ascorbic-acid and morin

Small molecules with antioxidative properties have been implicated in amyloid disorders. Curcumin is the active ingredient present in turmeric and known for several biological and medicinal effects. Adequate evidence substantiates the importance of curcumin in Alzheimer's disease and recent evidence suggests its role in Prion and Parkinson's disease. However, contradictory effects have been suggested for Huntington's disease. This difference provided a compelling reason to investigate the effect of curcumin on glutamine-rich (Q-rich) and non-glutamine-rich (non Q-rich) amyloid aggregates in the well established yeast model system. Curcumin significantly inhibited the formation of htt72Q-GFP (a Q-rich) and Het-s-GFP (a non Q-rich) aggregates in yeast. We show that curcumin prevents htt72Q-GFP aggregation by down regulating Vps36, a component of the ESCRT-II (Endosomal sorting complex required for transport). Moreover, curcumin disrupted the htt72Q-GFP aggregates that were pre-formed in yeast and cured the yeast prion, [PSI(+)].

Topics: Adenosine Triphosphatases; alpha-Tocopherol; Ascorbic Acid; Curcumin; Endosomal Sorting Complexes Required for Transport; Flavonoids; Gene Deletion; Green Fluorescent Proteins; Humans; Peptides; Protein Stability; Protein Structure, Quaternary; Saccharomyces cerevisiae; Saccharomyces cerevisiae Proteins

Protection of ascorbic acid (AA) (vitamin C) from Cu(II)-catalyzed autoxidation is an important aspect of antioxidant chemistry. The autoxidation of AA in the absence and presence of Cu(II) ions was investigated in aerated solution at room temperature and I = 0.1 ionic strength (KNO(3)); the effects of three different flavonoids of similar structure (quercetin, morin and catechin) and their mixtures on the AA system were studied. The concentration of unoxidized AA remaining in solution was measured with the modified cupric ion reducing antioxidant capacity spectrophotometric method. The Cu(II)-catalyzed oxidation at pH 4.5 followed first-order kinetics with respect to AA concentration. Catalytic autoxidation of AA was inhibited to a greater extent by stable quercetin and morin complexes of Cu(II) than by catechin complex. The inhibitive effectiveness order of mixtures gives information about possible synergistic or antagonistic combinations of flavonoid antioxidants, which should be further confirmed with other antioxidant tests.

Topics: Ascorbic Acid; Catalysis; Catechin; Copper; Flavonoids; Molecular Structure; Oxidation-Reduction; Quercetin

Antioxidants are compounds that can delay or inhibit lipid oxidation. The peroxidation of linoleic acid (LA) in the absence and presence of Cu(II) ion-ascorbate combinations was investigated in aerated and incubated emulsions at 37°C and pH 7. LA peroxidation induced by copper(II)-ascorbic acid system followed first order kinetics with respect to hydroperoxides concentration. The extent of copper-initiated peroxide production in a LA system assayed by ferric thiocyanate method was used to determine possible antioxidant and prooxidant activities of the added flavonoids. The effects of three different flavonoids of similar structure, i.e. quercetin (QR), morin (MR) and catechin (CT), as potential antioxidant protectors were studied in the selected peroxidation system. The inhibitive order of flavonoids in the protection of LA peroxidation was: morin>catechin≥quercetin, i.e. agreeing with that of formal reduction potentials versus NHE at pH 7, i.e. 0.60, 0.57 and 0.33V for MR, CT, and QR, respectively. Morin showed antioxidant effect at all concentrations whereas catechin and quercetin showed both antioxidant and prooxidant effects depending on their concentrations. The structural requirements for antioxidant activity in flavonoids interestingly coincide with those for Cu(II)-induced prooxidant activity, because as the reducing power of a flavonoid increases, Cu(II)-Cu(I) reduction is facilitated that may end up with the production of reactive species. The findings of this study were evaluated in the light of structure-activity relationships of flavonoids, and the results are believed to be useful to better understand the actual conditions where flavonoids may act as prooxidants in the preservation of heterogeneous food samples containing traces of transition metal ions.

Topics: Antioxidants; Ascorbic Acid; Catechin; Copper; Flavonoids; Linoleic Acid; Lipid Peroxidation; Oxidation-Reduction; Protective Agents; Quercetin; Structure-Activity Relationship

Morin is a yellowish pigment extractable from the wood of Chlorophora tinctoria. In the present study, we have determined that morin protects three types of human cells--ventricular myocytes, saphenous vein endothelial cells, and erythrocytes--against damage by oxyradicals generated in situ. In myocytes and endothelial cells, morin prolonged substantially and in a concentration-dependent manner the survival of cells exposed to either xanthine oxidase-generated oxyradicals or superoxide radicals produced with menadione. Morin protected erythrocytes from lytic attack by peroxyl radicals generated with 2,2'-azo-bis (2-amidinopropane) dihydrochloride. In all three types of human cells, the protective effect of morin clearly excelled that displayed by Trolox (a vitamin E analog), ascorbate, or mannitol, which are water-soluble antioxidants of similar molecular size. Chemically, we verified that morin behaves as an antioxidant by diminishing markedly the amount of malondialdehyde (lipid peroxidation product) found in human cardiocytes despite their exposure to oxyradicals. In agreement with related reports, we also observed that morin is non-toxic in rats even when used at concentrations 2-3 orders of magnitude higher than those in our in vitro studies. Thus, morin acts as a broad-spectrum and non-toxic antioxidant.

Topics: Ascorbic Acid; Cells, Cultured; Chromans; Endothelium, Vascular; Erythrocytes; Flavonoids; Free Radical Scavengers; Heart Ventricles; Humans; Malondialdehyde; Mannitol; Reactive Oxygen Species; Vitamin K; Wood