魔芋葡甘聚糖酯化改性产物对空气中SO2吸附及抑菌效果研究

以魔芋葡甘聚糖为原料,分别采用苯甲酸、醋酸和没食子酸对魔芋葡甘聚糖进行酯化改性,研究了改性pH值、温度及改性处理时间对改性产物吸附空气中SO2和抑菌效果的影响,优化了改性工艺参数,得到了有较好使用效果的天然的有机大分子空气净化材料.研究结果表明:当采用苯甲酸为魔芋葡甘聚糖酯化改性剂时,改性产物对空气中的SO2吸附效果和抑菌作用效果优于使用醋酸和没食子酸的改性产物.其改性处理温度50℃,反应时间2 h,pH值3,改性反应产物对空气中SO2的吸附率可达98.7%,抑菌率可达到86.3%.     

磁性固体酸催化剂的合成及其酯化催化活性的研究

研究了以磁性体为核、催化活性体为壳的固体酸催化剂制备过程的结构转化及其酯化催化活性变化.在ZrOCl2/FeCl2投料为10∶1(质量比),酸浓度为1 mol/L,浸泡时间2 h,400℃焙烧1 h的条件下,制得了具有优异的催化活性的纳米磁性催化剂ZrO2/SiO2-Fe3O4.采用IR、扫描电镜(SEM)和孔径分布等...     

碳基固体酸催化生物油酯化降酸工艺参数优化

为了降低生物油中羧酸类物质的质量分数,提高生物油品质,本试验采用碳基固体酸作为催化剂,对生物油进行催化酯化降酸提质。以乙酸为模型与甲醇反应,用单因素和响应面法优化生物油催化酯化反应条件,得出最佳工艺参数:反应温度100℃、醇酸比3.37、反应时间2.49 h、催化剂质量分数为5.26%,乙酸平均转化率为94.72%,在此条件下,分别用甲醇、乙醇、正丁醇与生物油进行催化酯化反应。结果表明:酯化后生物油中羧酸类物质转化成酯,酸值降低了82.82%~91.41%,降酸效果明显。且酯化后,生物油的密度降低、黏度减小、热值增加,提高了生物油作为燃料的品质。本研究可为生物油降酸提质提供参考依据。     

高酸值米糠油酯化脱酸成生物柴油原料

为充分利用高酸值米糠毛油,将其脱酸成生物柴油原料。采用酯化脱酸方法,通过对多种酯化脱酸催化剂的比较,结果表明氧化锌具有较强的催化活性。氧化锌作为米糠油酯化脱酸的催化剂,分别考察了甘油添加量、催化剂添加量、反应温度、反应时间对酯化脱酸的影响。得到了以下较优工艺参数：真空度为0.1 MPa,甘油添加量为理论甘油量1.044 g,催化剂添加量为油质量的0.1%,反应温度200℃,反应时间6 h。在此优化条件下,米糠油的酸值从38.14 mg/g降至5.17 mg/g,满足了作为生物柴油生产原料的要求。     

豆油脱臭馏出物甲酯化处理的试验研究

以豆油脱臭馏出物为原料利用超临界CO2提取维生素E，原料的甲酯化处理是重要的步骤之一，甲酯化结果表明，影响甲酯化的主要因素是甲醇与豆油脱臭馏出物的重量比例、酯化温度、酯化时间，而催化剂硫酸浓度的影响较小，最佳酯化因素组合是甲醇与豆油脱臭馏出物的重量比为0.6、硫酸浓度1％、酯化温度80℃、酯化时间60min，酯化率可达75.59％。而影响维生素E保存率的主要因素是酯化时间、酯化温度，甲醇与豆油脱臭馏出物的重量比例，矿石浓度影响较小，在酯化过程中，维生素E的保存率最好可以达到95.82％。     

超声波在憎水性黑米色素制备中的应用

在超声波作用下,采用乙酸酐酯化处理水溶性黑米色素,制备了憎水性黑米色素.探讨了超声水浴温度、反应时间、黑米色素与乙酸酐料液比等因素对黑米色素酯化度、色价的影响.结果表明:采用料液比2 g∶10 mL、在70℃超声水浴中反应3 h,为制备憎水性黑米色素的最优条件.同时通过红外光谱、可见吸收光谱及溶解性对黑米色素的酯化进行了初步探讨.     

轻馏分生物油催化酯化脱水提质研究

为了得到稳定的含氧液体燃料及较好分离糖类及其衍生物,以Amberlyst-36离子交换树脂为催化剂在100℃下对粗生物油进行酯化脱水提质工艺优化,考察了反应时间、催化剂用量以及正丁醇和生物油质量比(醇油比)对提质的影响,得到最佳提质条件为醇油比1.5∶1.0、15%的催化剂用量、反应时间4 h,此条件下提质油酸值从72.23 mg/g降为3.98 mg/g,水分从53.06%降为3.34%,热值由8.75 MJ/kg升高至31.50 MJ/kg。GC-MS分析显示生物油中不稳定酸、醛、酮转化为稳定含氧化合物,稳定目标产物酯、醇、醚GC含量占74.70%。接着进行老化实验,保存3个月,粗生物油黏度从3.21 mm2/s增加到48.24 mm2/s,极不稳定,提质油理化性质显著提高并保持稳定。最后将20.00 g提质油、30.00 g蒸馏水和30.00 g二氯甲烷进行充分混合,萃取分液,可以基本将糖类及其衍生物从提质油中分离出来,得到粗糖质量为1.24 g,糖类物质总GC含量为87.92%,其中丁基-β-D-吡喃葡萄糖苷占到75.28%。     

非酯化脂肪酸对奶牛氧化应激的诱导作用及其机制

处于围产期的奶牛由于能量负平衡引起脂质动员,导致大量非酯化脂肪酸(NEFA)释放进入肝脏和血液。当NEFA处于较高浓度时,可改变机体抗氧化系统与氧化系统的平衡状态,并激活核因子κB信号通路及丝裂原活化蛋白激酶信号通路,同时也会抑制核因子E2相关因子2信号通路的活化,诱发机体炎性损伤,最终诱导奶牛产生氧化应激,从而直接影响奶牛养殖业的经济效益。本文主要综述了NEFA对围产期奶牛氧化应激的诱导作用及其机制的研究进展,旨在为奶牛生产中缓解氧化应激、提高免疫机能及促进生产性能的发挥提供理论依据。     

大豆油脱臭馏出物的酶法甲酯化

采用脂肪酶催化大豆油脱臭馏出物(SODD)中的脂肪酸进行甲酯化反应。对反应条件进行单因素试验,确定了最佳反应工艺参数。经分析初步得出脂肪酶催化法甲酯化最佳条件为:甲酯化温度45℃,甲酯化时间16h,转速180r/min,底物比0.1:1。最佳条件下脂肪酸甲酯化率达到96.2%。脂肪酶反复使用6个批次活性无明显降低。     

Utilization and metabolism of palmityl and oleoyl fatty acids and alcohols in caecal enterocytes of Atlantic salmon (Salmo salar L.)

The substitution of fish oil with wax ester‐rich calanoid copepod‐derived oil in diets for carnivorous fish, such as Atlantic salmon, has previously indicated lower lipid digestibility. This suggests that the fatty alcohols (FAlc) present in wax esters may be a poorer substrate for intestinal enzymes than the fatty acids (FA) in triacylglycerol (TAG), the major lipid in fish oil. The hypothesis tested was that the possible lower utilization of dietary FAlc by salmon enterocytes is at the level of uptake and that subsequent intracellular metabolism was identical to that of FA. A dual‐labelled FAlc–FA metabolism assay was employed to determine simultaneous FAlc and FA uptake and relative utilization in enterocytes isolated from pyloric caeca of Atlantic salmon fed either a diet supplemented with fish oil or wax ester‐rich Calanus oil. The diets were fed for 10 weeks before caecal enterocytes from each dietary group were isolated and incubated with equimolar mixtures of either [1‐¹⁴C]16:0 FA and [9,10(n)‐³H]16:0 FAlc, or [1‐¹⁴C]18:1n‐9 FA and [9,10(n)‐³H] 18:1n‐9 FAlc. Uptake was measured after 2 h with relative utilization of labelled FAlc and FA calculated as a percentage of uptakes. Differences in uptake were observed, with FA showing higher uptake than FAlc, and 18:1 chains a higher uptake than 16:0. A proportion of unesterified FAlc was possibly recovered in the cells, but the majority of FAlc was recovered in lipid classes such as TAG and phospholipids indicating substantial conversion of FAlc to FA followed by esterification. However, incorporation of FA and FAlc into esterified lipids was higher when derived from FA than from FAlc. Twenty‐five to fifty percentage of the absorbed 16:0 FA was recovered in TAG fraction of the enterocytes compared with 15–75% of 18:1 FA. Twenty to thirty percentage of the absorbed 16:0 FA was recovered in the phosphatidylcholine fraction of the enterocytes compared with only 5–15% of the 18:1 FA. Less than 15% of the fatty chains taken up by the cells were used for energy production, with significantly higher oxidation of 18:1 in enterocytes from fish fed the fish oil diet compared with the Calanus oil diet. However, overall, dietary copepod oil had little effect on FAlc and FA metabolism. Metabolic modification by elongation and/or desaturation was generally low at 1–5% of the uptake. We conclude that our hypothesis was generally proved in that the uptake of FAlc by salmon enterocytes was lower than the uptake of FA and that subsequent intracellular metabolism of FAlc was similar to that of FA. However, unesterified FAlc was possibly recovered in the cells suggesting that the conversion to FA may not be concomitant with uptake.