饲用植酸酶酶活测定过程中底物的影响研究

参照国标法测定饲用植酸酶活性,研究不同来源的底物植酸钠、底物浓度、底物pH对饲用植酸酶活性的影响。结果表明,以P8810为代表的植酸钠盐水合物作为底物,其测定出的植酸酶酶活显著高于使用以P3168为代表的植酸钠作为底物所测定的植酸酶酶活。以P8810作为底物时,其反应浓度在高于6.6 mmol/L时,会产生底物抑制效应。以P8810作为底物时,调节底物pH至国标中定义的5.5与未调节pH所测得的植酸酶酶活相比较,差异并不显著,且在低底物pH条件下,某些植酸酶同样能够释放出最大催化活性。因此现有的国标法测定饲用植酸酶活性已与实际应用有一定的差别,不能照搬国标方法测定现有饲用植酸酶产品。     

植酸酶的研究应用现状

本文从植酸性质，植酸酶的来源及特性，影响植酸酶活性的因素以及植酸酶对植酸磷的利用研究，应用现状方面对植酸酶的重要意义和应用前景作一简要综述。     

植酸酶酶活测定方法的研究

植酸及其盐类广泛存在于植物组织和相应的粮食产品中,占其总量的1%～3%,其中磷含量占植物总磷的60%～90%,是磷和肌醇的主要储存形式。而植酸形式的磷不但不能被单胃动物所消化利用,它还抑制多种营养成分的吸收和利用。植酸酶是催化植酸水解成肌醇与磷酸的一类酶的总称,由于植酸酶的这一特点,它已在饲料和食品工业中广泛地得到应用。植酸酶的产生主要是依靠微生物发酵获得,近年来有关微生物发酵生产植酸酶为目的的研究、开发报道很多,微生物发酵法生产植酸酶取得了很大进展。植酸酶酶活性的测定主要是检测分解产物无机磷的生成量。目前植酸酶…     

沉淀消解法测定植物性饲料中植酸磷含量

本试验对植物性饲料中植酸磷含量进行测定，从而评价饲料营养价值。饲料样品经稀盐酸提取，植酸磷游离出来，加铁盐使其生成植酸铁沉淀，将沉淀用硝酸、硫酸消解，PO4^3-在酸性条件下，与钼酸发生反应生成磷钼酸，用抗坏血酸将其还原为钼兰显色，在波长660nm下进行比色测定。方法操作简单，具有良好的精密度，适用于植物性饲料中植酸磷含量的分析。     

植酸酶在肉仔鸡消化道内环境下活性变化的体外研究

本研究在体外条件下对肉仔鸡消化道内pH环境以及蛋白质水解酶对黑曲霉植酸酶活性的影响进行了研究。结果表明,该植酸酶为酸性植酸酶,最适pH为5.5。该植酸酶对pH环境和蛋白质水解酶较为敏感。当环境pH远离其最适pH时其活性迅速下降,且大部分酶活损失发生在30 min内,然后趋于稳定。在pH3.0和pH6.0条件下,加入胃蛋白酶和胰酶后,植酸酶活性亦进一步迅速降低,然后趋于稳定,但与胃蛋白酶相比,胰酶对植酸酶活性的影响更大。从植酸酶在14、28和42日龄肉仔鸡胃和小肠稳定性的研究可以看出,植酸酶在胃存留率分别为42%、40%和49%,在小肠内的存留率仅19%。植酸酶在胃内的稳定性好于小肠,小肠内环境不利于植酸酶存活。植酸酶活性受肉仔鸡消化道pH和蛋白酶的影响较大,这可能是影响植酸酶作用效果的主要因素之一。     

植物性植酸酶及其应用

本文综述了植物性植酸酶的来源、特征、活性、对植酸磷的分解作用、影响植物性植酸酶活性大小的因素、植物性植酸酶与其他养分之间的关系、从麸皮中提取植酸酶的研究现状等，最后对植物性植酸酶在畜牧业中的应用进行了展望。     

植酸酶在畜禽养殖上的研究进展

植酸酶作为一种畜禽饲料添加剂,能有效地将植酸磷降解为肌醇和无机磷,消除植酸的抗营养作用。本文综述了植酸酶的来源、影响酶作用的因素及其在畜禽生产中的应用。     

植酸酶在畜禽消化道内的活性变化与定点释放

利用微生物植酸酶替代畜禽日粮中的磷酸氢钙已得到普遍应用,但植酸酶活性受多种因素影响,仍不能替代畜禽日粮中的全部磷酸氢钙。本文从植酸酶的酶学特性出发,通过总结畜禽消化道pH、蛋白水解酶和金属离子等因素对植酸酶活性的影响,探讨植酸酶的适宜作用位点,进而为植酸酶在畜禽消化道内实施定点释放提供参考。     

饲料加工工艺对不同剂型植酸酶加工损耗的影响

试验旨在研究热处理对2个进口品牌和2个国产品牌耐高温植酸酶的影响及挤压膨化加工工艺(140~175℃)、环膜硬颗粒加工工艺(70~90℃)、冷挤压平模硬颗粒加工工艺(60~66℃)对不同剂型植酸酶活性损耗率的影响。不同品牌耐高温植酸酶在80℃水浴中处理2 min后测定其活性,同时在饲料中添加4 000、5 000 FTU/kg和8 000 FTU/kg活性的普通酸性植酸酶和耐高温植酸酶,分别测定植酸酶在不同制粒加工工艺条件下的活性。结果表明:热处理对不同耐高温植酸酶活性损耗的影响不同,其活性损耗率范围为8.45%~80.07%。在挤压膨化加工工艺条件下,两种植酸酶基本全部失活;在环模硬颗粒加工工艺条件下,普通商品酸性植酸酶活性损耗率为77.71%,而耐高温植酸酶活性损耗率为34.81%;在冷挤压平模硬颗粒加工工艺条件下,普通商品酸性植酸酶活性损耗率为27.40%,耐高温植酸酶活性损耗率为21.15%。采用内添加方式添加植酸酶,不同加工工艺对植酸酶活性损耗率的影响由大到小依次为:挤压膨化加工工艺环膜硬颗粒加工工艺冷挤压平模硬颗粒加工工艺。     

使用植酸酶的五个注意事项

<正>植酸酶作为一种新型微生物饲料添加剂,不仅能提高植酸磷的利用率,促进蛋白质、氨基酸和矿物质等营养素的消化吸收,促进动物生长发育,而且能够减少磷、氮等元素的污染,大大提高养殖业的经济和社会效益,但使用植酸酶时还应注意以下问题。1选择酶活性高的合格产品植酸酸酶是一种微生物制品,商品制剂多由曲霉菌发酵而获得。植酸酶的主要指标是单位酶活性(1单位酶活(IFTU)是指在37℃、pH值     

Involvement of molybdenum in feather growth

1. A poor hatchability syndrome, characterised by a high incidence of weak chickens, with clubbed down and long ginger hairs, in commercial broiler breeding stock was investigated.

2. If the weak chick were given a single oral treatment of ammonium molybdate (40 μg Mo/chick at 1 d), there was a reduction in subsequent mortality in both sexes and an increase in the growth rate of feathers in males, but not in females.     

Effects of high dietary molybdenum in rabbits

To study the effects of high dietary molybdenum (Mo) content, rabbits were fed with commercial pellets and carrots containing 39 mg Mo/kg dry matter (DM) [Experiment 1] and with a commercial diet supplemented with 40 mg Mo/kg DM [Experiment 2] for 14 days. The high dietary Mo contents failed to reduce the growth performance of rabbits. Moreover, supplemental Mo given in a dose of 40 mg/kg non-significantly decreased the apparent digestibility of crude protein (CP) and crude fibre (CF) compared to the control (73.63 +/- 2.49 and 18.56 +/- 5.10 vs. 74.31 +/- 3.03 and 21.38 +/- 6.48, respectively). Molybdenum ingested with feeds was mainly excreted (57%) via the urine. The highest Mo levels were found in kidney and liver samples (3.464 +/- 0.872; 5.27 +/- 0.95 mg/kg DM [Experiment 1] and 1.878 +/- 0.283; 1.62 +/- 0.16 mg/kg DM [Experiment 2], respectively), and Mo could also be detected in limb meat (0.336 +/- 0.205 mg/kg DM). It was stated that the testes were more sensitive to Mo exposure than the female reproductive organs because the number of germ cells was reduced. Due to the high dietary Mo intake free radicals could be generated, resulting in a marked increase of creatine kinase (CK) activity.     

锌、铜对实验性钼中毒绵羊肝脏、肾脏中钼含量的影响

小尾寒羊20只,随机分为5组,分别口服钼、铜和锌(mg/kg),Ⅰ组30mg/kg钼、Ⅱ组30mg/kg钼+15mg/kg铜、Ⅲ组30mg/kg钼+15mg/kg锌、Ⅳ组30mg/kg钼+15mg/kg铜+15mg/kg锌,Ⅴ组去离子水。试验90d期满,采取肝脏和肾脏,硫酸-高氯酸消化,原子吸收法测定钼、锌、铜含量,结果显示,Ⅰ组肝脏钼含量与第Ⅱ、Ⅲ、Ⅳ、Ⅴ组差异极显著(P<0.01),Ⅱ、Ⅲ组与Ⅳ、Ⅴ组差异极显著(P<0.01);Ⅳ组肝脏铜含量与Ⅰ、Ⅲ、Ⅴ组差异极显著(P<0.01),与Ⅱ组差异显著(P<0.05),Ⅱ组肝铜含量与Ⅰ、Ⅲ、Ⅴ组差异极显著(P<0.01);组间肝脏锌含量均差异极显著(P<0.01)。Ⅰ、Ⅲ组肾钼含量显著高于Ⅱ、Ⅳ、Ⅴ组(P<0.01);Ⅱ与Ⅳ、Ⅴ组差异极显著(P<0.01);肾铜含量Ⅲ组与Ⅰ组差异极显著(P<0.01);Ⅱ、Ⅲ、Ⅳ组与Ⅰ、Ⅴ组差异极显著(P<0.01);各组肾脏锌含量差异均极显著(P<0.01)。结果表明,30mg的钼可使肝脏钼含量显著增加(P<0.01),锌、铜含量降低。锌对肝脏钼有很好的颉抗作用,铜、锌有效地降低了钼在组织中的蓄积。     

Copper balance in mature geldings fed supplemental molybdenum

Four mature sedentary geldings were used in a 4×4 Latin square designed experiment to evaluate the effects of supplemental molybdenum (Mo) on copper (Cu) balance. Four diets were formulated to contain 0 (control), 5, 10 and 20 ppm of supplemental Mo and were fed for a 21-day adjustment period followed by a 72-hour fecal and urine collection. Diets consisted of a pelleted concentrate based on corn, soybean meal and cotton seed hulls fed in a 50:50 ratio of concentrate to native prairie grass hay. All diets were formulated to be isonitrogenous and isocaloric with similar concentrations of Cu. Urine was collected every four hours for 72 hours and multiple fecal grab samples were taken every two hours post feeding. On the third collection day, blood samples were drawn at the time of feeding, each hour for five hours post feeding, and eight hours post feeding for serum Cu analysis. Balance data were analyzed using a general linear model procedure with horse, period and treatment as main effects. Serum Cu data were analyzed using the general linear model procedure with horse, treatment and period as main effects and time as the repeated variable. The intake of Cu was similar among all diets fed. There was no difference (p>.05) in serum Cu concentrations over time or between treatments due to supplemental Mo. Urinary and fecal excretion of Cu did not differ (p>.05) between diets. Consequently, the balance of Cu was similar among diets consumed. Excretion of Mo in the urine was higher (p<.05) in horses fed the 20 ppm Mo diet versus the 0, 5 and 10 ppm Mo diet. As Mo intake increased, fecal excretion increased (p<.05) across all diets. Additionally, Mo balance was higher (p<.05) on the 20 ppm Mo diet than all other diets. In conclusion, supplemental Mo appeared to have no adverse effect on the absorption and retention of Cu when fed to mature geldings.     

钼对小鼠免疫功能的影响

钼（Mo）是动物、植物、微生物及人类必需的微量元素，是黄嘌呤氧化酶，醛氧化酶，亚硫酸氧化酶的组成成分，参与电子传递及铁的释放与运输，影响多种物质的代谢，具有重要的生理学功能。但过量的钼可导致动物中毒，并以反刍动物最为敏感。1938年Ferguson首次报道了牧草中钼含量过高，可使放牧牛产生以剧烈腹泻为特征的中毒性疾病。目前，有关钼对动物免疫功能的影响研究较少。本试验通过对小鼠日常饮水中加入不同剂量的钼，研究钼对小鼠免疫功能的影响，为动物钼中毒防治及科学饲养提供资料。     

钼对羊的中毒性试验

选择杂交波尔山羊8只, 小尾寒羊2只(4组), 分为5组, 前四组每日依次灌服150、100、60、100mg的钼(Na2MoO4·2H2O), 5d后剂量减半; 5组灌自来水。试验45d。结果表明: 试验羊出现磨牙、咳嗽、呻吟、跛行、腹泻及贫血等明显的临床症状。各试验组RBC、Hb和PCV均显著低于对照组; 1组RBC、MCV、MCH极显著低于3组(P<0 01); 4组PCV、MCV、MCH极显著低于2组(P<0 01 ), Hb显著低于2组(P<0 05)。剖检表明, 试验组羊尸体消瘦, 血液稀薄; 肝脏肿大且发生脂肪变性; 肾脏体积肿大, 肾小管上皮细胞肿胀; 肠黏膜肿胀、出血, 小肠壁有红白相间的花斑样病理变化。     

Copper, zinc and molybdenum in goat liver.

The concentrations of copper, zinc and molybdenum were measured in the liver of goats from western and south-eastern Norway. The mean copper concentrations in the liver of goats from these two districts were 23±19 µg Cu/g and 59±31 µg Cu/g wet weight, respectively. As for zinc and molybdenum, no difference was found between the two groups of animals. No correlations were detected between copper and zinc, zinc and molybdenum, or copper and molybdenum. The copper levels in Norwegian goat liver are considerably lower than in sheep liver, and the ranges are significantly more narrow. The concentrations of molybdenum in goat liver are at the same levels as in sheep and swine, while the levels of zinc are somewhat lower.     

The influence of tungsten on the molybdenum status of poultry

1. Large doses of tungsten, administered to the chick either by injection or by feeding, increased tissue concentrations of tungsten and decreased tissue concentrations of molybdenum and tissue activities of xanthine dehydrogenase.

2. The rate of loss of large doses of tungsten from the liver occurred in an exponential manner with a half‐life of 27 h.

3. When tungsten was administered to chicks fed on a semi‐synthetic diet containing abnormally low concentrations of molybdenum, the activity of hepatic xanthine dehydrogenase was reduced to negligible levels.

4. The alterations in molybdenum metabolism resulting from the administration of large doses of tungsten to the chick appears to be the result of tungsten toxicity and not of molybdenum deficiency.

5. Deaths from tungsten toxicity occurred when tissue concentrations of tungsten were increased to approximately 25 μzg/g liver. At this tissue tungstencon centration the activity of xanthine dehydrogenase was zero.