The effects of maternal n-6 and n-3 fatty acid (FA) supplementation on hatched chick tissue FA profile, antioxidant status, and ex vivo eicosanoid production by the cardiac tissue were investigated. ...Eggs with low, medium, and high levels of n-3 FA were obtained by feeding Cobb breeder hens were fed a corn-soybean meal-based diet containing 3.5% sunflower oil (low n-3), 1.75% sunflower oil plus 1.75% fish oil (medium n-3), or 3.5% fish oil (high n-3). Total n-3 FA in the yolk ranged from 1.8, 10.3, and 13.3% for low, medium, and high n-3 eggs, respectively (P < 0.001). Total long-chain (>20 C) n-6 FA in the egg yolk were 7.4, 2.1, and 1.3 for low n-3, medium n-3, and high n-3 eggs, respectively (P < 0.001). No differences were observed in total fat content of the eggs, which was 33.3, 31.6, and 31.9% for low n-3, medium n-3, and high n-3 eggs, respectively (P > 0.05). Hatchability for the low, medium, and high n-3 eggs was 89, 85, and 83%, respectively (P > 0.05). The total lipid content of chick liver, heart, brain, and lungs can be placed in the following descending order: liver > brain > heart > lung and was not affected by egg FA (P > 0.05). Total n-3 FA were higher in the tissues of medium and high n-3 chicks than in the tissue of low n-3 chicks (P < 0.05). There was no effect of egg FA on docosahexaenoic acid (22:6n-3) in the heart of low, medium, and high n-3 chicks (P > 0.05). There were no differences in total glutathione, glutathione peroxidase, glutathione reductase, or superoxide dismutase activities in the tissues of chicks from low n-3, medium n-3, and high n-3 eggs (P > 0.05). The medium n-3 and high n-3 chicks had lower catalase activity in the heart than did the low n-3 chicks (P = 0.013). The TBA reactive substances were significantly lower in the liver of high n-3 chicks than in that of low and medium n-3 chicks (P < 0.05). Heart tissue prostaglandin E₂ concentration was higher in low n-3 chicks than in those hatched from medium or high n-3 eggs (P < 0.05). Heart tissue thromboxane A₃ was lowest in low n-3 chicks (P < 0.05). There was no effect of yolk FA on ex vivo prostaglandin E₃ or thromboxane A₂ production in cardiac tissue (P > 0.05). These results indicate that modulating egg yolk n-3 FA enhances tissue n-3 FA and reduces proinflammatory cardiac eicosanoid production without affecting hatchability.
Lophocladines A (1) and B (2), two 2,7-naphthyridine alkaloids, were isolated from the marine red alga Lophocladia sp. collected in the Fijian Islands. Their structures were deduced on the basis of ...high-resolution mass spectra and one- and two-dimensional NMR spectroscopy. Lophocladine A (1) displayed affinity for NMDA receptors and was found to be a δ-opioid receptor antagonist, whereas lophocladine B (2) exhibited cytotoxicity to NCI-H460 human lung tumor and MDA-MB-435 breast cancer cell lines. Immunofluorescence studies indicated that the cytotoxicity of lophocladine B (2) was correlated with microtubule inhibition. This is the first reported occurrence of alkaloids based on a 2,7-naphthyridine skeleton from red algae.
Abstract The effects of feeding n-6 and n-3 fatty acids to broiler hens on cardiac ventricle fatty acid composition, and prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) production of hatched chicks ...were investigated. Fertile eggs obtained from hens fed diets supplemented with 3.5% sunflower oil (Low n-3), 1.75% sunflower+1.75% fish oil (Medium n-3), or 3.5% fish oil (High n-3) were incubated. The hatched chicks were fed a diet containing 18:3 n-3, but devoid of longer chain n-6 and n-3 fatty acids for 42 days. Arachidonic acid content was lower in the cardiac ventricle of High n-3 and Medium n-3 compared to Low n-3 birds for up to 2 weeks ( P <0.002). Long chain n-3 fatty acids were higher in the cardiac ventricle of chicks from hens fed High and Medium n-3 diets when compared to chicks from hens fed the Low n-3 diet. Differences in long chain n-3 fatty acids persisted up to four weeks of age ( P <0.001). Peripheral blood mononuclear cells (PBMNC) of 7-day-old High n-3 broilers produced significantly lower PGE2 and TXA2 than PBMNC from Low n-3 and Medium n-3 birds. These results indicate that maternal dietary n-3 fatty acids increases cardiac ventricle n-3 fatty acids while reducing arachidonic acid and ex vivo PGE2 and TXA2 production during growth in broiler chickens.
Cytotoxicity-guided fractionation of a strain of the marine cyanobacterium Lyngbya majuscula collected from Papua New Guinea led to the isolation of aurilides B (1) and C (2). The planar structures ...of 1 and 2 were established by spectroscopic analysis, including HR-FABMS, 1D (1)H and (13)C NMR, and 2D COSY, HSQC, HSQC-TOCSY, and HMBC spectra. The absolute configuration was determined by spectroscopic analysis and chiral HPLC analysis of acid hydrolysates of 1 and 2. Both aurilides B and C showed in vitro cytotoxicity toward NCI-H460 human lung tumor and the neuro-2a mouse neuroblastoma cell lines, with LC(50) values between 0.01 and 0.13 microM. Aurilide B (1) was evaluated in the NCI 60 cell line panel and found to exhibit a high level of cytotoxicity (the mean panel GI(50) concentration was less than 10 nM) and to be particularly active against leukemia, renal, and prostate cancer cell lines.
Five new lyngbyabellin analogs along with a known compound, dolabellin, have been isolated from the marine cyanobacterium Lyngbya majuscula collected from Papua New Guinea. The structures of ...lyngbyabellins E–I were elucidated through extensive spectroscopic analysis, including HR-FABMS and 1D and 2D NMR experiments. The absolute configurations of lyngbyabellin E and H were ascertained by chiral HPLC and GC/MS analysis of degradation products, in combination with NMR experiments. All five lyngbyabellins showed cytotoxicity to NCI-H460 human lung tumor and neuro-2a mouse neuroblastoma cell lines with LC50 values between 0.2 and 4.8μM.
Graphical Abstract
Brine shrimp toxicity and TLC analysis guided the isolation of five new and biologically active meroditerpenoids 2β,3α-epitaondiol (1), flabellinol (2), flabellinone (3), stypotriolaldehyde (4), and ...stypohydroperoxide (5) along with five known compounds from the marine brown alga Stypopodium flabelliforme collected in Papua New Guinea. The planar structures of compounds 1−5 were determined by extensive spectroscopic analysis (1D and 2D NMR, LRMS, HRMS, IR, and UV), while relative configuration was determined by 1D and 2D NOE experiments. X-ray crystallography confirmed the relative configuration of 2β,3α-epitaondiol (1), and the modified Mosher's ester method was used to establish its absolute configuration. All of the new metabolites were moderately toxic to murine neuro-2a cells (LC50 2−25 μM), and three 2β,3α-epitaondiol (1), flabellinol (2), and flabellinone (3) possessed potent sodium channel blocking activity. Stypotriolaldehyde (4) had a biphasic effect on the concentration of intracellular Ca2+ in rat cerebellar granule neurons (CGN). The previously known compound, stypoldione (6), also modulated intracellular calcium concentration and was cytotoxic in CGN. Metabolites 2β,3α-epitaondiol (1), flabellinol (2), and flabellinone (3) displayed moderate cytotoxicity to the NCI-H460 human lung cancer cell line.
The coexistence of factors considered to contribute to development of porphyria cutanea tarda was studied in 39 consecutive patients. Highly prevalent factors were alcohol intake in 79%, smoking in ...86%, hepatitis C virus infection in 74%, estrogen use in 73% of 11 females, and at least one mutation in the HFE (hereditary hemochromatosis) gene in 65%. The C282Y mutation was found in 29%, H63D in 47%, and S65C in 0%. HFE genotypes included C282Y/C282Y in 9%, H63D/H63D in 9%, C282Y/H63D in 12%, C282Y/wild type in 9%, and H63D/wild type in 26%. Less prevalent were HIV infection in 15% (or 25% of those tested, N = 24) and erythrocyte uroporphyrinogen decarboxylase deficiency, which distinguishes familial (type 2) from "sporadic" (type 1) porphyria cutanea tarda, in 19%. Multiple contributing factors coexisted in both types 1 and 2, with 92% of all patients having three or more factors. These observations indicate that this porphyria is multifactorial in the individual patient, and therefore is seldom attributable to a single identifiable cause. Profiling for all potentially contributing factors is important for individualizing management.
The rate of neutrino-electron elastic scattering interactions from 862 keV Be7 solar neutrinos in Borexino is determined to be 46.0±1.5(stat)-1.6+1.5(syst)counts/(day*100ton). This corresponds to a ...νe-equivalent Be7 solar neutrino flux of (3.10±0.15)×109cm-2s-1 and, under the assumption of νe transition to other active neutrino flavours, yields an electron neutrino survival probability of 0.51±0.07 at 862 keV. The no flavor change hypothesis is ruled out at 5.0σ. A global solar neutrino analysis with free fluxes determines Φpp=6.06-0.06+0.02×1010cm-2s-1 and ΦCNO<1.3×109cm-2s-1 (95% C.L.). These results significantly improve the precision with which the Mikheyev-Smirnov-Wolfenstein large mixing angle neutrino oscillation model is experimentally tested at low energy.
Coumarin (1,2-benzopyrone), a natural dietary constituent and drug currently under evaluation for treatment of certain cancers and lymphedema, reduces polycyclic aromatic hydrocarbon-induced ...neoplasms in rodents. Because most rodents metabolize coumarin through 3,4-epoxidation, whereas 7-hydroxylation predominates in humans, their suitability as a model for coumarin effects in humans has been questioned. We examined coumarin chemoprotection against the promutagen and dietary contaminant aflatoxin B1 with human liver S9 bioactivation in the Chinese hamster ovary cell/hypoxanthine-guanine phosphoribosyltransferase mutation assay. Coumarin in the absence of aflatoxin B1 was not mutagenic or cytotoxic up to 500 microM. When included with either 1 or 10 microM aflatoxin B1, coumarin produced a dose-dependent increase in mutant frequency and cytotoxicity. At concentrations greater than 50 microM, coumarin stimulated human liver S9 bioactivation of aflatoxin B1 to the mutagenic 8,9-epoxide. This increase was 12- and fivefold at 500 microM coumarin with 1 and 10 microM aflatoxin B1, respectively, compared with incubations with aflatoxin B1 alone. These findings differ from previous results with liver S9 from other species, and indicate that coumarin co-mutagenicity with aflatoxin B1 and human liver S9 is through increased aflatoxin B1 bioactivation.
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