Controlled synthesis and Li-electroactivity of rutile TiO2 nanostructure with walnut-like morphology.

Herein, we report on the synthesis of phase-pure rutile walnut-like TiO(2) (W-TiO(2)) spheres composed of single-crystalline nanorod-building blocks using a surfactant-free non-aqueous acidic modified "benzyl alcohol route". Based on the various HCl concentration- and reaction time-dependent experiments, an effect of hydrochloric acid on the phase formation mechanism in a non-aqueous system is suggested. As anodes for Li-ion batteries, the W-TiO(2) sphere electrodes exhibited superior cycling performance at a rate of 0.2 C without any conducting layers coated onto the anodes; this result is attributed to their high crystallinity and large surface area.

Facile synthesis of nano-Li4 Ti5O12 for high-rate Li-ion battery anodes.

One of the most promising anode materials for Li-ion batteries, Li4Ti5O12, has attracted attention because it is a zero-strain Li insertion host having a stable insertion potential. In this study, we suggest two different synthetic processes to prepare Li4Ti5O12 using anatase TiO2 nanoprecursors. TiO2 powders, which have extraordinarily large surface areas of more than 250 m2 g-1, were initially prepared through the urea-forced hydrolysis/precipitation route below 100°C. For the synthesis of Li4Ti5O12, LiOH and Li2CO3 were added to TiO2 solutions prepared in water and ethanol media, respectively. The powders were subsequently dried and calcined at various temperatures. The phase and morphological transitions from TiO2 to Li4Ti5O12 were characterized using X-ray powder diffraction and transmission electron microscopy. The electrochemical performance of nanosized Li4Ti5O12 was evaluated in detail by cyclic voltammetry and galvanostatic cycling. Furthermore, the high-rate performance and long-term cycle stability of Li4Ti5O12 anodes for use in Li-ion batteries were discussed.

Quercetin inhibits hydrogen peroxide-induced DNA damage and enhances DNA repair in Caco-2 cells.

Flavonoids are known to have antioxidant activity that may limit DNA damage and help prevent degenerative diseases, including cancer. However, our knowledge of flavonoids' role in DNA protection/repair mechanism(s) is limited. This study investigated the effects of quercetin on DNA oxidation and DNA repair in Caco-2 cells with or without oxidant (H2O2) challenge. Quercetin (1, 100 microM) significantly reduced oxidative DNA damage, as measured by the number of single-strand breaks identified by single cell gel electrophoresis. Quercetin treatment also caused a measurable increase in the mRNA expression of human 8-oxoguanine DNA glycosylase (hOGG1) at 0 and 4h after H2O2 treatment (measured using RT-PCR). In addition, the highest level of quercetin tested (100 microM) maintained hOGG1 expression at basal levels or higher for up to 12h after H2O2 treatment, while oxidant treatment alone resulted in significant reduction of hOGG1 at 8h. Our study indicates that quercetin could protect DNA both by reducing oxidative DNA damage and by enhancing DNA repair through modulation of DNA repair enzyme expression.

Flavonoid effects on DNA oxidation at low concentrations relevant to physiological levels.

Flavonoids, which are abundant in fruits and vegetables, are known to have many beneficial health effects. Antioxidant activity is likely to be a main function but has been mostly studied at high flavonoid concentrations which are not feasible at the intracellular level. In this experiment, several flavonoids (e.g., catechin, quercetin, myricetin, luteolin, morin and cyanidin) were examined at low physiologically relevant concentrations. Calf thymus DNA was treated with different flavonoids at concentrations of 0.1, 1, 10 and 100 microM using Fenton conditions to induce oxidation and several oxidative adducts including 8-hydroxy guanine (7,8-dihydro-8-oxo-2'-deoxyguanosine; 8-OH guanine) were analyzed using gas chromatography-mass spectrometry-selective ion monitoring (GC-MS-SIM). Catechin, quercetin and cyanidin inhibited 8-OH guanine formation by 92%, 33% and 45%, respectively, at low concentrations (0.1 microM). In addition catechin and quercetin showed antioxidant activities on 8-OH guanine formation over all concentrations. When the oxidative DNA adduct 4,6-diamino-5-formamidopyrimidine (fapy-adenine) was measured, however, the highest concentrations of catechin and quercetin actually increased adduct formation. These results indicate that flavonoids can act as antioxidants at low concentrations relevant to physiological levels. However measuring only one oxidative DNA adduct as a biomarker may result in misleading conclusions regarding antioxidant activities of natural products.

Anthocyanin Interactions with DNA: Intercalation, Topoisomerase I Inhibition and Oxidative Reactions.

Anthocyanins and their aglycone anthocyanidins are pigmented flavonoids found in significant amounts in many commonly consumed foods. They exhibit a complex chemistry in aqueous solution, which makes it difficult to study their chemistry under physiological conditions. Here we used a gel electrophoresis assay employing supercoiled DNA plasmid to examine the ability of these compounds (1) to intercalate DNA, (2) to inhibit human topoisomerase I through both inhibition of plasmid relaxation activity (catalytic inhibition) and stabilization of the cleavable DNA-topoisomerase complex (poisoning), and (3) to inhibit or enhance oxidative single-strand DNA nicking. We found no evidence of DNA intercalation by anthocyan(id)ins in the physiological pH range for any of the compounds used in this study-cyanidin chloride, cyanidin 3-O-glucoside, cyanidin 3,5-O-diglucoside, malvidin 3-O-glucoside and luteolinidin chloride. The anthocyanins inhibited topoisomerase relaxation activity only at high concentrations (> 50 muM) and we could find no evidence of topoisomerase I cleavable complex stabilization by these compounds. However, we observed that all of the anthocyan(id)ins used in this study were capable of inducing significant oxidative DNA strand cleavage (nicking) in the presence of 1 mM DTT (dithiothreitol), while the free radical scavenger, DMSO, at concentrations typically used in similar studies, completely inhibited DNA nicking. Finally, we propose a mechanism to explain the anthocyan(id)in induced oxidative DNA cleavage observed under our experimental conditions.

The potentiating and protective effects of ascorbate on oxidative stress depend upon the concentration of dietary iron fed C3H mice.

Ascorbic acid (AA) is an antioxidant that, in the presence of iron and hydrogen peroxide, increases the production of hydroxyl radicals in vitro. Whether AA has similar pro-oxidant properties in vivo may depend upon the relative balance of iron and AA concentrations. In this study, C3H mice were fed diets supplemented with 100 or 300 mg/kg iron, with or without AA (15 g/kg), for 12 months. Liver AA concentrations were greater in mice fed AA-supplemented diets with either low or high iron (P=.0001), while the high-iron diet was associated with a significantly lower liver AA concentration regardless of AA supplementation (P=.0001). Only mice fed the high-iron diet with AA had a significantly greater liver iron concentration (P=.05). In the high-iron group, AA reduced oxidative stress, as measured by greater activities of glutathione peroxidase, superoxide dismutase (SOD) and catalase and by significantly lower concentrations of 4-hydroxylalkenal (HAE) and malondialdehyde (MDA). In mice fed the low-iron diet, AA was associated with greater concentrations of HAE and MDA and with lower activities of SOD. However, AA did not increase the concentrations of modified DNA bases with the low-iron diet but was associated with significantly lower concentrations of modified DNA bases in mice fed the high-iron diet. In conclusion, dietary AA appears to have mild pro-oxidant properties at low-iron concentrations but has a strong antioxidant effect against oxidative stress and DNA damage induced by dietary iron in mouse liver.