维生素E对大鼠肝脏中硒氧化态的影响。

The effect of vitamin E on the oxidation state of selenium in rat liver.

作者信息

Diplock A T, Baum H, Lucy J A

出版信息

Biochem J. 1971 Aug;123(5):721-9. doi: 10.1042/bj1230721.

DOI:10.1042/bj1230721

PMID:5124381

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1177073/

Abstract

(75)Se as Na(2) (75)SeO(3) was administered orally to rats under different nutritional conditions. 2. The selenium found in the liver subcellular organelle fractions was present in at least three oxidation states: acid-volatile selenium, assumed to be selenide, zinc-hydrochloric acid-reducible selenium, assumed to be selenite, and higher oxidation states of selenium and organic derivatives, called selenate for convenience. 3. The proportion of the total selenium present as selenide present as selenide is susceptible to oxidation in vitro, which can be prevented by the addition of antioxidants in vitro. 4. The proportion of selenide is also directly related to the vitamin E status of the rats, and treatment of vitamin E-deficient rats with vitamin E results in an increase in the proportion of selenide. 5. Freezing the liver in situ before preparation of the organelle fractions did not alter the susceptibility of the selenide proportion to dietary vitamin E, indicating that the observed effects occur in vivo and not as a result of oxidation post mortem. 6. Intravenous administration of Na(2) (75)SeO(3), to rats whose alimentary tract was partially sterilized by neomycin treatment, gave a similar result to that in paragraph 4, indicating that the reduction of selenite to selenide probably occurs in vivo, and that intestinal micro-organisms are not responsible. 7. Treatment of vitamin E-deficient rats with silver produced a fall in the total (75)Se content of the liver, an effect only partially reversed by vitamin E administration. The proportion of the total selenium present as selenide was also lowered by the treatments with silver, and vitamin E significantly reversed this trend in most cases. 8. These results are consistent with the hypothesis that the active form of Se may be selenide and that the selenide may form part of the active centre of an uncharacterized class of catalytically active non-haem-iron proteins that are protected from oxidation in vivo by vitamin E.

摘要

在不同营养条件下，将（75）硒酸钠（2）（75）亚硒酸钠经口给予大鼠。2. 在肝脏亚细胞细胞器组分中发现的硒至少以三种氧化态存在：酸挥发性硒，假定为硒化物；锌 - 盐酸可还原硒，假定为亚硒酸盐；以及硒的较高氧化态和有机衍生物，为方便起见称为硒酸盐。3. 以硒化物形式存在的总硒比例在体外易被氧化，体外添加抗氧化剂可防止这种氧化。4. 硒化物的比例也与大鼠的维生素E状态直接相关，用维生素E治疗维生素E缺乏的大鼠会导致硒化物比例增加。5. 在制备细胞器组分之前原位冷冻肝脏，并未改变硒化物比例对膳食维生素E的敏感性，表明观察到的效应发生在体内，而非死后氧化的结果。6. 对经新霉素处理使消化道部分灭菌的大鼠静脉注射（75）硒酸钠（2），得到与第4段相似的结果，表明亚硒酸盐还原为硒化物可能发生在体内，且肠道微生物不是原因。7. 用银处理维生素E缺乏的大鼠会导致肝脏中总（75）硒含量下降，维生素E给药仅部分逆转这种效应。用银处理也会降低以硒化物形式存在的总硒比例，在大多数情况下维生素E能显著逆转这一趋势。8. 这些结果与以下假设一致：硒的活性形式可能是硒化物，且硒化物可能构成一类未表征的具有催化活性的非血红素铁蛋白活性中心的一部分，该活性中心在体内受到维生素E的保护而不被氧化。