摘要
用1日龄Arbir Acres雏鸡64只(1/2,1/2♀),分成2组,分别喂以含锰(Mn)17ppm的缺Mn玉米-豆饼基础饲粮和含Mn137ppm的补Mn(试剂级MnSO_4·H_2O)饲粮28天。结果表明,实用饲粮Mn缺乏促使肝和心的Mn含量降低(P<0.01),心脏含Mn超氧化歧化酶(MnSOD)活性降低约26％(P<0.01),而对肝MnSOD无影响(P>0.05)。Nn缺乏导致心和肝线粒体超微结构异常,包括心线粒体萎缩退化、“分裂”趋势、肝线粒体的“融合”趋势、心肝线粒体的脊排列不规则和有的外膜丢失,且心和肝粗面内质网均明显扩张。Mn缺乏使鸡腿病发生率增加,血浆谷草转氨酶(GOT)、谷丙转氨酶(GPT)活性和尿酸含量升高(P<0.01),肌酸磷酸激酶(CPK)活性虽有增加趋势,但不显著(P<0.05)。鸡的生长性能无显著变化(P>0.05)。
Sixty-four day-old Arbor Acres broilers ( 1/2 male, 1/2 female ) ,were randomly allotted to two treatments and fed ad libitum either a basal corn-soybean meal Mn-deficient diet containing 17ppm Mn or the Mn-supplemented ( reagent grade MnSO4·H2O ) diet containing 137ppm Mn for 28 days. Mn deficiency caused the reductions of Mn concentrations of liver and heart ( P<0.01 ) and also MnSOD activity of heart about 26% ( P<0.01 ) , but not MnSOD of liver ( P>0.05 ). Abnormalities of mitochondrial ultrastructures were observed both in heart and liver as shown by heart mitochondrial degeneration with a 'split' trend, liver mitochondrial 'combination' and irregular sequences of critae and losses of some outer membrances of some mitochondria both in heart and liver. Coarse reticulum enlargements of both heart and liver were also observed. Mn deficiency caused higher incidence of leg abnormality and higher plasma glutamate oxalacetate transaminase(GOT) and glutamate pyruvate transaminase ( GPT ) activity and uric acid level ( P<0.01 ), and plasma creatine phosphokinase ( CPK ) activity ( P>0.05 ) , nevertheless the growth performance of chicks was not affected ( P>0.05 ) .
出处
《畜牧兽医学报》
CAS
CSCD
北大核心
1992年第2期97-101,共5页
ACTA VETERINARIA ET ZOOTECHNICA SINICA
关键词
线粒体
超微结构
肉鸡
锰
缺乏
Mn deficiency, Tissue MnSOD activity, Mitochondrial ultrastructures, Broiler chicks
