几种鱼油的脂肪酸组成及贮藏期间的变化

对国内外几种鱼油进行了脂肪酸成分的分析与比较,并对鱼油的氧化特性进行了评估。结果表明,鱼油脂肪酸随种类不同而有较大的差异。毛鳞鱼鱼油、鲱鱼鱼油、鲐鱼鱼油、步丁鱼鱼油PUFA(ω3)含量分别为11.3％、14.3％、21.0％和27.6％;SFA含量分别为17.52％、21.2％、24.12％和31.15％;MUFA含量分别为62.46％、52.9％、40.04％和26.26％。鳀鱼鱼油EPA+DHA总量在15％～35％,特别是国产鳀鱼油的DHA含量高于EPA,C_(20:1)、C_(22:1)含量较低,而南非、智利、加利福尼亚、秘鲁产的鳀鱼鱼油EPA含量高于DHA。鱼油的SFA随储存时间而增加,PUFA则相反,温度是影响鱼油氧化的重要因素。     

服用鱼油多不饱和脂肪酸对血液中脂肪酸组成的影响

高脂血症患者摄食含DHA33％、EPA10％的鱼油脂肪酸制剂,可增加全血脂肪酸组成中DHA的相对含量,降低EPA、AA的含量;可增加血小板膜脂肪组成中DHA、EPA的相对含量,增加DHA/AA、EPA/AA的比值;也可增加HDL_2、HDL_3的脂肪组成中EPA的相对含量。     

红毛菜的氨基酸和脂肪酸分析

分析了红毛菜中氨基酸和脂肪酸的组成与含量，结果表明，红毛菜氨基酸含量为40．27％，必需氨基酸含量为20．30％，且组成十分均衡，游离氨基酸含量为4992．68ug.g^-1干品，其中大部分是呈味氨基酸和牛磺酸，不饱和脂肪酸占总脂肪酸的83．98％，EPA占51．739％，因此红毛菜是一种味道鲜美，营养丰富的天然保健食品。     

柄海梢中21种化学元素的研究分析

对柄海鞘中21种化学元素进行了分析,发现其中有多种矿物元素的含量高于海水,表明柄海鞘富集金属元素的能力较强,为进一步研究其药理及临床效用提供了必要的依据。     

鱼油多烯脂肪酸酯胶丸的制备及其在兔体内的药动学

从制罐的剥皮鲀下脚料提取的鱼油,经皂化、冷却得多烯脂肪酸(PUFA),续经酯化得其乙酯(PUFA-E)。后者用气相色谱法测定含二十碳五烯酸(EPA)18.1％,二十二碳六烯酸(DHA)49.0％,两者合计为鱼油的69.5％。 PUFA-E的各项指标符合药用的一般     

海燕Asterina pectinifera生殖腺营养成分的研究

对黄海产海燕生殖腺进行了营养成分分析。结果如下：海燕生殖腺蛋白质含量为43.25％，脂肪含量为14.22％，还原糖含量为3.48％，总糖含量为18.60％。并进一步对氨基酸、不饱和脂肪酸作了定性定量分析，其中总氨基酸中必需氨基酸含量为36.24％，半必需氨基酸含量为10.46％，其它氨基酸含量为53.30％；高不饱和脂肪酸含量丰富，其中二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）分别占总不饱和脂肪酸的22.39％和0.30％，EPA含量显著。     

柄海鞘中21种化学元素的研究分析

对柄海鞘中 2 1种化学元素进行了分析 ,发现其中有多种矿物元素的含量高于海水 ,表明柄海鞘富集金属元素的能力较强 ,为进一步研究其药理及临床效用提供了必要的依据。     

扇贝中肠腺脂质的提取及脂肪酸分析

对大连沿海地区养殖的栉孔扇贝Chlamys farreri、虾夷扇贝Pecten yesoensis中肠腺中的脂质的提取方法及脂质中脂肪酸进行比较研究。结果表明,在冲气隔氧、提取温度为100℃、时间为60min、料水比为1:2条件下,脂质的水提取率最高,为3.01%。栉孔扇贝、虾夷扇贝中肠腺脂质中的不饱和脂肪酸分别占脂肪酸总量的32.0%和32.8%,其中2种扇贝中肠腺中EPA DHA的含量分别为13.6%和13.8%。     

硝酸银-水法提纯高含量DHA和EPA的实验研究

目的 从鱼油中分离提纯高含量的DHA和EPA方法 用硝酸银一水法对鱼油乙酯化产品进行分离提纯。结果 用硝酸银一水法分离粗鱼油得到(1)DHA、EPA总含量大于95％的产品；(2)DHA含量大于95％的产品；(3)EPA含量高于DHA的产品。结论 研究的工艺可降低生产高含量鱼油DHA、EPA的成本，降低现售DHA、EPA产品的副作用，提高DHA、EPA产品的稳定性。     

19种湛江地区海产贝类中脂肪酸组成GC-MS分析

目的运用GC-MS检测广东湛江地区19种常见的海洋经济贝类19种主要脂肪酸的组成和含量。方法借鉴Kang等组织样品前处理方法,再运用GC-MS分析脂肪酸组成和含量。结果19种海洋贝类脂肪酸含量介于0.08%～0.59%。饱和脂肪酸(SFA)占32.75%～62.35%,单不饱和脂肪酸(MUFA)达到1.55%～22.79%,多不饱和脂肪酸(PUFA)达到22.31%～57.32%。在19种贝类中n-3PUFA含量较高,其中头足纲的贝类要远高于腹足纲和双壳纲的16种贝类,3种头足类EPA和DHA在鲜贝中达到0.518～1.00g.kg-1和0.402～1.377g·kg-1。结论19种贝类都属于低脂肪酸高PUFA生物,在3个纲中n-6/n-3PUFA比值,腹足纲(1.00～14.34)要高于双壳纲(0.16～0.65)和头足纲(0.12～0.44),因此,头足纲贝类是人体补充n-3PUFA的极好来源。贝类的脂肪酸组成和含量分析结果表明,结合19种贝类在分类学和生物学特征的不同,贝类的脂肪酸组成与其分类学上的地位具有一定的联系。     

烤鳗加工废料鳗骨的综合利用

测定了烤鳗加工废弃物鳗骨的成分，系统研究了鳗骨为原料提取鳗骨油，经盐形成法和尿素包合法制取鱼油多不饱和脂肪酸，喷雾干燥法制备鳗油微胶囊的工艺条件。结果表明，该工艺简便易行，鳗骨油提取完全率达７６％以上；纯化后鳗骨油脂肪酸中ＥＰＡ，ＤＨＡ含量由７．４％提高至４５％以上，总回收率为６４％；微胶囊制品中ＰＵＦＡ含量达２６．２％左右，其抗氧化稳定远高未经包囊的混合物。     

Health effects of oleic acid and long chain omega-3 fatty acids (EPA and DHA) enriched milks. A review of intervention studies

Substitution of dietary saturated fat by oleic acid and/or polyunsaturated fatty acids (PUFA) has been described to reduce the cardiovascular risk by reducing blood lipids, mainly cholesterol. Additional benefits have been described for long chain omega-3 PUFA (eicosapentaenoic acid—EPA and docosahexaenoic acid—DHA) from fish oils. In recent years, food technology has been used to produce dairy drinks with a reduced content of saturated fat in favour of those fatty acids, most of them claiming cardiovascular benefits. This review summarises all the scientific evidence regarding the effects of milks enriched with long chain omega-3 PUFA (EPA + DHA) and/or oleic acid on cardiovascular health. Nine controlled intervention studies with enriched milks have reported effects on healthy volunteers, subjects with increased risk factors and cardiovascular patients. The main effects observed were reductions of blood lipids, mainly cholesterol, LDL-cholesterol and triglycerides.     

The induction of apoptosis in pre-malignant keratinocytes by omega-3 polyunsaturated fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) is inhibited by albumin

The long chain omega-3 polyunsaturated fatty acids (PUFA) have been reported to exert anti-cancer effects. At this study we tested the effect of the omega-3 PUFA, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), on pre-malignant keratinocytes growth in the well-characterised human pre-malignant epidermal cell line, HaCaT and attempted to identify a PUFA serum antagonist. Both EPA and DHA inhibited HaCaT growth and induced apoptosis. At the 10% (v/v) foetal bovine serum (FBS) medium, limited growth inhibition (3–20% for 50 μM DHA and EPA respectively) and negligible apoptosis were observed with PUFA use. However, at 3% (v/v) FBS medium, 30–50 μM of PUFA caused impressive levels of growth inhibition (82–83% for 50 μM DHA and EPA respectively) and increase of apoptosis (8–19% increase in 72 h). None of the numerous serum growth factors present in FBS or the antioxidant n-tert-butyl-α-phenylnitrone could inhibit the PUFA-induced cytotoxicity. In contrast, bovine and human albumin (0.1–0.3%, w/v) significantly antagonized the growth inhibitory and apoptosis-inducing effects of PUFA. In conclusion, we have shown for the first time that omega-3 PUFA inhibit the growth and induce apoptosis of pre-malignant keratinocytes and identified albumin as a major antagonistic factor in serum that could limit their effectiveness at pharmacologically-achievable doses.     

A comparative study on the effect of algal and fish oil on viability and cell proliferation of Caco-2 cells.

Polyunsaturated fatty acid (PUFA) rich micro-algal oil was tested in vitro and compared with fish oil for antiproliferative properties on cancer cells in vitro. Oils derived from Crypthecodinium cohnii, Schizochytrium sp. and Nitzschia laevis, three commercial algal oil capsules, and menhaden fish oil were used in cell viability and proliferation tests with human colon adenocarcinoma Caco-2 cells. With these tests no difference was found between algal oil and fish oil. The nonhydrolysed algal oils and fish oil showed a much lower toxic effect on cell viability, and cell proliferation in Caco-2 cells than the hydrolysed oils and the free fatty acids (FFAs). Eicosapentaenoic acid (EPA; C20:5n-3) and docosahexaenoic acid (DHA; C22:6n-3) were used as samples for comparison with the tested hydrolysed and nonhydrolysed oils. The hydrolysed samples showed comparative toxicity as the free fatty acids and no difference between algal and fish oil. Oxidative stress was shown to play a role in the antiproliferative properties of EPA and DHA, as alpha-tocopherol could partially reverse the EPA/DHA-induced effects. The results of the present study support a similar mode of action of algal oil and fish oil on cancer cells in vitro, in spite of their different PUFA content.     

Docosahexaenoic and eicosapentaenoic acids increase neuronal death in response to HuPrP82-146 and Abeta 1-42

Dietary supplements containing polyunsaturated fatty acids (PUFA) are frequently taken for their perceived health benefits including a possible reduction in cognitive decline in the elderly. Here we report that pre-treatment with docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA) significantly reduced the survival of cortical or cerebellar neurons incubated with HuPrP82-146, a peptide derived from the prion protein, or with Abeta 1-42, a peptide found in Alzheimer's disease. Treatment with DHA or EPA reduced the free cholesterol content of neuronal membranes. This did not affect the amount of FITC-HuPrP82-146 ingested by neurons, but increased the kinetics of incorporation. In untreated neurons, FITC-HuPrP82-146 migrated to caveolin-1 containing lipid rafts. The addition of HuPrP82-146 also triggered the migration of cytoplasmic phospholipase A2 (cPLA2) into caveolin-1 containing rafts, and increased prostaglandin E2 production. Activation of cPLA2 and prostaglandin E2 production were both increased in neurons pre-treated with DHA. These results are consistent with DHA or EPA altering cell membranes resulting in increased amounts of HuPrP82-146 localising to caveolin-1 containing rafts, increased activation of cPLA2, prostaglandin E2 production, caspase-3 activity and reduced neuronal survival. Such observations raise the possibility that some PUFA supplements may accelerate neuronal loss in the terminal stages of prion or Alzheimer's diseases.     

哈蟆油延缓衰老的作用机制研究

目的：研究哈蟆油抗衰老的作用机制。方法：实验分为空白对照、衰老/免疫低下模型与哈蟆油高、中、低剂量（0.4、0.2、0.1g·kg-1）组。采用皮下注射D-半乳糖复制小鼠衰老模型,测定肾脏丙二醛（MDA）、一氧化氮（NO）、还原型谷胱甘肽（GSH）的含量和髓过氧化物酶（MPO）、黄嘌呤氧化酶（XOD）的活性;采用深部X射线照射复制小鼠免疫低下模型,以气相色谱法测定小鼠血液中脂肪酸的含量。结果：与空白对照组比较,衰老模型组小鼠肾脏MDA含量显著上升,XOD活性显著升高,NO、GSH含量显著下降,MPO活性显著下降（P〈0.01或P〈0.05）;与衰老模型组比较,哈蟆油高、中、低剂量组小鼠MDA含量显著降低,XOD活性显著减弱,MPO活性显著增强（P〈0.01或P〈0.05）,哈蟆油低剂量组NO含量显著升高（P〈0.01）。与空白对照组比较,免疫低下模型组二十碳五烯酸（EPA）/二十碳四烯酸（AA）、EPA、脂肪酸总量、单不饱和脂肪酸、多不饱和脂肪酸（PUFA）含量显著降低（P〈0.05或P〈0.01）;与免疫低下模型组比较,哈蟆油高、中、低剂量组二十二碳六烯酸（DHA）、EPA、脂肪酸总量、n-3系PUFA、单不饱和脂肪酸、PUFA含量显著增加（P〈0.05或P〈0.01）,哈蟆油中、低剂量组EPA/AA显著降低（P〈0.01）,蛤蟆油低剂量组DHA/AA、饱和脂肪酸含量显著减少（P〈0.05或P〈0.01）。结论：哈蟆油具有显著的抗氧化作用,可以增加免疫力低下小鼠体内不饱和脂肪酸含量,这些可能是其延缓衰老的机制之一。     

Eicosapentaenoic acid and docosahexaenoic acid modulate mitogen-activated protein kinase activity in endothelium

Omega-3 polyunsaturated fatty acids (PUFA) regulate inflammation and immunoreaction partially via affecting endothelial functions. However, the intracellular signaling mechanisms for inhibiting endothelial activation by omega-3 PUFA remain unclear. We investigated the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on mitogen-activated protein kinases (MAPK) of endothelium. We analyzed the expression of extracellular signal-related kinases (ERK1/2), Jun amino-terminal kinases (JNK), and p38 mRNA by real-time RT-PCR and the kinases activity by western blotting in tumor necrosis factor-alpha (TNF-alpha)-activated human umbilical vein endothelial cells (HUVEC). We observed that EPA or DHA alone significantly reduced the TNF-alpha-induced activation of p38 and JNK kinases at a concentration of 20 microM, but EPA is a more potent inhibitor than DHA. In contrast, both EPA and DHA significantly counteracted the TNF-alpha-mediated deactivation of ERK1/2 kinases. Meanwhile, both EPA and DHA significantly attenuated the TNF-alpha-induced expression of p38 and ERK1/2 mRNA, and DHA but not EPA also reduced the TNF-alpha-induced JNK mRNA expression. We present data show that both EPA and DHA alone diminish activation of p38 and JNK kinases, while maintaining the activation of ERK1/2 kinases of TNF-alpha-stimulated HUVEC. This may contribute to the inhibiting effects of omega-3 PUFA on endothelial activation by proinflammatory stimuli.