204 research outputs found
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No full textAscorbate and flavonoids as protectors against mutant Cu/Zn superoxide dismutase-induced oxidative damage in a mouse model of amyotrophic lateral sclerosis
No full textThe experiments in this thesis tested in vitro and in vivo the proposal that zinc-deficient superoxide dismutase, resulting from mutations or oxidative damage to the enzyme, gains ascorbate oxidase activity that contributes to the pathology of amyotrophic lateral sclerosis (ALS). They also tested whether flavonoids can help protect against this activity.The in vitro experiments showed that zinc-extracted Cu/Zn-SOD (Cu-SOD) as well as SOD treated with H2O2 or H2O2 plus ascorbate accelerated ascorbate oxidation 100 to 300 %, while native SOD had no effect. With Cu-SOD, the activity was unaffected by EDTA, EGTA, or catalase, showing that the catalytic copper was firmly bound and that the H2O2 product of SOD activity was not responsible. Catechin and uric acid slowed ascorbate oxidation by Cu-SOD by 72% and 67%, respectively.The in vivo study investigated tissue levels of ascorbate and biomarkers of oxidative stress in a transgenic mice bearing a mutation in Cu/Zn-SOD as a model of familial ALS (FALS mice), and the effects of dietary ascorbate and quercetin. In FALS mice on control modified AIN93G diet for 10 weeks compared to the wild-type, liver thiobarbituric acid reactive substances (TBARS) were 47% higher and liver oxidized vitamin C was 2800% higher. These results support, in liver, that mutant SOD acquired ascorbate oxidase activity and increased oxidative stress. The only difference in other tissues was a 136% increase in GSH/GSSG ratio in thigh muscle of FALS mice.In dietary treatments of FALS mice, spinal cord TBARS was 93 % higher with ascorbate-supplemented diet compared to control diet, suggesting that dietary ascorbate increased oxidative stress. Also in spinal cord, oxidized-vitamin C was 250% higher in ascorbate + quercetin-fed FALS mice, which suggests there is no protection by quercetin against ascorbate oxidation. In brain, protein thiols were 56% and 58% lower in quercetin-fed and ascorbate + quercetin-fed FALS mice, suggesting that quercetin worsened oxidative damage. In liver, quercetin feeding produced a 40% decrease in vitamin C, total vitamin C and oxidized-vitamin C, perhaps by down-regulating ascorbate biosynthesis.
Overall the results support a gain of ascorbate oxidase activity of mutant SOD in ALS, but do not support protection by dietary treatment with ascorbate or quercetin
In vitro studies to assess the potential of Quercetin as a topical sunscreen; photooxidative properties, photostability and inhibition of UV radiation-mediated skin damage
No full textProtection from the negative effects of solar radiation can be achieved by wearing protective clothing, avoiding exposure to sunlight or by the application of topical sunscreens. In this thesis, a number of studies were designed to determine if quercetin is suitable for use as a topical sunscreen.
The first objective was to determine if quercetin could protect against UV-induced lipid oxidation. Quercetin is twice as effective at preventing UVB-induced oxidation as preventing UVA-induced oxidation.The difference between UVA- and UVB- induced oxidation is believed to be due to the presence of an excited state form of quercetin in the UVA system.
The second objective was to determine the UV photostability of quercetin in solution. Three photoproducts of quercetin form regardless of whether UVA or UVB radiation is used. These photoproducts are 2,4,6-trihydroxybenzaldehyde, quercetin depside and hydroxytyrosol. . The slow rate of formation, less than 20% loss of starting material over 11 hours, and non-toxic nature of the photoproducts indicate that photostability of quercetin is not an obstacle to its use as a sunscreen.
The third objective was to determine the ability of quercetin to inhibit photosensitization by ketoprofen. Quercetin was shown to be effective in preventing decomposition of ketoprofen until it was consumed in the formation of the three quercetin photoproducts. This abilty of quercetin to prevent ketoprofen photosensitization indicates a beneficial effect for the use of quercetin as a topical sunscreen.
The fourth objective was to determine if quercetin can prevent UV-induced damage in a biological system. Quercetin was found to significantly reduce secretion of matrix metalloprotease 1 (MMP-1) upon UVA or UVB exposure, but had no effect on secretion of tumor necrosis factor á (TNF-á) in HaCaT cells. , Topical application of quercetin to UVA or UVB exposed EpiDerm skin mimics significantly reduced both MMP-1 and TNF-á secretion.
These results indicate that quercetin is effective in decreasing or eliminating several harmful effects of UVA and UVB radiation in the skin without major loss of starting material and without formation of toxic photoproducts. As such, quercetin appears to be a good candidate for inclusion into topical sunscreen formulations
The protective effect of ascorbate and catechin against myocardial ischemia-reperfusion injury in an isolated rat heart model
No full textMyocardial ischemia-reperfusion (I/R) injury is an important health concern in myocardial infarction and situations such as angioplasty and cardiac surgeries. Therefore, patients and physicians need therapeutic interventions that are applicable at the time of surgery. Flavonoids and ascorbate (vitamin C) are known for their antioxidant activity and may be involved in the currently known health benefits of plant based foods and drinks. The objectives of this study were to 1) determine the extent to which ascorbate or catechin alone at levels which could be in blood after dietary supplementation, can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic protective effect of ascorbate and catechin when given together. Isolated rat hearts (n=48) were perfused in the retrograde mode with modified Krebs-Henseleit buffer, and following the induction of 30 min global ischemia, ascorbate (150 µM) and/or catechin (5 µM) were added directly into the perfusate during 90 min reperfusion. To determine the histopathological features, hematoxylin and eosin (H&E) stain was used in one heart per condition; while to assess the biochemical analysis, the heart tissues were assessed for apoptosis (caspase-3 activity), oxidative stress (thiobarbituric acid reactive substances (TBARS) and total malondialdehyde (MDA) levels), and redox status (reduced and oxidized glutathione tissue levels). A comparison of IR hearts with two controls, sham (perfused for a 15 min stabilization period) and continuous perfusion (perfused for 135 min), showed in most but not all measurements that this was a suitable model of IR injury. The treatment experiments showed that 150 µM ascorbate protected the heart against lipid peroxidation and cell apoptosis by 100%, while 5 µM catechin protected by 67% and 90% respectively. No cooperative protective effect could be observed when ascorbate and catechin were used together. None of the treatments significantly affected either reduced or oxidized glutathione levels. In conclusion, this study showed strong protection by ascorbate, which could be used in clinically relevant situations, and is the first to report the protection by catechin at this dose under conditions of myocardial ischemia-reperfusion injury
Mitochondrial uptake of anthocyanidins and protection from oxidative stress
No full textThe anthocyanins show efficient antioxidant properties and free radical scavenging properties which result in various health-promoting benefits. This research investigated the ability of anthocyanidins to distribute into mitochondria and protect mitochondria from oxidative stress.
In an in vitro study, the uptake of pure cyanidin and quercetin, and their 3-glucosylated forms into isolated rat liver mitochondria was tested, along with their effects on mitochondrial oxidative stress parameters. The absorption of cyanidin was significantly higher (67% uptake of 125 µM) than the other three flavonoids. Measurements indicated that the cyanidin was taken up into or tightly bound by mitochondria. Also, results suggested that cyanidin uptake was partially dependent on membrane potential. When incubated together (internally and externally) with mitochondria all tested flavonoids decreased reactive oxygen species (ROS) generation during mitochondrial respiration, and inhibited lipid peroxidation to different extents. Importantly, pre-loaded CY showed much stronger effects against oxidative stress in two analyses than other flavonoids. Due to its greater uptake by mitochondria, cyanidin may provide greater protection in vivo.
In an in vivo study, cyanidin, quercetin and their 3-glucosides were administered into rat tail vein to give a dose of 7.6 µmol/Kg body weight. Cyanidin and its glucoside had greater affinity to liver and kidney than did quercetin and its glucoside; particularly, all test tissues contained a significantly higher amount of cyanidin than other test flavonoids. Also, cyanidin accumulated more in liver mitochondria than other flavonoids, and consistent with in vitro results was present in mitochondria to a much greater extent than cyanidin glucoside. However, delivery of the flavonoids at this dose did not significantly affect the liver mitochondria susceptibility to lipid peroxidation or the level of endogenous tissue oxidative damage.
Altogether the results show that cyanidin can rapidly and efficiently accumulate in mitochondria, wherein it exhibits strong bio-antioxidant activity against oxidative stress and may help protect mitochondrial function and integrity. Also, the anthocyanidin and its 3-glucoside have greater ability than flavonols to accumulate in organs; especially cyanidin presented in liver mitochondria to a much greater extent. Cyanidin could be a potent natural antioxidant compound that is effective in mitochondria-protective therapies
A record of successful incubation of Bandy Bandy (Vermicella annulata) eggs
No full textVolume: 24Start Page: 45End Page: 4
Photochemical trajectory modeling studies of the North Atlantic region during August 1993
No full textA Lagrangian photochemical trajectory model has been used to assess the factors affecting O-3 production during transport of polluted air masses across the North Atlantic Ocean. Sensitivity studies have been performed along idealized trajectories, and it is found that the potential impact of North American emission sources is maximized by transport of air at high altitudes, in drier conditions and in conditions where mixing of the air with background air masses is relatively limited. Measurements taken from the NCAR King Air aircraft as part of the North Atlantic Regional Experiment (NARE) August 1993 intensive have been used to initialize forward trajectories, calculated using European Centre for Medium-Range Weather Forecasting analyzed wind fields, from eastern North America to assess O-3 production over the Atlantic during this period. The effects of dilution of a polluted air parcel with air from the upper troposphere have also been studied, and the contribution of photochemical O-3 production to the air mass composition is found to be smaller than that of dilution, particularly for long trajectories and for conditions where dilution is relatively rapid or involves air from the stratosphere. Measurements taken from the Meteorological Research Flight Hercules aircraft over the eastern Atlantic as part of the Oxidizing Capacity of the Tropospheric Atmosphere campaign have been examined in the light of these studies. A backward trajectory analysis has been performed from one of the vertical profiles taken off the coast of Portugal on August 31, 1993, to assess the origin of the different air masses intercepted. While the lower levels are characteristic of air from the European boundary layer advected over the ocean, the upper levels show strong evidence for anthropogenic influence from North American sources, with elevated levels of O-3, NOy, CO, and aerosol. Although it cannot be concluded that this air mass definitely originated from over North America, the measured concentrations are shown to be consistent with those for an air mass from this source region experiencing some mixing with air masses in the upper troposphere
From Women and Sport to Gender and Sport: Transnational, Transdisciplinary, and Intersectional Perspectives
No full texthttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000303571900001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701HistoryHospitality, Leisure, Sport & TourismA&HCISSCI1EDITORIAL MATERIAL5,SI667-6742
INVESTIGATION OF SOME MOLECULAR MECHANISMS OF CYTOTOXIC 1,5-DIARYL-3-OXO-1,4-PENTADIENES
No full textGlutathione S-transferase GSTð has been one of the significant targets for cancer treatment in the
past several years. The reason behind that is 1) its overexpression in some cancer cells compared
to normal ones 2) its ability to cause resistance against cancer chemotherapeutics and 3) its
protective role against reactive oxygen species (ROS). We have synthesized a large number of
compounds which have strong potency against different cancer cell lines. These compounds
possess a 1,5-diaryl-3-oxo-1,4-pentadienyl pharmacophore. In the present study some
investigations as to the way in which cytotoxicity is mediated was undertaken. Our results have
demonstrated that the analogs NC 2067 and NC 2081 behaved as substrates for GSTð and
reduced the level of GSH. This was apparent by the decrease in the concentrations of both
compounds after the addition of GSTð and GSH. In addition, both agents caused about 3-7 folds
increase in ROS levels. The dichlorodihydrofluorescein dye was used for this purpose due to its
fluorescence characteristic after being oxidized by ROS. High levels of these species cause a
drop in the mitochondrial membrane potential. This phenomenon was detected when the
monomeric form of JC-1 levels were increased after treatment. The reduction of 2-3 folds was
seen when the cells were treated with the IC50 values of both compounds. In addition, both
agents inhibited oxygen consumption implicating their ability to inhibit oxidative
phosphorylation. We also evaluated the effect of both agents on mitochondrial swelling. NC
2081 caused swelling using concentrations of 10 ìM and 50 ìM. This was apparent when the
absorption of an isolated rat liver mitochondrial solution decreased after the addition of the
compound. The addition of the higher concentration caused about 2 fold greater effect than the
lower one. On the other hand, compound NC 2067 produced minimal swelling only at a
concentration of 50 ìM
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