纳米氧化铜对小白鼠铜表观消化率的影响

选40只20 g左右的健康昆明种小白鼠,随机分为4组.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组在基础日粮中以纳米氧化铜的形式添加铜10mg/kg.采用全收粪法,研究纳米氧化铜对小白鼠铜表观消化率的影响.结果显示,硫酸铜组、氧化铜组、纳米氧化铜组小白鼠铜的表观消化率分别为54.74%、48.30%、71.88%,纳米氧化铜组铜的表观消化率显著高于硫酸铜组(P<0.05),极显著高于氧化铜组(P<0.01).试验表明,与添加硫酸铜和氧化铜相比,日粮中添加纳米氧化铜能提高小白鼠铜的表观消化率.     

纳米氧化铜对小白鼠铜表观消化率的影响

选40只20 g左右的健康昆明种小白鼠,随机分为4组。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组在基础日粮中以纳米氧化铜的形式添加铜10mg/kg。采用全收粪法,研究纳米氧化铜对小白鼠铜表观消化率的影响。结果显示,硫酸铜组、氧化铜组、纳米氧化铜组小白鼠铜的表观消化率分别为54.74%、48.30%、71.88%,纳米氧化铜组铜的表观消化率显著高于硫酸铜组（P〈0.05）,极显著高于氧化铜组（P〈0.01）。试验表明,与添加硫酸铜和氧化铜相比,日粮中添加纳米氧化铜能提高小白鼠铜的表观消化率。     

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.     

不同铜源对鸡嗉囊ATP7A和ATP7B基因和蛋白表达的影响

为研究不同水平的硫酸铜、微米氧化铜和纳米氧化铜对鸡嗉囊铜转运蛋白基因ATP7A和ATP7B mRNA相对表达量及蛋白表达量的影响,将105只1日龄的SPF蛋鸡随机分为7组,每组15只。第1组为对照组,饲喂低铜半纯化日粮;第2组~第4组,在基础日粮中分别以硫酸铜、微米氧化铜和纳米氧化铜的形式添加铜8 mg/kg;第5组~第7组,在基础日粮中分别以硫酸铜、微米氧化铜和纳米氧化铜的形式添加铜160 mg/kg,试验期30 d。结果表明,日粮中添加硫酸铜和纳米氧化铜显著提高雏鸡嗉囊铜含量(P0.05),微米氧化铜没有明显变化。与硫酸铜和微米氧化铜相比,纳米氧化铜显著提高雏鸡嗉囊ATP7A和ATP7B mRNA和蛋白表达量(P0.05)。由此可见,嗉囊ATP7A和ATP7B对纳米氧化铜的转运发挥重要作用。     

纳米氧化铜时对小白鼠灌胃接种大肠杆菌致病性的影响

为了研究纳米氧化铜对小白鼠灌胃接种大肠杆菌致病性的影响,试验选择140只体重20 g左右的昆明种小白鼠随机分为7组:1组为正常对照组,饲喂基础日粮;2组为感染对照组,饲喂基础日粮;3组为硫酸铜组,在基础日粮中以硫酸铜的形式添加铜180 mg/kg;4,5,6,7组为纳米氧化铜组,分别在基础日粮中以纳米氧化铜的形式添加铜10,60,120,180 mg/kg.结果表明:3组发病率明显低于2组;3组小白鼠肠道大肠杆菌数量显著少于2组(P<0.05),3,7组显著少于1组(P<0.05).说明日粮中添加高剂量纳米氧化铜能降低大肠杆菌致病性,但效果不如添加相同水平的硫酸铜.     

纳米氧化铜对鸡肝细胞CP mRNA表达及培养基质中肝酶活性的影响

将培养48h的鸡原代肝细胞随机分为13组,每组3个重复。第1组为对照组,第2～5、6～9和10～13组分别以硫酸铜、氧化铜和纳米氧化铜的形式添加铜2、4、8、16mg/L,继续培养24h后检测上清中AKP、AST、ALT、γ-GT和LDH活性,用实时荧光定量PCR法检测肝细胞CP mRNA表达量。结果显示,以硫酸铜形式添加铜2～16mg/L、以氧化铜形式添加铜8～16mg/L和以纳米氧化铜形式添加铜16mg/L,培养基质中γ-GT活性均显著高于对照组（P〈0.05）;添加铜2mg/L时,硫酸铜组γ-GT活性显著高于纳米氧化铜组（P〈0.05）,添加铜8mg/L时,氧化铜组γ-GT活性显著高于纳米氧化铜组（P〈0.05）。添加铜2mg/L时,硫酸铜和氧化铜组AST和LDH活性显著高于对照组和纳米氧化铜组（P〈0.05）。添加铜2mg/L时,氧化铜组ALT活性显著高于纳米氧化铜组（P〈0.05）。添加铜8mg/L时,硫酸铜和氧化铜组AKP活性显著高于对照组和纳米氧化铜组（P〈0.05）。添加铜2～8mg/L时,肝细胞CP mRNA表达量显著高于对照组（P〈0.05）;添加铜2mg/L时,纳米氧化铜组肝细胞CP mR-NA表达量显著高于氧化铜组（P〈0.05）,氧化铜组显著高于硫酸铜组（P〈0.05）;肝细胞CP mRNA表达量随铜添加量的增加而降低。结果表明,基质中铜达到2mg/L时,纳米氧化铜比硫酸铜、氧化铜更有利于肝细胞生长,纳米氧化铜对体外培养肝细胞的损害作用低于硫酸铜和氧化铜。     

纳米氧化铜对小白鼠血浆抗氧化机能的影响

选144只20g左右的健康昆明种小白鼠,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、20mg/kg。研究不同剂量纳米氧化铜对小白鼠血浆抗氧化能力的影响,试验期30d。结果表明,添加纳米氧化铜显著提高小白鼠血浆铜蓝蛋白活力(P<0.05),显著提高小白鼠血浆细胞色素C氧化酶活性(P<0.05),显著降低30d小白鼠血浆丙二醛含量(P<0.05)。     

不同剂量纳米氧化铜对肉鸡免疫功能的影响

将180只1日龄健康AA肉仔鸡随机分为6组,每组设3个重复,第1、2、4、6组分别以硫酸铜、氧化铜、纳米氧化铜、纳米铜的形式在基础日粮中添加铜8mg/kg,3组和5组以纳米氧化铜形式在基础日粮中分别添加铜4mg/kg和16mg/kg,研究不同剂量纳米氧化铜对肉鸡免疫功能的影响.结果表明,与硫酸铜、氧化铜组相比,在饲料中以纳米氧化铜形式添加铜8mg/kg和16mg/kg,显著提高肉鸡免疫器官指数、新城疫抗体效价、淋巴细胞转化率和白细胞介素-2(IL-2)活性,以纳米氧化铜形式添加铜4mg/kg未引起机体免疫低下.由此可见,与硫酸铜相比,日粮中添加纳米氧化铜可提高肉鸡免疫功能.     

纳米氧化铜时小白鼠灌胃接种大肠杆菌致病性的影响

为了研究纳米氧化铜对小白鼠灌胃接种大肠杆菌致病性的影响,试验选择140只体重20 g左右的昆明种小白鼠随机分为7组:1组为正常对照组,饲喂基础日粮;2组为感染对照组,饲喂基础日粮;3组为硫酸铜组,在基础日粮中以硫酸铜的形式添加铜180 mg/kg;4,5,6,7组为纳米氧化铜组,分别在基础日粮中以纳米氧化铜的形式添加铜10,60,120,180 mg/kg.结果表明:3组发病率明显低于2组;3组小白鼠肠道大肠杆菌数量显著少于2组(P＜0.05),3,7组显著少于1组(P＜0.05).说明日粮中添加高剂量纳米氧化铜能降低大肠杆菌致病性.但效果不如添加相同水平的硫酸铜.     

纳米铜对绵羊瘤胃液铜浓度、pH值及日粮表观消化率的影响

选用4只体重(55±2)kg、3岁装有永久性瘤胃瘘管的阉公羊,采用4×4拉丁方设计,研究日粮中添加纳米铜(添加量分别为:对照组0 mg Cu/kg、处理A组10 mg Cu/kg、处理B组20 mg Cu/kg、处理C组30 mg Cu/kg)对瘤胃液铜浓度、pH值及日粮表观消化率的影响。结果表明:(1)处理C组的瘤胃液铜浓度平均值显著高于对照组和处理B组(P<0.05);(2)瘤胃液铜浓度与瘤胃pH呈高度正相关(P<0.01),纳米铜有提高瘤胃液pH的趋势,处理C组的瘤胃液pH平均值显著高于对照组(P>0.05);(3)瘤胃液铜浓度与日粮OM的表观消化率呈高度负相关(P<0.05),处理C组CP、EE的表观消化率显著低于对照组(P<0.05)。根据试验结果推断,添加纳米铜低于30 mg/kg时不会影响日粮表观消化率。     

Effects of source and level of copper on performance and liver copper stores in weanling pigs

Five 28- to 33-d experiments involving 460 crossbred pigs weaned at 28 +/- 2 d of age (initial weight, 6.7 to 8.1 kg) were conducted to determine the effects of feeding high dietary levels of Cu sulfate (CuSO4) or Cu oxide (CuO) on rate and efficiency of gain and liver Cu stores of weanling pigs. The pigs were housed in groups of five to six/pen and fed a fortified, unmedicated, corn-soybean meal-dried whey basal diet (1.1% lysine, 30 ppm Cu). In Exp. 1 and 2, pigs (eight replicates) were fed the basal or the basal plus 125 or 250 ppm Cu from CuSO4 or CuO for 28 d. In Exp. 3 and 4, four replications were fed the same diets as in Exp. 1 and 2 plus two additional diets (500 ppm Cu from CuSO4 or CuO). In Exp. 5, dietary levels of 0, 125, 250, 375 or 500 ppm Cu from CuSO4 were evaluated using four replications. At the end of each experiment, the liver from one pig in each pen was collected for Cu analysis. Overall, rate and efficiency of gain were improved (P less than .01) by feeding 125 or 250 ppm Cu as CuSO4, with the 125 ppm dietary level being about 75% as effective in stimulating growth as 250 ppm. Performance of pigs was not different from controls when the highest (500 ppm) level of Cu (from CuSO4) was fed. Liver Cu increased 10- to 70-fold when 250 to 550 ppm Cu from CuSO4 was included in the feed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of supplementing combinations of inorganic and complexed copper on performance and liver mineral status of beef heifers consuming antagonists.

Performance, immune response, and liver trace mineral status were measured in growing heifers supplemented with different copper (Cu) concentrations and sources when diets contained the Cu antagonists Mo, S, and Fe. Sixty Angus x Hereford heifers were managed in two groups for 112 d and were either individually fed diets and mineral treatments using individual feeding stalls (Stall) or pen-fed grass hay and individually supplemented mineral treatments (Pen). The basal diet of grass hay, rolled barley, and soybean meal was analyzed to contain 6 mg Cu/kg DM. The treatments consisted of 1) no supplemental Cu (Control); 2) 49 mg Cu/kg DM from Cu sulfate (i.e. approximately five times NRC recommendation for Cu from CuSO4) (5X-SO4); 3). 22 mg Cu/kg DM from CuSO4 (2X-SO4); 4). 22 mg Cu/kg DM from a combination of 50% CuSO4 and 50% Cu-amino acid complex (50-50); and 5). 22 mg Cu/kg DM from a combination of 25% CuSO4, 50% Cu-amino acid complex, and 25% Cu oxide (CuG) (25-50-25). All heifers were supplemented with the Cu antagonists Mo (10 mg/kg DM), S (2,900 mg/kg DM), and Fe (500 mg/kg DM). These diets resulted in dietary Cu:Mo ratios that averaged 0.5:1 for Control, 4.5:1 for the 5X-SO4, and 2.4:1 for 2X-SO4, 50-50, and 25-50-25. Rate and efficiencies of gain and cell-mediated immune function were not different (P > 0.10) among treatments. Data suggest supplements containing combinations of inorganic and complexed Cu interacted differently in the presence of Mo, S, and Fe. Heifers consuming the 25-50-25 supplement in the Stall group initially lost hepatic Cu rapidly but this loss slowed from d 50 to d 100 compared to the Control (P = 0.07), 50-50 (P < 0.05), and 2X-SO4 (P < 0.05) heifers and was similar (P > 0.10) to that in the 5X-SO4 heifers. In the Pen group, total hepatic Cu loss tended to be greater for 25-50-25 and 2X-SO4 compared to 5X-SO4 heifers (P = 0.09 and P = 0.06, respectively); Cu loss in the 50-50 heifers was similar (P > 0.10) to that in the 5X-SO4 heifers. This suggests that supplementing combinations of inorganic and amino acid-complexed Cu was as effective in limiting hepatic Cu loss during antagonism as was increasing dietary Cu levels to five times the NRC recommendation. A combination of 25% CuSO4 , 50% Cu-amino acid complex, and 25% CuO limited liver accumulation of Mo compared to supplements without CuO and could provide a strategic supplementation tool in limiting the systemic effects of Cu antagonism in beef cattle.     

Effects of dietary protein level and clinoptilolite on the weight gain and liver mineral response of growing lambs to copper supplementation

Growing male Synthetic I (1/2 Finnish Landrace x 1/4 Dorset x 1/4 Rambouillet) lambs were used in two experiments (64 lambs in Exp. 1 and 63 in Exp. 2) to test the hypothesis that dietary CP level (9 or 14% of diet as fed) and(or) clinoptilolite (clino; 0 or 2% of diet) affects growth and tissue mineral concentrations of growing lambs fed supplemental Cu. Lambs were individually fed their respective diets ad libitum and killed after 12 wk (Exp. 1) or 16 wk (Exp. 2) to obtain carcass measurements, organ weights and liver mineral concentrations. In Exp. 1, 20 ppm added Cu (as CuSO4.5H2O) increased mortality and depressed BW gain (P less than .01) and daily feed intake (P less than .05) in the presence or absence of clino and at both levels of CP. Liver Cu concentration was greater (P less than .01) in lambs fed added Cu than in those not fed Cu (408 ppm vs 110 ppm, respectively). Neither CP nor clino affected liver Cu concentration. Clinoptilolite increased daily gain of lambs fed high CP but not low CP (P less than .01). In Exp. 2, clino in the diet had no effect on daily gain or daily feed, but 20 ppm Cu addition depressed daily gain (P less than .01) and gain/feed (P less than .07). Organ weights and levels of trace elements other than Cu in the liver generally were not affected by diet in either experiment. It is concluded that high dietary CP or 2% dietary clino did not protect against toxic signs of Cu when Cu was added to the basal diet (10 ppm Cu) at 10 or 20 ppm.     

Pathologic study of specific-pathogen-free chicks and hens inoculated with adenovirus isolated from hydropericardium syndrome.

The mortality and pathology caused by serotype 4 adenovirus, isolated from chickens with hydropericardium syndrome (HPS) in Japan, was investigated in specific-pathogen-free (SPF) chickens. One-day-old to 15-mo-old SPF chickens were inoculated intramuscularly, orally, and intranasally with liver homogenates from HPS chickens or isolated serotype 4 adenovirus. There were no clinical signs before death. The mortality rate in all groups of 1-day-old chicks was 100%, irrespective of the inoculum or inoculation route. Four-week-old chickens inoculated with liver homogenate also had a 100% mortality rate. Five-week-old chickens inoculated with cell culture of HPS adenovirus had a 40% mortality rate. The mortality rates of 7-mo-old hens inoculated with liver homogenates intramuscularly and orally were 75% and 25%, respectively. In 15-mo-old hens inoculated with liver homogenates intramuscularly, the mortality rate was 70%. Gross lesions were hydropericardium and swelling and congestion of the liver with occasional petechial hemorrhages. Histologically, the liver had diffuse or multifocal hepatic necrosis and hemorrhage with intranuclear inclusion bodies noted within hepatocytes. In the spleen, macrophages containing erythrocytes and yellow pigment were prominent in the red pulp. In the lung, a moderate diffuse macrophage infiltration was noted throughout the lung parenchyma, and these macrophages contained yellow pigment. In the pancreas of the chicks inoculated at 1 day old, there was multifocal necrosis of glands with intranuclear inclusion bodies. Intranuclear inclusion bodies were seen also in the gizzard, proventriculus, duodenum, cecum, kidney, and lung of the chicks inoculated at 1 day old. Immunohistochemically, the intranuclear inclusion bodies of various organs showed positive reactions against group I avian adenovirus. Adenovirus was recovered from the liver of chickens with HPS. This study indicates that HPS adenovirus is able to reproduce HPS lesions and mortality in SPF chicks and even adult chickens and that it is a highly pathogenic strain.     

Pathogenicity of serotype 8 fowl adenovirus isolated from gizzard erosions of slaughtered broiler chickens

The pathogenicity of serotype 8 fowl adenovirus (FAV), isolated from gizzard erosions of slaughtered broiler chickens, was investigated. In experiment 1, 29 5-day-old specific-pathogen-free (SPF) chickens were inoculated with the isolates of serotype 8 FAV, M013 (group 1) or G0054 (group 2) strain, via an oral route. There were no clinical signs in any of chickens after inoculation, and mild gizzard erosions were observed macroscopically and microscopically in three inoculated chickens of group 2. FAV was recovered from gizzards and rectums but was not recovered from pancreas and livers from chickens in both inoculated groups. In experiment 2, 27 1-day-old SPF chickens were inoculated with the G0054 strain by intramuscular route. Five, 6, and 3 inoculated chickens died on days 3, 4, and 5 postinoculation (PI), respectively. Four, 3, 1, and 1 inoculated chickens became moribund with severe clinical signs such as ruffled feathers, severe depression and closed eyes from days 3 to 6 PI, respectively. Macroscopically, the common characteristic of the gross lesions of dead chickens and euthanized moribund chickens was discoloration of liver. FAV was recovered from the gizzard, liver, pancreas and rectum. Virus titers in the liver and pancreas were high until day 6 PI. Histologically, necrotizing hepatitis and pancreatitis with intranuclear inclusion bodies were observed in the inoculated chickens. These results indicate that some strains of serotype 8 FAV are able to reproduce not only gizzard erosion by oral inoculation but inclusion body hepatitis (IBH) by intramuscular inoculation.     

蛋氨酸形式和饲粮蛋白质水平对黄羽肉鸡生产性能的影响

选用1日龄快长型岭南黄羽肉鸡公雏1500只,随机分为5个处理,每处理6个重复,每重复50只鸡,分别饲喂以下5种饲粮:正常蛋白质加Alimet饲粮(处理1)、正常蛋白质加DLM饲粮(处理2)、低蛋白质(比正常水平降低约1.5个百分点)加Alimet饲粮(处理3)、低蛋白质加DLM组饲粮(处理4)、正常蛋白质未加蛋氨酸饲粮(处理5)。结果表明,在等摩尔量有效成分添加基础上,Alimet比DLM更有利于提高黄羽肉鸡生长性能,降低饲料成本和死亡率;饲粮蛋白质水平和蛋氨酸形式对43～63日龄和0～63日龄黄羽肉鸡生长性能的影响存在互作效应,表现为在正常蛋白质水平时添加Alimet对黄羽肉鸡生长性能的改善效果优于DLM,且更有利于降低饲料成本,而在低蛋白质水平时添加Alimet和DLM则无显著差异;在本试验条件下,降低饲粮蛋白质水平会对黄羽肉鸡的生长性能、饲料成本和成活率产生不利影响。