Muller Andreas S, Pallauf Josef, Most Erika
Institute of Animal Nutrition and Nutrition Physiology, Justus Liebig University Giessen, Germany.
J Trace Elem Med Biol. 2002;16(1):47-55. doi: 10.1016/S0946-672X(02)80008-6.
4 x 5 growing female rabbits (New Zealand White) with an initial live weight of 610 +/- 62 g were fed a torula yeast based semisynthetic diet low in selenium (<0.03 mg/kg diet) and containing <2 mg alpha-tocopherol per kg (group I). Group II received a vitamin E supplementation of 150 mg alpha-tocopherylacetate per kg diet, whereas for group III 0.40 mg Se as Na-selenite and for group IV both supplements were added. Selenium status and parameters of tissue damage were analyzed after 10 weeks on experiment (live weight 2,355 +/- 145 g). Selenium depletion of the Se deficient rabbits (groups I and II) was indicated by a significantly lower plasma Se content (group I: 38.3 +/- 6.23 microg Se/mL plasma, group II: 42.6 +/- 9.77, group III: 149 +/- 33.4, group IV: 126 +/- 6.45) and a significantly lower liver Se content (group I: 89.4 +/- 18.2 microg/kg fresh matter, group II: 111 +/- 26.2) as compared to the Se supplemented groups III (983 +/- 204) and IV (926 +/- 73.9). After 5 weeks on the experimental diets differences in the development of plasma glutathione peroxidase were observed. As compared to the initial status group (45.2 +/- 4.50) pGPx activity in mU/mg protein was decreased in group I (19.1 +/- 7.08), remained almost stable in the vitamin E supplemented group II (46.3 +/- 11.2) whereas an elevated enzyme activity was measured in the Se supplemented groups III (62.4 +/- 23.9) and IV (106 +/- 19.9). In the rabbit organs investigated 10 weeks of Se deficiency caused a significant loss of Se dependent cellular glutathione peroxidase activity (GPx1) of 94% (liver), 80% (kidney), 50% (heart muscle) and 60% (musculus longissimus dorsi) in comparison to Se supplemented control animals. Damage of cellular lipids and proteins in the liver was due to either Se or vitamin E deficiency. However damage was most severe under conditions of a combined Se and vitamin E deficiency. It can be concluded that the activity of plasma glutathione peroxidase is a sensitive indicator of Se deficiency in rabbits. The loss of GPx1 activity indicates the selenium depletion in various rabbit organs. Both selenium and vitamin E are essential and highly efficient antioxidants which protect rabbits against lipid and protein oxidation.
选用4×5只生长中的雌性新西兰白兔,初始体重为610±62克,给它们喂食一种以圆酵母为基础的半合成日粮,这种日粮含硒量低(<0.03毫克/千克日粮),每千克含α-生育酚<2毫克(第一组)。第二组每千克日粮补充150毫克α-生育酚醋酸酯形式的维生素E,第三组补充0.40毫克亚硒酸钠形式的硒,第四组同时添加这两种补充剂。实验进行10周后(体重2355±145克),分析硒状态和组织损伤参数。缺硒兔子(第一组和第二组)的硒缺乏表现为血浆硒含量显著降低(第一组:38.3±6.23微克硒/毫升血浆,第二组:42.6±9.77,第三组:149±33.4,第四组:126±6.45),肝脏硒含量也显著降低(第一组:89.4±18.2微克/千克鲜重,第二组:111±26.2),与补充硒的第三组(983±204)和第四组(926±73.9)相比。实验日粮喂养5周后,观察到血浆谷胱甘肽过氧化物酶活性发展存在差异。与初始状态组(45.2±4.50)相比,第一组中以毫单位/毫克蛋白计的血浆谷胱甘肽过氧化物酶(pGPx)活性降低(19.1±7.08),在补充维生素E的第二组中几乎保持稳定(46.3±11.2),而在补充硒的第三组(62.4±23.9)和第四组(106±19.9)中酶活性升高。在研究的兔子器官中,与补充硒的对照动物相比,缺硒10周导致硒依赖性细胞谷胱甘肽过氧化物酶活性(GPx1)显著丧失,肝脏中丧失94%,肾脏中丧失80%,心肌中丧失50%,背最长肌中丧失60%。肝脏中细胞脂质和蛋白质的损伤是由于缺硒或维生素E缺乏。然而,在硒和维生素E联合缺乏的情况下损伤最为严重。可以得出结论,血浆谷胱甘肽过氧化物酶活性是兔子缺硒的敏感指标。GPx1活性的丧失表明兔子各器官中硒的缺乏。硒和维生素E都是必需的且高效的抗氧化剂,可保护兔子免受脂质和蛋白质氧化。