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缺硒牛红细胞对氧化损伤的抵抗力及白细胞还原硝基蓝四氮唑的能力。

Erythrocyte resistance to oxidative damage and leucocyte capacity to reduce nitroblue tetrazolium in selenium-deficient cattle.

作者信息

Gutzwiller A

机构信息

Swiss Federal Research Station for Animal Production, Posieux, Switzerland.

出版信息

Zentralbl Veterinarmed A. 1998 Jul;45(5):271-8. doi: 10.1111/j.1439-0442.1998.tb00827.x.

Abstract

Simmental x Red Holstein steers which were fed roughage with a low selenium (Se) content received either a Se-delivering bolus orally (group Se+) or no Se supplement (group Se-). Weight gain was not influenced by Se supplementation. When blood for the in-vitro assays was drawn 8 weeks after bolus administration, erythrocyte glutathione peroxidase (GSH-Px) activity was much higher in the Se+ than in Se- animals (P < 0.01). The addition of acetylphenylhydrazine to the blood samples induced significantly fewer Heinz bodies in erythrocytes of Se+ animals (P < 0.01). It was shown that H2O induced the formation of identical amounts of thiobarbituric acid reactive substances (TBARS) in the erythrocytes of Se+ and Se- animals. Thus, GSH-Px seems to be more important for the protection of haemoglobin than for the protection of erythrocyte lipids from oxidative damage. After addition of endotoxin and nitroblue tetrazolium to blood samples, leucocytes of Se+ and of Se- animals reduced the same amount of nitroblue tetrazolium. Thus, selenium deficiency apparently had no negative effect on the oxidative burst of leucocytes.

摘要

西门塔尔牛与红荷斯坦牛杂交的阉牛,饲喂低硒(Se)含量的粗饲料,一组口服含硒大丸剂(Se+组),另一组不补充硒(Se-组)。补硒对体重增加没有影响。在给予大丸剂8周后采集用于体外试验的血液时,Se+组动物红细胞谷胱甘肽过氧化物酶(GSH-Px)活性比Se-组动物高得多(P<0.01)。向血样中添加乙酰苯肼后,Se+组动物红细胞中诱导产生的海因茨小体明显较少(P<0.01)。结果表明,H2O在Se+组和Se-组动物红细胞中诱导产生相同量的硫代巴比妥酸反应性物质(TBARS)。因此,GSH-Px对血红蛋白的保护作用似乎比对红细胞脂质免受氧化损伤的保护作用更重要。向血样中添加内毒素和硝基蓝四氮唑后,Se+组和Se-组动物的白细胞还原相同量的硝基蓝四氮唑。因此,缺硒显然对白细胞的氧化爆发没有负面影响。

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