This study aimed to get an optimum level of combined organic selenium, inorganic selenium and vitamin E in obtaining the best production and reproduction of quails as well as the highest antioxidant level in quail egg...This study aimed to get an optimum level of combined organic selenium, inorganic selenium and vitamin E in obtaining the best production and reproduction of quails as well as the highest antioxidant level in quail eggs. Seven hundred twenty quails （360 females and 360 males） at the age of six weeks old were used in this research. Nine treatment diets were： To （commercial diet/control）, Tl （diet containing 0.46 ppm inorganic Se ＋ 43.50 ppm vitamin E）, T2 （diet containing 0.46 ppm inorganic Se ＋ 87.00 ppm vitamin E）, T3 （diet containing 0.92 ppm inorganic Se ＋ 43.50 ppm vitamin E）, T4 （diet containing 0.92 ppm inorganic Se ＋87.00 ppm vitamin E）, Ts （diet containing 0.46 ppm organic Se ＋ 43.50 ppm vitamin E）, T6 （diet containing 0.46 ppm organic Se ＋ 87.00 ppm vitamin E）, T7 （diet containing 0.92 ppm organic Se ＋ 43.50 vitamin E） and Ts （diet containing 0.92 ppm organic Se 0.92 ＋ 87.00 ppm vitamin E）. The design of the experiment was a factorial nested design. Any significant differences among the treatments were analyzed by using Duncan＇s test. The results of this study indicated that 0.92 ppm organic selenium ＋ 43.50 ppm vitamin E （T7） in general gave the highest content of selenium in meat, in egg albumin, and in egg yolk as well as hatchability. The antioxidants as represented by vitamin E and glutathione peroxidase enzyme in the quail eggs were significantly higher as compared to that of quails fed other treatment diets.展开更多
AIM： To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells （HSCs）, in acute liver injury induced by CCI4, and to explore their role ...AIM： To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells （HSCs）, in acute liver injury induced by CCI4, and to explore their role in the recovery from hepatic fibrosis phase. METHODS： An acute liver damage model of rats was established by intraperitoneal injection of carbon tetrachloride （0.3 ml/100 g body weight） twice a week, then the rats were killed at 6, 24, 48, and 72 h after the first and third injection, respectively. A liver fibrosis model was established by the same injection for 8 wk. Then three rats were killed at 3, 7, 14, and 28 d after the last injection, respectively. The rats from the intervention group were fed with chow supplemented with vitamin E （250 mg/kg） and selenium （0.2 mg/kg）, and the rats in the normal control group and pathological group were given standard chow. Livers were harvested and stained with hematoxylin and eosin, Sirius red. Activated HSCs were determined by s-smooth muscle actin immunohistochemistry staining. Apoptotic HSCs were determined by dual staining with the terminal deoxynucleotidyl transferase UTP nick end labeling （TUNEL） and α-smooth muscle actin immunohistochemistry. Serum alanine aminotransferase and aspartate aminotransferase were also analyzed. RESULTS： In the acute liver damage model, the degree of liver injury was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, while the number of apoptotic HSCs was more in the intervention group than in the pathological group. In the liver fibrosis model, the degree of liver fibrosis was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, and the number of apoptotic HSCs was more in the intervention group than in the pathological group. CONCLUSION： Vitamin E and selenium supplementation at the given level can inhibit CCI4-induced activation and proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage phase. Vitamin E and selenium can also effectively decrease the degree of hepatic fibrosis and promote the recovery process.展开更多
文摘This study aimed to get an optimum level of combined organic selenium, inorganic selenium and vitamin E in obtaining the best production and reproduction of quails as well as the highest antioxidant level in quail eggs. Seven hundred twenty quails （360 females and 360 males） at the age of six weeks old were used in this research. Nine treatment diets were： To （commercial diet/control）, Tl （diet containing 0.46 ppm inorganic Se ＋ 43.50 ppm vitamin E）, T2 （diet containing 0.46 ppm inorganic Se ＋ 87.00 ppm vitamin E）, T3 （diet containing 0.92 ppm inorganic Se ＋ 43.50 ppm vitamin E）, T4 （diet containing 0.92 ppm inorganic Se ＋87.00 ppm vitamin E）, Ts （diet containing 0.46 ppm organic Se ＋ 43.50 ppm vitamin E）, T6 （diet containing 0.46 ppm organic Se ＋ 87.00 ppm vitamin E）, T7 （diet containing 0.92 ppm organic Se ＋ 43.50 vitamin E） and Ts （diet containing 0.92 ppm organic Se 0.92 ＋ 87.00 ppm vitamin E）. The design of the experiment was a factorial nested design. Any significant differences among the treatments were analyzed by using Duncan＇s test. The results of this study indicated that 0.92 ppm organic selenium ＋ 43.50 ppm vitamin E （T7） in general gave the highest content of selenium in meat, in egg albumin, and in egg yolk as well as hatchability. The antioxidants as represented by vitamin E and glutathione peroxidase enzyme in the quail eggs were significantly higher as compared to that of quails fed other treatment diets.
基金Supported by the Science Research Foundation of Ministry of Public Health of China, No. 98-2-280
文摘AIM： To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells （HSCs）, in acute liver injury induced by CCI4, and to explore their role in the recovery from hepatic fibrosis phase. METHODS： An acute liver damage model of rats was established by intraperitoneal injection of carbon tetrachloride （0.3 ml/100 g body weight） twice a week, then the rats were killed at 6, 24, 48, and 72 h after the first and third injection, respectively. A liver fibrosis model was established by the same injection for 8 wk. Then three rats were killed at 3, 7, 14, and 28 d after the last injection, respectively. The rats from the intervention group were fed with chow supplemented with vitamin E （250 mg/kg） and selenium （0.2 mg/kg）, and the rats in the normal control group and pathological group were given standard chow. Livers were harvested and stained with hematoxylin and eosin, Sirius red. Activated HSCs were determined by s-smooth muscle actin immunohistochemistry staining. Apoptotic HSCs were determined by dual staining with the terminal deoxynucleotidyl transferase UTP nick end labeling （TUNEL） and α-smooth muscle actin immunohistochemistry. Serum alanine aminotransferase and aspartate aminotransferase were also analyzed. RESULTS： In the acute liver damage model, the degree of liver injury was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, while the number of apoptotic HSCs was more in the intervention group than in the pathological group. In the liver fibrosis model, the degree of liver fibrosis was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, and the number of apoptotic HSCs was more in the intervention group than in the pathological group. CONCLUSION： Vitamin E and selenium supplementation at the given level can inhibit CCI4-induced activation and proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage phase. Vitamin E and selenium can also effectively decrease the degree of hepatic fibrosis and promote the recovery process.
