 citations
TL;DR: The present study investigates the inhibition of lipid peroxidation by dehydrozingerone and curcumin in rat brain homogenates by inhibiting the formation of conjugated dienes and spontaneous lipid per oxidation.
Abstract: The present study investigates the inhibition of lipid peroxidation by dehydrozingerone and curcumin in rat brain homogenates. Both the test compounds inhibited the formation of conjugated dienes and spontaneous lipid peroxidation. These compounds also inhibited lipid peroxidation induced by ferrous ions, ferric-ascorbate and ferric-ADP-ascorbate. In all these cases, curcumin was more active than dehydrozingerone and dl-alpha-tocopherol.
TL;DR: The antioxidant activity of curcumin, 1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione, a natural antioxidant obtained from rhizome of Curcume longa L., and related compounds was measured against lipid peroxidation in various media as discussed by the authors.
Abstract: The antioxidant activity of curcumin, 1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione, a natural antioxidant obtained from rhizome of Curcume longa L., and related compounds was measured against lipid peroxidation in various media. Curcumin reacted with stable radicals such as galvinoxyl and N,N-diphenyl-1-picrylhydrazyl, indicating it to possibly serve as a potent hydrogen donor, but no curcumin radical could be observed directly by electron spin resonance spectroscopy. Neither could the radical be spin trapped with a-(4-pyridyl-1-oxide)-N-t-butylnitrone. Curcumin suppressed the oxidation of methyl lineolate in organic homogeneous solution and aqueous emulsions, soybean phosphatidylcholine liposomal membranes, and rat liver homogenate induced by free radicals. Curcumin was a stronger antioxidant than 2,6-di-t-butyl-4-methylphenol. Comparable to isoeugenol, but weaker than 3,4-dihydroxycinnamic acid and 2-t-butyl-4-methoxyphenol
TL;DR: Direct determination of curcumin in RBC indicated that the liposomes retained most of theCurcumin, thus allowing its incorporation into RBC at concentrations providing stable protective effects against PQ-induced lysis.
TL;DR: Detergents could increase the Na+−K+ ATPase activity more in the control group than in the retinol deficient groups, and curcumin or turmeric improved the detergent action on the enzyme.
Abstract: The effect of retinol deficiency and curcumin and turmeric feeding on brain microsomal Na(+)-K(+)ATPase activity was investigated. The brain Na(+)-K(+)ATPase activity registered an increase of 148.5% as compared to the control group. Upon treating retinol deficient rats with curcumin or turmeric, the abnormally elevated activity showed a decrease of 36.9 and 47.1%, respectively, when compared to the retinol deficient group. An increase in Vmax by 67% and Km by 66% for ATP was observed in the retinol deficient group. Curcumin or turmeric fed retinol-deficient groups reduced the Vmax by 25 and 33%, while Km was reduced by 25 and 31%, respectively, compared to the retinol deficient group. Arrhenius plot of Na(+)-K(+) ATPase showed a typical bi-phasic pattern in all the groups. Cholesterol:Phospholipid ratio showed a decrease in the retinol-deficient group by 67.8%, which showed a marked increase in curcumin or turmeric treated groups. Detergents could increase the Na(+)-K(+) ATPase activity more in the control group than in the retinol deficient groups. Curcumin or turmeric improved the detergent action on the enzyme. Subsequent freezing and thawing over a period of 30 min decreased the enzyme activity by 22.8% in the retinol deficient group compared to 15.9% decrease in the control group. Curcumin or turmeric treated groups showed a decrease in the enzyme activity by 22.0 and 19.2%, respectively, when compared to the zero time in each group. In the presence of concanavalin-A (Con-A) there was only 52.4% stimulation in the enzyme activity in retinol deficient groups, compared to 108.0% in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The results indicate that the assay of DNA biosynthesis is not of predictive value with respect to the chemopreventive effect of a chemical, while assay of carcinogen—DNA interaction shows correlation between the chemosynthetic property and the inhibition of the interaction of carcinogens with DNA.
Abstract: Our earlier experiments have shown that the plant phenols—hydroxychavicol, eugenol, catechin, curcumin, and the vitamins—β-carotene and α-tocopherol—are potent inhibitors of polycyclic aromatic hydrocarbon (PAH) induced mutagenesis and carcinogenesis. In an attempt to elucidate their mode of action, we studied their effect on mouse skin DNA synthesis following 7,12 dimethylbenzanthracene (DMBA) treatment and 3H-7,12 dimethylbenzanthracene—DNA interaction in vitro (in the presence of mouse skin S9). With the exception of eugenol, all the phenols and vitamins tested inhibited 3H-DMBA-DNA interaction in vitro. In the DNA biosynthesis assay, of the chemopreventive agents tested only β-carotene effectively modulated DMBA suppressed DNA synthesis in the mouse skin. Our results indicate that the assay of DNA biosynthesis is not of predictive value with respect to the chemopreventive effect of a chemical, while assay of carcinogen—DNA interaction shows correlation between the chemopreventive property and the inhibition of the interaction of carcinogen with DNA.
05 May 1994
01 Jan 1994