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Deficient and excess dietary selenium levels affect growth performance, blood cells apoptosis and liver HSP70 expression in juvenile yellow catfish Pelteobagrus fulvidraco

文献类型： 外文期刊

作者： Hu, Jun-Ru 1 ; Huang, Yan-Hua 2 ; Wang, Guo-Xia 2 ; Wu, Ying-Xia 1 ; Xian, Jian-An 1 ; Wang, An-Li 1 ; Cao, Jun-Ming 3 ;

作者机构： 1.S China Normal Univ, Coll Life Sci, Guangdong Prov Key Lab Healthy & Safe Aquaculture, Key Lab Ecol & Environm Sci Guangdong Higher Educ, Guangzhou 510631, Guangdong, Peoples R China

2.Guangdong Acad Agr Sci, Inst Anim Sci, Guangzhou 510640, Guangdong, Peoples R China

3.Guangdong Acad Agr Sci, Inst Anim

关键词： Selenium (Se);Growth;Apoptosis;Heat shock protein 70;Yellow catfish

期刊名称：FISH PHYSIOLOGY AND BIOCHEMISTRY （ 影响因子：2.794； 五年影响因子：2.876 ）

ISSN：

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收录情况： SCI

摘要： We investigated the effects of deficient and excess dietary selenium (Se) on growth, blood cells apoptosis and liver heat shock protein 70 (HSP70) expression in juvenile yellow catfish (Pelteobagrus fulvidraco). After 8 weeks, yellow catfish (initial weight: 2.12 +/- A 0.01 g) fed isonitrogenous and isolipid diets containing < 0.05 (deficient dietary Se) or 6.5 (excess dietary Se) mg Se/kg displayed a significantly lower weight gain ratio (WGR) than those fed a diet containing 0.23 (normal dietary Se) mg Se/kg. As dietary Se levels increased, liver Se concentration, glutathione peroxidase activity and the hepatosomatic index increased significantly. Plasma glucose concentration was highest in the normal treatment compared with the excess dietary Se treatment. Both deficient and excess dietary Se lead to increased reactive oxygen species (ROS) production and apoptosis ratio in blood cells, whereas only excess dietary Se increased their cytoplasmic free-Ca2+ (CF-Ca2+) concentration. Excess dietary Se also resulted in the highest level of HSP70 expression, thereby possibly providing a protective mechanism against oxidative stress. These results indicate that both deficient and excess dietary Se restrained the growth of juvenile yellow catfish and caused oxidative stress. The overproduction of ROS may act as a signal molecule mediate apoptosis when dietary Se deficiency. Both ROS and CF-Ca2+ were recorded when dietary Se excess, suggesting that Ca2+ may be activated by Se and play a major role during Se-induced oxidative stress and cell apoptosis.

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