Fish oil supplementation in CCl4 injured rodents exclusively suppressed enzymatic and non-enzymatic lipid peroxidation of DHA and EPA

Poster Session 1: abstract no. M4.07The Conference abstracts' website is located at http://www.issfal.org/conferences/2014-stockholm/abstractsFish oil contains high amount of omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and helps in reducing risk of neurodegenerative diseases and coronary heart diseases. Because of the high numbers of double bonds, they are prone to undergo lipid peroxidation in vitro and in vivo. Many of the products generated through this process are claimed either to be bioactive or toxic. We, therefore, investigated the effect of fish oil supplementation with CCl4 liver injured rats. Male Sprague Dawley rats were randomized into five groups: 1) water (Control), 2) canola oil, 3) CCl4, 4) fish oil (omega-3, 350 mg/kg), 5) fish oil + CCl4. Rats were treated ...postprin

Hyperoxia Elevates Adrenic Acid Peroxidation in Marine Fish and Is Associated with Reproductive Pheromone Mediators

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Maternal-fetal evaluation of oxidized lipid products of polyunsaturated fatty acid induced by environmental contaminant perfluorooctante sulfonate

Poster Session 3: abstract no. N9.06The Conference abstracts' website is located at http://www.issfal.org/conferences/2014-stockholm/abstractsPerfluorooctane sulfonate (PFOS) is synthetic fluorinated hydrocarbons. However the carbon-fluoride bonds render these compounds to be non-biodegradable, leading to their persistence in the environment and lengthy elimination half-life in vivo. PFOS could also penetrate the placental barrier and the blood brain barrier, and produce neurotoxic effect. High dose of PFOS leads to neonatal mortality and neurologic delays. It is known PFOS generate a dose-dependent ROS production, but the effect in PUFA lipid peroxidation, especially adrenic, arachidonic, docosahexaenoic and eicosapentaenoic acids that are ...postprin

Nonenzymatic lipid mediators, neuroprostanes, exert the antiarrhythmic properties of docosahexaenoic acid

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Redox imbalance and morphological changes in skin fibroblasts in typical Rett syndrome.

Evidence of oxidative stress has been reported in the blood of patients with Rett syndrome (RTT), a neurodevelopmental disorder mainly caused by mutations in the gene encoding the Methyl-CpG-binding protein 2. Little is known regarding the redox status in RTT cellular systems and its relationship with the morphological phenotype. In RTT patients (n = 16) we investigated four different oxidative stress markers, F2-Isoprostanes (F2-IsoPs), F4-Neuroprostanes (F4-NeuroPs), nonprotein bound iron (NPBI), and (4-HNE PAs), and glutathione in one of the most accessible cells, that is, skin fibroblasts, and searched for possible changes in cellular/intracellular structure and qualitative modifications of synthesized collagen. Significantly increased F4-NeuroPs (12-folds), F2-IsoPs (7.5-folds) NPBI (2.3-folds), 4-HNE PAs (1.48-folds), and GSSG (1.44-folds) were detected, with significantly decreased GSH (−43.6%) and GSH/GSSG ratio (−3.05 folds). A marked dilation of the rough endoplasmic reticulum cisternae, associated with several cytoplasmic multilamellar bodies, was detectable in RTT fibroblasts. Colocalization of collagen I and collagen III, as well as the percentage of type I collagen as derived by semiquantitative immunofluorescence staining analyses, appears to be significantly reduced in RTT cells. Our findings indicate the presence of a redox imbalance and previously unrecognized morphological skin fibroblast abnormalities in RTT patients

Chronic Melatonin Administration Reduced Oxidative Damage and Cellular Senescence in the Hippocampus of a Mouse Model of Down Syndrome

Previous studies have demonstrated that melatonin administration improves spatial learning and memory and hippocampal long-term potentiation in the adult Ts65Dn (TS) mouse, a model of Down syndrome (DS). This functional benefit of melatonin was accompanied by protection from cholinergic neurodegeneration and the attenuation of several hippocampal neuromorphological alterations in TS mice. Because oxidative stress contributes to the progression of cognitive deficits and neurodegeneration in DS, this study evaluates the antioxidant effects of melatonin in the brains of TS mice. Melatonin was administered to TS and control mice from 6 to 12 months of age and its effects on the oxidative state and levels of cellular senescence were evaluated. Melatonin treatment induced antioxidant and antiaging effects in the hippocampus of adult TS mice. Although melatonin administration did not regulate the activities of the main antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase) in the cortex or hippocampus, melatonin decreased protein and lipid oxidative damage by reducing the thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PC) levels in the TS hippocampus due to its ability to act as a free radical scavenger. Consistent with this reduction in oxidative stress, melatonin also decreased hippocampal senescence in TS animals by normalizing the density of senescence-associated â-galactosidase positive cells in the hippocampus. These results showed that this treatment attenuated the oxidative damage and cellular senescence in the brain of TS mice and support the use of melatonin as a potential therapeutic agent for age-related cognitive deficits and neurodegeneration in adults with DS

Enantioselective access to isoquinuclidines by tropenone desymmetrization and homoallylic radical rearrangement: synthesis of (+)-ibogamine.

[reaction: see text]. Chiral lithium amide-induced desymmetrization of a tropenone and subsequent Bu3SnH-catalyzed nitrogen-directed homoallylic radical rearrangement constitute key steps in a new strategy to dehydroisoquinuclidines. The strategy was applied in a synthesis of (+)-ibogamine

Enantioselective total synthesis of (-)-xialenon A.

The first total synthesis of (-)-xialenon A (1) via conjugate allylation of a 1,5-cyclooctadiene-derived bicyclo[3.3.0]octenone 3 and an alpha'-hydroxylation on the more hinderd face of enone 9 using hypervalent iodine chemistry, is described