Showing papers on "Galangin published in 1997"

Antioxidative Activities of Natural Compounds Found in Plants

Abstract: The antioxidative activity of natural plant productslacinilene A, naringin, galangin, and rutinwas examined using lipid peroxidation systems consisting of either ethyl linoleate, ethyl linolenate, or ethyl arachidonate plus Fenton's reagent. Inhibitory activity of plant products toward malonaldehyde (MA) formation from lipids was measured using gas chromatography. Lacinilene A, which showed the strongest antioxidative acitivity among the chemicals tested, inhibited MA formation from ethyl linolenate and ethyl arachidonate by 100% at the levels of 3.0 and 0.5 μmol, respectively. Natural flavonoid compounds naringin, galangin, and rutin exhibited appreciable antioxidative activities at doses lower than 0.125 μmol. Rutin, which exhibited the strongest activity among the three flavonoids, inhibited MA formation from ethyl arachidonate by 70% at the level of 0.125 μmol. These flavonoids exhibited only slight inhibition of MA formation at levels higher than 0.5 μmol from the ethyl esters of the three fatty acid...

Pharmacological effects of selected flavonoids on rat isolated ileum : Structure-activity relationship

Abstract: 1. Eleven selected flavonoids were studied to evaluate their effects on the rat isolated ileum and to determine their structure-activity relationships. 2. The flavonoids rutin and 3',5,7-trihydroxy-4' methoxyflavone-7-rutinoside, which have a sugar moiety (O-rha-glu), had no significant effect on the ileum, indicating that the presence of sugar substitution reduces the biological activity of the flavonoids. 3. Nine other flavonoids caused inhibition of tonic and phasic contractions of the ileum with the following order of potency from highest to lowest: galangin, quercetin, chrysin, xanthomicrol, flavone, naringenin, fisetin, morin, and flavanone. 4. Flavones were more potent than flavanones, indicating that the double bond at carbon 2-3 increases the potency of the flavonoid. 5. Galangin, quercetin, chrysin, and xanthomicrol, which have hydroxyl substituents on carbon 3 and/or 5, showed higher potency than flavone, indicating that such hydroxyl groups are essential for the activity. 6. Galangin was more potent than quercetin, morin, and fisetin, suggesting that the hydroxyl substituents on ring B attenuate the potency. 7. Quercetin caused more potent relaxation of the ileum than morin, suggesting that the presence of a hydroxyl group at C-2' of ring B attenuates the myolytic activity.

Metabolism of galangin by rat cytochromes P450: relevance to the genotoxicity of galangin.

Abstract: The mutagenicity of flavonols seems to depend on the number and position of hydroxyl groups in the B ring. Galangin is a flavonol that does not have any hydroxyl group in the B ring and has been suggested to be a substrate of cytochromes P450 which, through the hydroxylation of the B ring, could metabolise it to more genotoxic products. The present study was undertaken to test this hypothesis. Using high performance liquid chromatography we show that galangin is sequentially transformed to kaempferol and then to quercetin by a mechanism dependent on cytochrome P450 reactions. The metabolites of galangin are responsible for its mutagenicity in Salmonella typhimurium reversion assay and for the induction of chromosomal aberrations in V79 cells.

Specific Antimutagenicity of Flavonoids Against Dietary Carcinogen Trp-P-2

Abstract: Antimutagenic mechanism of flavonoids was investigated in one of the dietary carcinogens, Trp-P-2(3-amino-l-methyl-5H-pyrido[4,3-b]indole). Flavonoids such as galangin and quercetin suppressed the mutagenicity of Trp-P-2 to Salmonella typhimurium TA98 strain in the presence of S9 with a dose-dependent manner. Conversely, they had no effect on the mutagenicity of N-hydroxy-Trp-P-2, the ultimate carcinogenic form of Trp-P-2, or the previously mutated TA98 cell. Thus flavonoids are a desmutagen against Trp-P-2 before or while being activated to the ultimate carcinogen. The desmutagenicity did not associate with hydroxy number or position on the flavonoid skeleton and hence did not contribute to the antioxidative potency of flavonoids. Flavonoids were also unable to absorb Trp-P-2 before being incorporated into the cell. On the other hand, the desmutagenicity of flavonoids closely coincided with their inhibitory effects on cytochrome P-450c monooxygenase to catalyze Trp-P-2 to N-hydroxy-Trp-P-2. The desmutagenic mechanism of flavonoids was due to inhibition of the activation process of Trp-P-2. The inhibitory effect of flavonoids was specific to heterocyclic amines such as Trp-P-2 because flavonoids did not suppress the mutagenicity of other carcinogens such as benzo[a]pyrene, 1-nitropyrene, 2-acetylaminofluorene, and N-methyl-N′-nitro-N-nitrosoguanidine.