紫苏醛合成紫苏葶的工艺研究

在酸碱缓冲溶液中由紫苏醛与盐酸羟胺缩合合成紫苏葶,经红外光谱、气相色谱-质谱联机、氢核磁共振谱图确定了产物紫苏葶的结构。研究了反应体系的pH、反应温度以及紫苏醛和盐酸羟胺的投料比对紫苏葶收率的影响,确定优化工艺条件为:反应体系的pH为6.5,紫苏醛与盐酸羟胺的摩尔投料比为1∶7,40℃下反应6h,紫苏葶的产率和纯度可分别达到91.1%和98.20%。优化后的实验条件有效地抑制了紫苏葶的酸性分解,与文献方法相比,明显提高了紫苏葶的收率和纯度。     

添加助剂的非木浆二氧化氯漂白

研究了添加醛类助剂对非木浆二氧化氯漂白的活化效果。在ClO2脱木素（D）段添加1.0%～1.5%的甲醛助剂,可以有效地促进和改善ClO2脱木素的速率和效率。与对照样相比,ClO2脱木素（D）后和碱抽提（DE或DEP）后纸浆的卡伯值均有所降低,ClO2的实际消耗量增大,表明甲醛对ClO2脱木素有较好的活化作用。除了甲醛以外,乙醛、乙二醛、葡萄糖等醛类或醛糖也可以起到一定的活化效果。甲醛的活化效果与未漂浆初始卡伯值的高低有关。未漂浆初始卡伯值越高,甲醛对ClO2脱木素段的活化效果越好。对原浆卡伯值为21.7的烧碱-蒽醌法麦草浆,在D段添加1.5%的甲醛助剂,采用DEPP漂序,可使漂白终点白度达到81.8%,比对照样提高了2.5个点,部分强度指标有所下降。     

氧化淀粉的制备及特性研究

利用两步氧化法,首次将玉米淀粉改性为同时含羧基和醛基的氧化淀粉,为制革工业提供了一种新型的清洁化鞣剂。第一步通过正交试验确定了含羧基量最多的初氧化淀粉,优化工艺为pH=9·0,时间4h,温度45℃,双氧水用量为玉米淀粉的30%。第二步得到含醛基量最多的氧化淀粉,优化工艺为pH=1·2,时间4h,反应温度40℃,高碘酸钠与初氧化淀粉摩尔比为1·2。电导滴定法测得最终氧化淀粉含羧基量的质量分数为0·75%,紫外分光光度法测得含醛基量质量分数为0·83%。高效液相色谱得到初氧化淀粉的重均分子质量为7238·70,氧化淀粉重均分子质量为2915·44。     

基于香气活力值分析白酒风味化合物对乙醇代谢关键酶的影响

以香气活力值（OAV）为基础,通过体外酶学实验研究了浓香型白酒中酯类、醇类物质对乙醇脱氢酶（ADH）和乙醛脱氢酶活性（ALDH）的影响。结果表明,浓香型白酒中己酸乙酯香气活力值最大（OAV≥7 284）,其次分别为戊酸乙酯（OAV≥1 276）和丁酸乙酯（OAV≥845）;白酒中风味化合物对两种酶活性的影响差异很大,醇类和酯类的加入会抑制ADH活性,其中正戊醇、异丁醇和戊酸乙酯的抑制率最高,分别为27.64%、29.32%和26.72%,且具有剂量依赖性（R2＞0.9）;然而,除了正丙醇,大部分醇类和酯类的加入会不同程度的促进ALDH活性。     

Quantification of aroma vapours sorbed in polyethene films using supercritical carbon dioxide

Extraction with supercritical carbon dioxide was used to quantity the amounts of seven different aroma vapours sorbed in polyethene films. The method was found to completely extract all aroma compounds from the films. The solution of aroma compounds in the polymer films decreased with increasing polymer density. Monoterpenes were always completely sorbed in the films, whereas aldehydes and ketones had a much lower affinity for the films. The sulphur-containing compound, thiophene, was difficult to analyse due to its adsorption on metal surfaces.     

Taurine ameliorates alcoholic steatohepatitis via enhancing self-antioxidant capacity and alcohol metabolism

Chronic alcohol consumption or alcohol abuse is the main cause of alcoholic steatohepatitis or further cirrhosis. This study was to exam if the antioxidant capacity and alcohol metabolism in livers of chronic alcohol-fed rats were improved by supplementing taurine (Tau). Rats were randomly divided into four groups with five times per week of treatment: 1) isocaloric solution; 2) 3 g alcohol/kg BW/day; 3) 3 g alcohol/kg BW/day + 1 g taurine (Tau)/kg BW/day; and 4) 3 g alcohol/kg BW/day + 2 g Tau/kg BW/day. A 6-week alcohol consumption resulted in lower (p < 0.05) body weight gain and self-antioxidant capacities, as well as increased (p < 0.05) liver size, serum/hepatic lipids, and AST and ALT values. However, alcohol-fed rats co-treated with Tau have decreased (p < 0.05) liver lipid levels via increasing fecal lipid output and cholesterol metabolism. Besides, co-treatment of Tau also enhanced (p < 0.05) self-antioxidant capacities and alcohol metabolism in livers via enhancing GSH contents, CAT, GSH-Px, ADH, and ALDH activities, but decreasing MDA contents. In a histological examination of rat liver, microvesicular steatosis and necrotic cells were observed in alcohol-fed rats without Tau while largely suppressed microvesicular steatosis and no necrotic cells were observed in alcohol-fed rat supplemented with Tau. Therefore, Tau could be an effective hepatoprotective agent against alcohol-induced damage via enhancing self-antioxidant capacity and alcohol metabolism.     

Low ergosterol content in yeast adh1 mutant enhances chitin maldistribution and sensitivity to paraquat-induced oxidative stress

Alcohol dehydrogenases catalyse the reversible oxidation of alcohols to aldehydes or ketones, with concomitant reduction of NAD(+) or NADP(+) . Adh1p is responsible for the reduction of acetaldehyde to ethanol, while Adh2p catalyses the reverse reaction, the oxidation of ethanol to acetaldehyde. Lack of Adh1p shifts the cellular redox balance towards excess NADH/NADPH and acetaldehyde, while absence of Adh2p does the opposite. Yeast mutant adh1Δ had a slow growth rate, whereas adh2Δ grew like the isogenic wild-type (WT) during prediauxic shift fermentative metabolism. After 48 h WT and mutants reached the same number of viable cells. When exponentially growing (LOG) cells were exposed to calcofluor white, only mutant adh1Δ displayed an irregular deposition of chitin. Quantitative analyses of both LOG and stationary-phase cells showed that adh1Δ mutant contained significantly less ergosterol than cells of WT and adh2Δ mutant, whereas the erg3Δ mutant contained extremely low ergosterol pools. Both adh1Δ and adh2Δ mutants showed higher-than-WT resistance to heat shock and to H(2) O(2) but had WT resistance when exposed to ultraviolet (UV) light and the DNA cross-linking agent diepoxyoctane, indicating normal DNA repair capacity. Mutant adh1Δ was specifically sensitive to acetaldehyde and to membrane peroxidizing paraquat. Our results link the pleiotropic phenotype of adh1Δ mutants to low pools of ergosterol and to reductive stress, and introduce the two new phenotypes, resistance to heat shock and to H(2) O(2) , for the adh2Δ mutant, most probably related to increased ROS production in mitochondria, which leads to the induction of oxidative stress protection.     

Susceptibility of anthocyanins to ex vivo degradation in human saliva

Some fruits and their anthocyanin-rich extracts have been reported to exhibit chemopreventive activity in the oral cavity. Insights regarding oral metabolism of anthocyanins remain limited. Anthocyanin-rich extracts from blueberry, chokeberry, black raspberry, red grape, and strawberry were incubated ex vivo with human saliva from 14 healthy subjects. All anthocyanins were partially degraded in saliva. Degradation of chokeberry anthocyanins in saliva was temperature dependent and decreased by heating saliva to 80 °C and after removal of cells. Glycosides of delphinidin and petunidin were more susceptible to degradation than those of cyanidin, pelargonidin, peonidin and malvidin in both intact and artificial saliva. Stability of di- and tri-saccharide conjugates of anthocyanidins slightly, but significantly, exceeded that of monosaccharide compounds. Ex vivo degradation of anthocyanins in saliva was significantly decreased after oral rinsing with antibacterial chlorhexidine. These results suggest that anthocyanin degradation in the mouth is structure-dependent and largely mediated by oral microbiota.