不同硒源对肉鸡组织硒含量及谷胱甘肽过氧化物酶活力的影响

为了比较不同硒源对肉仔鸡组织硒含量及对肝脏和全血中谷胱甘肽过氧化物酶(GSH -Px)活力的影响 ,以不同的指标确定4种硒源在肉鸡饲料中的应用效果及适宜添加量 ,采用4×3因子完全随机设计 ,包括4种硒源 (硒化卡拉胶、硒蛋氨酸、富硒酵母、亚硒酸钠 ) ,3个水平 ,设基础日粮对照。测定21日龄和42日龄肉鸡的全血、肝脏、血浆、红细胞、肌肉的硒含量和GSH -Px活性。结果表明 ,硒蛋氨酸组在所有组织中均有最高的硒含量 ,4种硒源均能有效提高肝脏及全血GSH -Px活力 ,硒蛋氨酸和富硒酵母可显著提高红细胞中的硒含量 ,而亚硒酸钠则能有效提高红细胞的GSH -Px活力     

硒对黄粉虫谷胱甘肽过氧化物酶活性的影响

为探讨亚硒酸钠对黄粉虫幼虫血淋巴谷胱甘肽过氧化物酶（GSH—PX）活性的影响,将黄粉虫的中龄幼虫随机分成6组,饲喂含不同浓度的亚硒酸钠饲料。采用DTNB比色法测定GSH—PX活性。结果显示,饲喂含亚硒酸钠的饲料后黄粉虫幼虫血淋巴GSH—PX活力都明显上升：饲喂同一浓度的亚硒酸钠,幼虫血淋巴GSH—PX活力均比对照组高,只有加硒浓度为20mg／kg．80mg／kg在第16d时,黄粉虫血淋巴GSH—PX活力随着饲喂时间的延长而显著上升;饲喂不同浓度的亚硒酸钠,在硒浓度为5mg／kg、10mg／kg时,黄粉虫血淋巴GSH-PX活力随亚硒酸钠浓度的增加显著上升,在硒浓度为20mg／kg时开始下降。     

两种来源硒对肉仔鸡体内硒沉积和谷胱甘肽过氧化物酶活性的影响

应用有机硒和无机硒 (Na2 SeO3·5H2 O)饲喂艾维因肉仔鸡 ,在基础日粮中分别添加 0 .15、0 .30、0 .5 0、0 .70、1.0 0mg kg硒 ,以研究两种硒在肉仔鸡器官中的积累和对GSH -PX活性的影响。结果表明 :两种硒在组织器官中的积累率为肝脏 >胰脏 >胸肌 ,有机硒的沉积率高于无机硒。当添加两种来源硒的水平在 0 .1～ 1.0 0mg kg范围内 ,GSH -PX的活性随添加日粮硒浓度增加而增高 ;组织器官中的GSH -PX活性在添加有机硒浓度为 0 .30mg kg或无机硒浓度为0 .5 0mg kg为最高     

低硒日粮对畜禽淋巴器官组织结构和含硒量及谷胱甘肽过氧化物酶活性影响的研究

应用雏鸡、雏鸭、仔猪和奶山羊研究了低硒日粮对动物淋巴器官组织结构、含硒量及谷胱甘肽过氧化物酶(GSH—PX)活性的影响,结果表明,低硒日粮可显著地降低实难组动物淋巴器官及白细胞的含晒量和GSH—PX活性。淋巴器官含硒量与GSH—PX活性之间显著地正相关(P<0.01),低硒营养时两者同步降低。病理组织学检查,仔猪、雏鸡和雏鸭的淋巴组织发生明显的变性和坏死性变化;但奶山羊则以淋巴组织变性为主,坏死性变化不明显。     

谷胱甘肽过氧化物酶和谷胱甘肽转硫酶研究进展

谷胱甘肽过氧化物酶（GSH—Px）和谷胱甘肽转硫酶（GST）是一对抗氧化酶。GSH—Px为含硒半胱氨酸,至少有4种同工酶,催化还原H2O2和有机氢过氧化物。GST不合硒,有多种同工酶,不能分解H2O2,但具有清除过氧化物和解毒的双重功能。二者广泛存在于组织细胞、红细胞、血浆和乳中,与细胞损伤、缺氧、中毒、衰老、多种疾病的发生有关;GSH—Px活性也与机体硒水平密切相关。文章综述了GSH—Px和GST的分类与结构、性质、作用、检测原理、动物临床方面的应用及研究进展。     

酵母硒对肉仔鸡的生物安全性评价

本试验旨在研究饲粮添加不同水平酵母硒对爱拔益加(AA)肉仔鸡生长性能、血液血红蛋白含量和红细胞压积、血浆生化指标、器官指数和组织结构变化的影响,进而评价酵母硒对肉仔鸡的生物安全性。试验采用单因子完全随机设计,选用288只1日龄AA肉仔鸡,随机分为4个组,每个组6个重复,每个重复12只鸡(公母各占1/2)。各组分别在玉米-豆粕型基础饲粮中添加0、0.4、2.4和4.9 mg/kg(以硒计)的酵母硒试验。试验期为42 d。结果表明:1)与对照组相比,饲粮添加0.4和2.4 mg/kg酵母硒显著提高了22~42日龄肉仔鸡平均日采食量(P0.05);饲粮添加0.4、2.4和4.9 mg/kg酵母硒显著提高了1~42日龄肉仔鸡平均日增重(P0.05),而各酵母硒添加组之间差异不显著(P0.05)。2)饲粮添加不同水平酵母硒除对21日龄肉仔鸡血浆尿素氮含量和谷胱甘肽过氧化物酶(GSH-Px)活性以及42日龄肉仔鸡血浆GSH-Px活性有显著影响(P0.05)外,对其他血浆生化指标均无显著影响(P0.05)。与对照组相比,各酵母硒添加组21和42日龄肉仔鸡血浆GSH-Px活性随着酵母硒添加水平的增加均显著提高(P0.05),且饲粮添加2.4 mg/kg酵母硒显著降低了21日龄肉仔鸡血浆尿素氮含量(P0.05)。3)饲粮添加不同水平酵母硒对21和42日龄肉仔鸡血液血红蛋白含量和红细胞压积及42日龄肉仔鸡器官指数均无显著影响(P0.05),且并未引起主要器官的组织结构变化。综上所述,肉仔鸡饲粮中酵母硒的添加水平为0.4 mg/kg(饲粮中总硒含量为0.41 mg/kg)时,具有10倍的安全系数,即饲粮中以酵母硒形式添加硒对肉仔鸡是安全的。     

硒、碘营养缺乏对大鼠血浆甲状腺激素水平和肾脏、肝脏和甲状腺组织中γ—谷氨酰转肽酶活性的影响

硒营养缺乏导致大鼠甲状腺、肝脏、肾脏组织中γ—谷氨酰转肽酶活性显著上升,而碘缺乏不影响此酶的活性;单纯硒缺乏导致血浆T_3浓度下降;单纯碘缺乏和硒碘双重缺乏都不影响血浆T_3浓度,单纯碘缺乏导致血浆T_4浓度下降和TSH的浓度升高,硒缺乏加大这些变化。说明硒缺乏会加剧碘缺乏引起的甲状腺机能低下,γ—谷氨酰转肽酶活性不受甲状腺激素代谢水平的影响。     

不同硒水平对生长育肥猪血液生化指标的影响

试验研究了宁夏常用饲料中不同硒水平对生长育肥猪血液生化指标的影响。结果表明 :(1 )谷胱甘肽过氧化物酶 (GSH PX)活性随饲粮硒水平的增加 ,呈现下降 上升 下降的动态变化趋势。谷胱甘肽硫转移酶可反映缺硒的程度。 (2 )缺硒组仔猪血硒含量和全血中GSH PX均处于缺硒边缘状态 ,在临界值以下 ,不能满足仔猪的代谢需要。 (3)随饲粮硒水平的逐渐增加 ,猪瘟的抗体水平和淋巴细胞转化率明显升高 ,以饲粮中添加硒 0 45mg/kg时达到最高 ,仔猪发病率最低     

母种猪饲粮添加DL-硒代蛋氨酸对后代乳猪胰脏硒含量、抗氧化能力、消化酶活性以及GSH-Px mRNA表达的影响

本试验旨在研究母种猪饲粮中添加DL-硒代蛋氨酸对后代乳猪胰脏硒含量、抗氧化功能、消化酶活性以及谷胱甘肽过氧化物酶(GSH-Px)基因表达的影响.选取健康的胎次相同、妊娠后期的"长×大"二元杂交母猪12头,随机分为2组(亚硒酸钠组和DL-硒代蛋氨酸组),每组6个重复,每个重复1头猪.在基础饲粮(硒的实测值为0.04 mg/kg)中添加亚硒酸钠和DL-硒代蛋氨酸各0.3 mg/kg.试验分为妊娠后期(32 d)和泌乳期(28 d),共计60 d.结果表明:与亚硒酸钠组相比,DL-硒代蛋氨酸组使后代乳猪胰脏中硒含量增加54.29%(P<0.01),GSH-Px活性、超氧化物歧化酶(SOD)活性、总抗氧化能力(T-AOC)和还原型谷胱甘肽(GSH)水平分别提高22.84%(P<0.01)、24.60%(P<0.01)、112.52%(P<0.01)和131.14%(P<0.01),而丙二醛(MDA)含量降低了25.55%(P<0.01);胰淀粉酶、蛋白酶和脂肪酶活性分别提高50.81%(P<0.01)、17.61%(P<0.05)和14.87%(P<0.05);GSH-Px mRNA表达增高了31.00%(P<0.01).结果提示,母种猪饲粮中添加DL-硒代蛋氨酸较亚硒酸钠能显著提高后代乳猪胰脏组织硒含量,增强抗氧化功能和消化酶分泌,并能提高GSH-Px mRNA表达量.     

1～21日龄岭南黄羽肉仔鸡饲粮硒适宜供给量的研究

本试验旨在研究饲粮不同硒添加水平对1~21日龄岭南黄羽肉仔鸡生长性能和抗氧化性能的影响,以探讨快大型岭南黄羽肉仔鸡饲养前期的饲粮硒适宜供给量。选用1日龄健康、发育良好的快大型岭南黄羽肉公雏鸡1 200只,根据体重随机分为5个组,每组6个重复,每个重复40只鸡,试验1组(对照组)饲喂基础饲粮(硒水平为0.039 mg/kg),试验2~5组饲粮在基础饲粮中分别添加0.075、0.150、0.225和0.300 mg/kg硒,试验期21 d。结果表明:本试验条件下:1)与对照组相比,饲粮添加0.300 mg/kg硒显著降低1~21日龄岭南黄羽肉仔鸡的末重(P0.05),显著提高料重比(P0.05),且0.300 mg/kg硒添加组的平均日增重显著低于其他各水平硒添加组(P0.05)。2)与对照组相比,饲粮添加0.075和0.150 mg/kg硒显著提高21日龄岭南黄羽肉仔鸡的血浆谷胱甘肽过氧化物酶(GSH-Px)活性(P0.05),饲粮添加0.225和0.300 mg/kg硒显著降低血浆丙二醛(MDA)含量(P0.05)。各水平硒添加组的红细胞GSH-Px活性均显著高于对照组(P0.05)。3)与对照组相比,饲粮添加0.075、0.150和0.225mg/kg硒显著提高21日龄岭南黄羽肉仔鸡的肝脏GSH-Px活性(P0.05),0.075和0.150 mg/kg硒添加组的肝脏MDA含量显著低于对照组和0.300 mg/kg硒添加组(P0.05)。综合考虑,为获得较好生长性能和抗氧化性能,1~21日龄岭南黄羽肉仔鸡饲粮硒适宜添加水平为0.075 mg/kg,基础饲粮中硒水平为0.039 mg/kg,则1~21日龄岭南黄羽肉仔鸡饲粮硒适宜供给量为0.114 mg/kg;以肝脏MDA含量为依据,通过非线性回归分析估测得到1~21日龄岭南黄羽肉仔鸡饲粮硒适宜供给量为0.130 mg/kg。     

硒和维生素E在硒缺乏动物自由基代谢中作用机制的研究

为阐明硒缺乏动物自由基代谢与硒缺乏症发病学的关系，以及硒和ＶＥ在自由基代谢中的作用采用低Ｓｅ日粮饲喂小鼠，并对血液、肝组织丙二醛、硒谷胱甘肽过氧化物酶、相关向量元素及自由基水平进行了系统检测。     

低硒雏鸡口服亚硒酸钠后机体硒浓度及谷胱甘肽过氧化物酶的活性动态变化规律

低硒雏鸡口服亚硒酸钠后，对不同时间血液（清）、肝、肾、胰、心、脾硒浓度及谷胱甘肽过氧化物酶活性的动态变化规律测定。结果发现随着硒浓度的变化，酶活性也发生相应变化，但１９２ｈ后肾、脾酶活性出现第２次升高而其硒浓度仍降低。值得注意的是酶活性的变化总滞后于硒浓度的变化     

Thyroid hormone concentrations in selenium deficient and selenium sufficient cattle

Selenium deficient calves when compared to selenium supplemented calves had increased plasma thyroxine concentrations and decreased plasma tri-iodothyronine concentrations. These changes in the selenium deficient calves were accompanied by significant increases in plasma urea and creatinine concentrations and decreased plasma alkaline phosphatase activity. The demonstration that low selenium status can cause imbalances in thyroid hormone metabolism may provide an explanation for some of the effects of the deficiency.     

有机硒对仔獭兔生长性能和组织抗氧化能力的影响

选择80只60日龄的法系獭兔研究酵母硒对生长性能和组织抗氧化能力及GSH-Px mRNA表达丰度的影响。随机分为4个处理组,对照组、硒添加组(1～3)的饲粮是在基础日粮中分别添加0、0.1、0.3、0.5 mg/kg酵母硒,试验期30 d。结果表明:硒添加2组与3组的饲料增重比分别降低12.86%与9.02%,而皮张面积却分别增加11.30%与11.97%(P<0.05);在血浆中,添加2组与3组的GSH-Px活性与CAT活性均极显著升高(P<0.01);在肝组织中,添加1组的GSH-Px活性与CAT活性显著升高(P<0.05),而添加2组的MDA含量降低得最多;在肌肉组织中,添加1～3组的GSH-Px活性分别显著升高17.66%、57.91%与65.02%(P<0.05);肝与背最长肌的GSH-Px mRNA表达水平随酵母硒添加水平升高而升高(P<0.01)。综合分析表明,仔獭兔饲粮中添加酵母硒的最适量为0.3 mg/kg。     

鸡血藤总黄酮对猪圆环病毒2型感染小鼠脾脏氧化应激的影响

试验旨在探讨鸡血藤总黄酮（TFSD）对猪圆环病毒2型（PCV2）感染小鼠脾脏氧化应激的影响。将70只昆明小鼠随机分为7组,对照组、TFSD组（100 mg/kg体重）、PCV2组、PCV2＋维生素C （VC）组、PCV2＋不同浓度TFSD （25、50和100 mg/kg体重）组,每组10只,连续3 d采用灌胃和腹腔注射PCV2病毒液的方法建立小鼠氧化应激模型,第4~6天每天按上述分别灌胃给予生理盐水、VC或TFSD。第7天剖杀小鼠,取脾脏分析黄嘌呤氧化酶（XOD）、髓过氧化物酶（MPO）和超氧化物歧化酶（SOD）活力,并检测还原型谷胱甘肽（GSH）和氧化型谷胱甘肽（GSSG）水平,计算GSH/GSSH。结果显示,PCV2感染小鼠后,脾脏中XOD与MPO的活力及GSSG水平显著上升（P＜0.05）,SOD活力、GSH水平及GSH/GSSG显著下降（P＜0.05）。TFSD处理小鼠脾脏的SOD活力、GSH水平和GSH/GSSG比值均显著高于PCV2组（P＜0.05）,而XOD、MPO活力和GSSG水平则显著低于PCV2组（P＜0.05）,对PCV2引起的氧化应激相关酶活力与相关分子水平变化的抑制作用优于VC。结果表明,鸡血藤总黄酮对PCV2诱导的小鼠脾脏氧化应激有良好的调节作用。     

Effect of Total Flavonoids of Spatholobus suberectus Dunn on Oxidative Stress in Mice Spleen Induced by PCV2

The aim of this study was to investigate the effect of total flavonoids of Spatholobus suberectus Dunn (TFSD) on porcine circovirus type 2 (PCV2) induced oxidative stress in mice spleen.70 Kunming mice were divided into 7 groups:Control group, TFSD group (100 mg/(kg·BW)), PCV2 group, PCV2+vitamin C (VC) group, and PCV2+various concentrations of TFSD groups (25, 50 and 100 mg/(kg·BW)). Mice were continuously treated with PCV2 via both intragastric administration and intraperitoneal injection for 3 d to establish oxidative stress models. From the 4th to 6th day, mice were intragastric administrated with saline, VC or TFSD, respectively, according to the grouping method. At the 7th day, the activities of xanthine oxidase (XOD), myeloperoxidase (MPO) and superoxide dismutase (SOD), the levels of glutathione (GSH) and oxidized glutathione (GSSG), and the ratio of GSH to GSSG in the mice spleen were analyzed. The results showed that PCV2 infection significantly upregulated the XOD and MPO activities and GSSG content(P <0.05), and dramatically downregulated the SOD activity, GSH level and the ratio of GSH to GSSG (P <0.05) in the mice spleen.Compared to PCV2 group, the SOD activity, GSH content and the ratio of GSH to GSSG in mice treated with TFSD were significantly increased (P <0.05), while the activities of XOD and MPO and the level of GSSG were significantly decreased (P <0.05), showing better performance in the inhibition of PCV2 induced changes of oxidative stress associated enzyme activities and moledule levels than VC.In conclusion,TFSD had regulative effect on the oxidative stress induced by PCV2 in mouse spleen.     

Down-regulation of GPx1 mRNA and the loss of GPx1 activity causes cellular damage in the liver of selenium-deficient rabbits

The effects of 10 weeks of dietary selenium and/or vitamin E deficiency (< 0.03 mg Se and 1.5 mg vitamin E per kg diet) on body Se and vitamin E stores and on the down-regulation of liver cellular glutathione peroxidase (GPx1) and plasma glutathione peroxidase (GPx3) were examined in growing female New Zealand White rabbits in comparison to Se (+ 0.40 mg Se/kg diet) and/or vitamin E (+ 150 I.U./kg diet) supplemented controls. Additionally plasma lactate dehydrogenase (LDH) activity, liver thiobarbituric acid-reactive substances (TBA-RS) and liver protein carbonyls were measured to assess the development of oxidative stress during an alimentary Se and/or vitamin E deficiency. Significantly decreased concentrations of Se and vitamin E in plasma (Se: − 70%; vitamin E: − 87%) and liver (Se: − 90%; vitamin E: − 95%) indicated an efficacious Se and vitamin E depletion of the rabbits within 10 weeks. GPx1 messenger RNA levels (GPx1 mRNA) in the livers of Se-depleted rabbits were down-regulated to 1/3–1/8 of the Se supplemented controls. GPx1 enzyme activity in the livers of Se-deficient rabbits declined to 10% of the Se-supplied control rabbits. A significantly elevated LDH activity in the blood plasma of Se- and vitamin E-deficient rabbits indicated a general impairment of tissues. Markedly increased TBA-RS concentrations and protein carbonyl contents in the livers of Se- and vitamin E-deficient rabbits gave further evidence for severe oxidative damage of cellular lipids and proteins during an alimentary Se and/or vitamin E deficiency. Both a full expresssion of GPx1 attained by dietary Se supplementation and dietary vitamin E supply effected an almost complete protection against oxidative cellular damage of the liver.     

滞育发动前家蚕滞育性与非滞育性卵的谷胱甘肽氧化还原循环状态分析

为了调查滞育和非滞育性家蚕卵的谷胱甘肽氧化还原循环在滞育发动前是否存在差异,利用分光光度法检测滞育发动前(25℃中蚕卵产下后0～24 h)滞育与非滞育蚕卵的谷胱甘肽含量和相关代谢酶活性。滞育发动前,滞育性家蚕卵中的还原型谷胱甘肽(GSH)含量、氧化型谷胱甘肽(GSSG)含量、总谷胱甘肽(GSH+2GSSG)含量和GSH/GSSG比值变化不显著,谷胱甘肽S-转移酶(GST)活性变化不显著,但硫氧还蛋白过氧化物酶(TPX)活性下降23%,谷胱甘肽还原酶(GR)活性升高57%;非滞育性家蚕卵中的GSH含量及TPX和GST活性变化不显著,但GSSG含量升高61%,GSH+2GSSG含量升高41%,GSH/GSSG比值下降33%,GR活性下降16%。与非滞育性家蚕卵相比,滞育发动前滞育性家蚕卵中的GSH含量、GSSG含量和GSH+2GSSG含量较低,GSH/GSSG比值较高,TPX活性较低,GST活性无显著差异,GR活性较高。两种蚕卵中都未能检测到谷胱甘肽过氧化物酶(GPX)和硫氧还蛋白还原酶(TrxR)活性。结果表明,滞育发动前滞育性家蚕卵中较低的TPX活性和较高的GR活性共同导致较高的GSH/GSSG比值,使其谷胱甘肽氧化还原循环处于相对还原态。     

Selenium reference ranges in New Zealand cattle

AIM: To compare serum selenium and liver selenium concentrations with whole blood concentrations in samples taken at the same time from unsupplemented cattle, and to use these comparisons to establish a reference range for use in diagnosing selenium deficiency. METHODS: Selenium was measured in concurrent whole blood, serum and liver samples obtained from cattle in unsupplemented herds in the Manawatu, Waikato and Wairarapa regions of New Zealand. The results were statistically analysed. RESULTS: The revised reference ranges are as follows. [table: see text] CONCLUSION: The serum and liver selenium concentrations used as reference values prior to this study were inaccurate for the detection of selenium deficiency.     

Studies on vitamin E and selenium deficiency in young pigs. IV. Effect on coagulation system.

An evaluation of the coagulation system has been conducted in vitamin E and/or selenium deficient swine. The partial thromboplastin time, plasma fibrinogen concentration, platelet lipid peroxides, as well as the fibrinogen/fibrin degradation products were not found to be significantly affected by either vitamin E deficiency, selenium deficiency, or deficiency of both. With selenium deficiency, the prothrombin time was shortened (p less than 0.05). The platelet count and platelet turnover were greatly decreased by both vitamin E (p less than 0.001) and selenium deficiency (p less than 0.005). Further-more, the survival of platelets labelled with 75Se-selenomethionine and the per cent isotope incorporated into platelets were reduced (p less than 0.05 and p less than 0.005) in association with vitamin E deficiency, but not with selenium deficiency. These results were interpreted as evidence of a platelet production defect and possibly a platelet function defect in vitamin E deficient animals. Selenium deficiency were also associated with decreased (p less than 0.05) survival of fibrinogen labelled with 75Se-selenomethionine and increased (p less than 0.05) turnover of fibrinogen. From these fibrinogen kinetic findings, it was considered that chronic low grade disseminated intravascular coagulation possibly occurs in selenium deficient animals, probably in relation to the development of hepatosis dietetica or widespread microvascular damage. However, other possibilities such as increased fibrinogenolysis in relation with hepatosis dietetica or an intrinsic fibrinogen defect due to selenium deficiency also need to be taken into consideration and have not been ruled out in the present study.