纳米氧化铜对小鼠全血及组织中铜和锌沉积的影响

选取240只体质量约22g健康的昆明种小白鼠,随机分为6组,每组设4个重复.1组饲喂基础日粮,2组在基础日粮中以硫酸铜的形式添加铜10mg/kg,3组在基础日粮中以氧化铜的形式添加铜10mg/kg,4～6组在基础日粮中以纳米氧化铜的形式分别添加铜5、10和20mg/kg.研究不同剂量纳米氧化铜对小白鼠全血和组织中铜及锌含量的影响.试验期30 d.结果表明,试验至15 d,添加纳米氧化铜显著提高小白鼠全血铜含量,显著降低小白鼠肝脏及胫骨锌含量;试验至30 d,添加纳米氧化铜显著提高小白鼠胫骨铜含量.     

福美双和铜对肉鸡胫骨软骨发育不良的影响

本试验旨在研究福美双和铜对肉鸡胫骨软骨发育不良、血清相关酶活性和组织铜含量的影响。100羽1日龄AA肉鸡随机分为4组,从8日龄起分别给予基础日粮(对照组),福美双日粮(基础日粮+福美双100 mg/kg),福美双低铜日粮(基础日粮+福美双100 mg/kg+CuSO4.5H2O 50 mg/kg),福美双高铜日粮(基础日粮+福美双100 mg/kg+CuSO4.5H2O 100 mg/kg),试验期至21日龄。结果表明:(1)日粮中添加福美双(100 mg/kg)能显著增加肉鸡TD的发生率;添加铜能降低福美双的这种作用,两者之间存在明显的互作关系;(2)与对照组相比,福美双组和福美双高铜日粮组肉鸡血清钙、磷水平明显升高(P<0.05);血清ALT水平在各组之间无显著差异;血清ALP、AST水平,福美双高铜日粮组与其余各组相比明显升高,差异显著(P<0.05);(3)与对照组相比,其余各组肉鸡胫骨长度均显著下降(P<0.05);(4)日粮中铜添加可提高各组织中铜的沉积;添加福美双能提高肝脏、肾脏、胰腺中铜的沉积,同时降低铜在肾脏中的沉积,而铜的添加能够降低福美双所引起的肾脏铜的增加。提示福美双可能通过损伤肝、肾功能,影响机体组织对铜的生物利用从而诱导肉鸡胫骨软骨发育不良的发生。     

1~21日龄黄羽肉鸡饲粮铜营养需要量的研究

本研究旨在通过研究饲粮铜添加水平对黄羽肉鸡生长性能、免疫器官发育、抗氧化性能、肝脏和血清铜含量等的影响,以探讨1~21日龄黄羽肉鸡铜的营养需要量。选用1日龄健康、发育良好的快大型岭南黄羽肉公雏鸡1440只,根据体重随机分为6个组,每组6个重复,每个重复40只鸡,组1(对照组)饲喂基础饲粮(2.80 mg/kg铜),组2、3、4、5、6饲粮在基础饲粮中分别添加4、8、16、32、64 mg/kg铜。试验期21 d。结果表明：本试验条件下,1)饲粮添加4和64 mg/kg铜显著提高试鸡平均日采食量( P<0.05),饲粮中铜添加水平对末重、平均日增重和料重比无显著影响( P>0.05)。2)与对照组相比,8 mg/kg组法氏囊指数显著升高( P<0.05),而饲粮铜添加水平对胸腺和脾脏指数无显著影响( P>0.05)。3)与对照组相比,8、16、32和64 mg/kg组血清和肝脏铜锌超氧化物歧化酶(CuZnSOD)活性显著升高(P<0.05),各组间血清和肝脏丙二醛含量均无显著差异(P>0.05);添加16、32、64 mg/kg铜显著降低血清铜蓝蛋白活性(P<0.05)。4)与对照组相比,16、32和64 mg/kg组血清铜含量显著降低(P<0.05),铜添加水平对肝脏铜含量和肝脏金属硫蛋白含量影响不显著( P>0.05)。综合考虑各项指标,为获得较好生长性能和免疫器官发育、抗氧化性能,1~21日龄快大型黄羽肉鸡饲粮铜适宜添加水平为8 mg/kg,加上基础饲粮铜含量2.80 mg/kg,则该阶段黄羽肉鸡铜需要量为10.80 mg/kg;以血清CuZnSOD活性为依据,通过非线性回归分析估测得到1~21日龄黄羽肉鸡铜需要量为13.38 mg/kg。     

43～63日龄黄羽肉公鸡铜需要量

本研究旨在通过研究饲粮铜添加水平对黄羽肉公鸡生长性能、抗氧化性能、肝脏和血清铜含量等的影响,以探讨43~63日龄黄羽肉公鸡铜的需要量。选用43日龄健康、发育良好的快大型岭南黄羽肉公鸡900只,根据体重随机分为6个组,每组6个重复,每个重复25只鸡,组1(对照组)为基础饲粮组(铜水平为2.74 mg/kg),组2~6饲粮在基础饲粮中分别添加4、8、16、32、64 mg/kg铜。结果表明:1)与对照组相比,16和32 mg/kg铜组显著提高试鸡末重、平均日增重和平均日采食量(P<0.05),饲粮中铜添加水平对料重比无显著影响(P>0.05)。2)与对照组相比,16和32 mg/kg铜组血清铜锌-超氧化物歧化酶(Cu Zn-SOD)活性显著升高(P<0.05),32和64 mg/kg铜组肝脏Cu Zn-SOD活性显著升高(P<0.05),饲粮铜添加水平对胸肌中Cu ZnSOD活性无显著影响(P>0.05);饲粮添加32和64 mg/kg铜显著降低了胸肌丙二醛(M DA)含量(P<0.05),各组间血清和肝脏MDA含量均无显著差异(P>0.05);添加16、32、64 mg/kg铜显著降低了血清铜蓝蛋白活性(P<0.05)。3)与对照组相比,8、16 mg/kg铜组肝脏铜含量显著降低(P<0.05),铜添加水平对血清铜含量和肝脏金属硫蛋白含量影响不显著(P>0.05)。综合考虑各项指标,为获得较好生长性能和抗氧化性能,43~63日龄黄羽肉公鸡饲粮铜适宜添加水平分别为16和32 mg/kg,加上基础饲粮铜水平为2.74 mg/kg,则该阶段黄羽肉公鸡铜需要量分别为18.74和34.74 mg/kg;以生长性能和肝脏Cu Zn-SOD活性为依据,通过折线回归分析估测得到43~63日龄黄羽肉公鸡铜需要量分别为19.94和38.34 mg/kg。     

生长肥育猪日粮铜添加水平与组织铜残留量动态关系初探

采用54头杂交猪(杜×大×约)研究大剂量日粮铜添加水平对组织铜含量的影响,建立日粮铜添加水平与组织铜残留量之间的动态模型,探讨保证猪肉及其副产品食用安全性的最适铜添加量。试验采用单因子设计,分别设0、100、200、300、400mg/kg的铜添加水平,试验从20kg开始,100kg结束。结果表明:添加100～400mg/kg的铜不同程度地增加了组织器官中铜的残留量,肝脏和肾脏中铜含量随饲粮添加水平的增加呈二次曲线变化规律。肝脏铜残留量(y,单位为mg/kg)与日粮铜添加水平(x,单位为mg/kg)之间的回归方程为:80kg体重时,y=5.4697-0.0814x+0.0009x2(R2=0.930,P=0.07);100kg体重时,y=11.3963-0.2920x+0.0022x2(R2=0.814,P=0.036)。肾脏铜残留量(y,单位为mg/kg)与日粮铜添加水平(x,单位为mg/kg)之间的回归方程为:y=8.7583-0.0043x+0.0002x2(R2=0.975,P=0.025)。在80kg屠宰时,为了保证肝脏中的铜含量不超过10mg/kg,饲粮铜添加水平不应高于129mg/kg。在100kg屠宰时,为了保证肝脏或肾脏中的铜含量不超过10mg/kg,饲粮铜添加水平不应高于128或90mg/kg。     

日粮锰对肉仔鸡组织器官锰、铜、锌沉积的影响

选用 1日龄艾维茵肉仔鸡 ,采用单因子多水平随机化试验设计 ,随机分成 6组 ,每组 3个重复 ,每个重复 8只鸡。在玉米 豆粕型基础日粮中分别添加锰 (MnSO4 ·H2 O) 0 ,40 ,80 ,1 2 0 ,1 60 ,2 0 0mg/kg ,研究日粮锰对肉仔鸡组织器官锰、铜、锌沉积的影响。结果表明 :在肉仔鸡日粮中添加 40 2 0 0mg/kg的锰 ,对胫骨锰、肝脏锰和肾脏锰的沉积有显著的影响 (P <0 0 5) ;日粮锰的添加对肝铜和肾铜沉积无明显影响 (P >0 0 5) ,但日粮锰添加量超过 1 2 0mg/kg时 ,能够减少胫骨铜的沉积 (P <0 0 5) ;对胫骨、肝和肾中锌的沉积无明显影响(P >0 0 5)。     

斜率比法评定肉仔鸡对铜源的相对生物学利用率

本试验旨在研究肉仔鸡对不同铜源的相对生物学利用率。试验采用3×2完全随机设计,3种铜源分别为硫酸铜、碱式氯化铜和蛋氨酸铜,2个铜添加水平分别为10和20 mg/kg,另设1个不添加铜的对照组,共7组。选择1日龄健康雄性爱拔益加(AA)肉仔鸡504只,随机分为7组,每组6个重复,每个重复12只鸡。试验期为21 d。结果表明:饲粮铜源和铜添加水平对1～21日龄肉仔鸡的末重、平均日采食量、平均日增重和料重比均无显著影响(P> 0. 05)。肝脏铜含量和血浆铜蓝蛋白活性均随饲粮铜添加水平的增加而极显著增加(P<0.01)。以血浆铜蓝蛋白活性为评价指标,碱式氯化铜和蛋氨酸铜相对于硫酸铜(100%)的生物学利用率分别为141.05%和142.07%;以肝脏铜含量为评价指标,碱式氯化铜和蛋氨酸铜相对于硫酸铜(100%)的生物学利用率分别为127.61%和137.64%。由此可见,饲粮铜添加水平≤20 mg/kg(基础饲粮中铜含量为9.65 mg/kg)时对1～21日龄肉仔鸡无显著促生长作用; 21日龄肉仔鸡对低铜饲粮(铜添加水平≤20 mg/kg)中3种铜源的相对生物学利用率为:蛋氨酸铜>碱式氯化铜>硫酸铜。     

日粮铜水平对育肥猪组织器官铜沉积及铜代谢的影响研究

研究日粮铜对育肥猪组织铜沉积和粪铜代谢率的影响,本试验选择来源相同且体重相近(30±1.05)kg健康状况较好的杜长大三元杂交生长猪共24头,随机分为4组,每组3个重复,每个重复2头猪。4个处理组分别饲喂4种不同硫酸铜水平的试验日粮,将最低剂量组的铜添加量设定为10 mg/kg(对照组),试验组分别添加铜含量为45 mg/kg(1组),135 mg/kg(2组),225 mg/kg(3组);添加后测定饲料中铜的实际含量分别为19.09 mg/kg(对照组),53.60 mg/kg(1组),154.00 mg/kg(2组),250 mg/kg(3组)。结果表明:在试验期间,胃、脾、胰脏和淋巴结组.织中铜含量在各个铜饲喂剂量下都处于较低水平,各组饲喂剂量之间差异不显著(P0.05);各处理组间心、肝、肺脏铜含量差异显著(P0.05);胫骨,肋骨、股骨骨质和股骨骨髓的积铜含量差异显著(P0.05);10 mg/kg(对照组)和45 mg/kg(1组)铜的消化率明显高于135 mg/kg(2组)和225 mg/kg(3组)(P0.05),但2,3组间铜的消化率差异极显著(P0.01)。结果表明,日粮中添加45 mg/kg的硫酸铜猪体内组织铜沉积率小,粪铜消化率高。     

饲粮铜添加水平对5～8周龄泰和乌骨鸡生产性能及组织黑色素含量的影响

本试验旨在研究饲粮铜添加水平对5～8周龄泰和乌骨鸡生产性能及组织黑色素含量的影响。选用29日龄泰和乌骨鸡270只,随机分成6组,每组3个重复,每个重复15只鸡。试验鸡饲喂在基础饲粮(铜含量为4.77 mg/kg)中分别添加0、5、15、30、60、125 mg/kg铜的饲粮,饲养至56日龄。结果表明:饲粮添加适量铜可显著影响5～8周龄泰和乌骨鸡平均日增重、平均日采食量和料重比(P<0.05),且在30 mg/kg时生产性能达到最佳。饲粮添加适量铜可显著或极显著影响血清、肝脏、肾脏、皮肤及肌肉的黑色素含量及酪氨酸酶活性(P<0.05或P<0.01),并呈现出随饲粮铜添加水平的提高先升后降的趋势。当饲粮铜添加水平为30 mg/kg时,血清和组织酪氨酸酶活性及组织黑色素含量达到峰值。由此可知,玉米-豆粕型基础饲粮中添加铜可提高生产性能和组织黑色素含量,其适宜添加水平为30 mg/kg。     

国外科技

比较评估肉鸡羟基氯化铜和硫酸铜生物学效价 摘要:本研究旨在采用小麦-豆粕为基础日粮,比较羟基氯化铜(CH)与硫酸铜(CuSO4)添加水平对的肉鸡在生长发育、胴体品质,胫骨性能和矿物质浓度的影响。选择308只1日龄公雏鸡随机分配到8个处理,每个处理6个重复,每个重复18只。设基础饲粮不添加铜作为阴性对照组,基础日粮以硫酸铜形式添加15和200 mg Cu/kg,基础日粮以羟基氯化铜添加15、50、100、150和200 mg Cu/kg。试验期分为1-14日龄和14-35日龄2个阶段。结果表明,硫酸铜形式添加15 mg Cu/kg组的肉鸡体重和料肉比(FCR)与阴性对照组无显著差异,而羟基氯化铜形式添加15 mg Cu/kg组肉鸡FCR阴性对照组(0-35天;P< 0.05)。硫酸铜形式添加200 mg Cu/kg组,羟基氯化铜形式添加200 mg Cu/kg组肉鸡日增重增加且FCR降低(P<0.01)。根据折线回归模型估测,以日增重和FCR作为评价指标,饲粮羟基氯化铜形式铜最佳添加水平分别为109.5和72.3 mg Cu/kg。饲粮铜源或水平对肉鸡胴体品质无影响(P> 0.05)。羟基氯化铜形式添加150 mg Cu/kg组肉鸡胫骨灰分含量最高,而硫酸铜形式添加200 mg Cu/kg组肉鸡胫骨灰分含量最低。与硫酸铜形式添加200 mg Cu/kg组,羟基氯化铜形式添加200 mg Cu/kg组肉鸡十二指肠粘膜Cu含量更高(P<0.001)。总之,在促生长营养剂量和药理剂量水平上来看,羟基氯化铜作为补充铜源在促进生长方面比硫酸铜更有效。     

羟基蛋氨酸铜中铜含量的测定

分别用PAN、二甲酚橙、紫脲酸铵作为指示剂,研究了EDTA配位滴定法测定羟基蛋氨酸铜螯合物中铜含量的方法,标准偏差均小于0.2%,相对标准偏差小于0.6%。结果表明,EDTA配位滴定法测定羟基蛋氨酸铜中铜含量,操作过程简单、方便,分析结果重现性好、准确度高,且三种指示剂均可用于铜的测定,其中紫脲酸铵最好,终点变色敏锐。本法可用于不同工艺所合成的羟基蛋氨酸铜中铜含量的测定。     

Copper status of ewes fed increasing amounts of copper from copper sulfate or copper proteinate

The Cu status of mature, crossbred ewes fed two sources (CuSO4 vs. Cu proteinate) and three levels (10, 20, or 30 mg/kg) of dietary Cu was determined in a 73-d feeding trial. Ewes (n = 30) were fed a basal diet containing rice meal feed, cottonseed hulls, cottonseed meal, meat and bone meal, cracked corn, and vitamin-mineral supplements at 2.5% of BW to meet NRC requirements for protein, energy, macrominerals, and microminerals, excluding Cu. The basal diet contained 5 mg/kg Cu, 113 mg/kg Fe, .1 mg/kg Mo, and .17% S. Copper sulfate or Cu proteinate was added to the basal diet to supply 10, 20, or 30 mg/kg of dietary copper in a 2x3 factorial arrangement of treatments. Ewes were housed in 3.7- x 9.1-m pens in an open-sided barn. Blood samples were collected on d 28 and 73. Ewes were slaughtered on d 74, and liver and other tissues were collected to determine Cu concentrations. An interaction (P = .08) occurred between source and level for liver Cu. The interaction existed due to an increase in liver Cu concentrations when ewes were fed increasing dietary Cu from CuSO4 but not when fed Cu proteinate diets. There was no source x level interaction (P>.10) for the blood constituents measured. On d 73, plasma ceruloplasmin activity was greater (P<.05) in ewes fed Cu proteinate than in those fed CuSO4 (33.1 vs. 26.8 microM x min(-1) x L(-1)). Increasing the concentration of dietary Cu did not affect (P>.10) plasma ceruloplasmin. Packed cell volume (PCV), red blood cell count (RBC), white blood cell count, whole blood hemoglobin (wHb), plasma hemoglobin, and plasma Cu were similar between sources of Cu. Ewes fed 20 mg/kg Cu had lower (P<.05) PCV, RBC, and wHb than those fed 10 or 30 mg/kg Cu diets. Feeding up to 30 mg/kg Cu from these sources did not cause an observable Cu toxicity during the 73-d period.     

Iatrogenic copper deficiency associated with long-term copper chelation for treatment of copper storage disease in a Bedlington Terrier

A 9-year-old Bedlington Terrier was evaluated because of weight loss, inappetence, and hematemesis. Copper storage disease had been diagnosed previously on the basis of high hepatic copper concentration. Treatment had included dietary copper restriction and administration of trientine for chelation of copper. A CBC revealed microcytic hypochromic anemia. High serum activities of liver enzymes, high bile acid concentrations, and low BUN and albumin concentrations were detected. Vomiting resolved temporarily with treatment, but the clinicopathologic abnormalities persisted. Results of transcolonic portal scintigraphy suggested an abnormal shunt fraction. Results of liver biopsy and copper quantification revealed glycogen accumulation and extremely low hepatic copper concentration. Serum and hair copper concentrations were also low. Chelation and dietary copper restriction were tapered and discontinued. Clinical signs and all clinicopathologic abnormalities improved during a period of several months.     

Pathobiology of copper toxicity

A review is presented of various aspects of copper (Cu) metabolism. The Cu absorption from the gastrointestinal tract in monogastric animals differs from that in ruminants. This is influenced by Cu binding compounds, sulphide production in the rumen, and molybdenum and zinc concentrations of the diet. Moreover, the valence of the Cu ions may influence the availability of Cu in the intestine. Metallothionein and lysosomes are involved in the accumulation of copper in the liver. The different findings in various Cu storage diseases may reflect different mechanisms of disease. Cu-induced liver cell damage and haemolysis may be the result of lipid peroxidation.     

Comparison of copper heptonate with copper oxide wire particles as copper supplements for sheep on pasture of high molybdenum content

OBJECTIVE: To assess the effectiveness of intramuscular injection of copper heptonate (CuHep) and an oral dose of copper oxide wire particles (COWP) in preventing Cu inadequacy in adult and young sheep on pasture of high Mo content. DESIGN: Field experiments with flocks of mature Merino wethers and crossbred weaners. PROCEDURE: Adult wethers were given 25 or 37.5 mg Cu as CuHep, 2.5 g COWP or no Cu treatment. The weaners were given 12.5 or 25 mg Cu as CuHep, 1.25 g COWP or no Cu treatment. At intervals over the next 12 (adults) or 8 (weaners) months the sheep were weighed and samples of blood and liver were collected for trace element assay. Wool samples collected from the adults at the end of the experiment were assessed for physical characteristics. RESULTS: The higher dosage of CuHep raised liver Cu above control group values for at least 9 months in adults and 3 months in weaners. The lower dosage of CuHep was similarly effective for 3 months in adults but was without effect in weaners. In adults the response to COWP matched that to the higher dosage of CuHep; in weaners it was greater, lasting at least 5 months. No changes indicative of Cu deficiency, apart from a depressed body weight in adults, were seen. CONCLUSIONS: In sheep on pasture of high Mo content a single intramuscular injection of CuHep providing 37.5 mg Cu to adults or 25 mg Cu to weaners will raise liver Cu reserves for at least 9 and 3 months respectively and may be an acceptable alternative to COWP for preventing seasonal Cu deficiency in sheep in southern Australia.     

Comparative metabolism of copper

Copper is required in trace amounts for many body functions. The prominent effects of Cu deficiency or Cu toxicosis differs greatly between animal species. Along with iron, Cu is necessary for the transfer of O2 via a cascade of enzymes so that energy may be available for vital body functions without overheating of the tissues through rapid oxidation. As a part of lysyl oxidase, Cu has an obligate function in the maturation of all connective tissue (including elastic tissue and bone) maintaining the form and integrity of all body organs. As a constituent of tyrosinase, Cu is involved in the formation of melanin, thus preventing albinism. Copper also is involved in the myelination of nerve fibers and the production of neutrophils, enkephalins, lipoproteins, and cholesterol. Copper must be properly sequestered to prevent toxicosis. Copper is stored primarily as metallothioneins and as superoxide dismutase and is transported primarily as ceruloplasmin or as low molecular weight proteins, peptides, and amino acids.