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本文引用的文献

1
Some effects of administering antithyroxine compounds to rats.给大鼠施用抗甲状腺素化合物的一些作用。
J Endocrinol. 1952 Jan;8(1):32-9. doi: 10.1677/joe.0.0080032.
2
Effect of metabolic inhibitors upon iodide transport in sheep thyroid slices.代谢抑制剂对绵羊甲状腺切片中碘转运的影响。
J Clin Endocrinol Metab. 1955 May;15(5):598-615. doi: 10.1210/jcem-15-5-598.
3
The relationship between metabolic activity and iodide-concentrating capacity of surviving thyroid slices.存活甲状腺切片的代谢活性与碘浓缩能力之间的关系。
J Clin Endocrinol Metab. 1955 Apr;15(4):442-58. doi: 10.1210/jcem-15-4-442.
4
THE EFFECT OF ATRACTYLATE AND OLIGOMYCIN ON THE BEHAVIOUR OF MITOCHONDRIA TOWARDS ADENINE NUCLEOTIDES.苍术酮和寡霉素对线粒体与腺嘌呤核苷酸相互作用的影响。
Biochem J. 1965 Jun;95(3):707-16. doi: 10.1042/bj0950707.
5
[METABOLIC INHIBITORS AND ACTION OF THYROTROPIN IN VITRO].[代谢抑制剂与促甲状腺素的体外作用]
C R Seances Soc Biol Fil. 1964;158:2500-4.
6
[RESPIRATORY CONTROL IN THYROID MITOCHONDRIA].[甲状腺线粒体中的呼吸控制]
C R Seances Soc Biol Fil. 1964;158:2504-8.
7
ENDOGENOUS ADP OF MITOCHONDRIA, AN EARLY PHOSPHATE ACCEPTOR OF OXIDATIVE PHOSPHORYLATION AS DISCLOSED BY KINETIC STUDIES WITH C14 LABELLED ADP AND ATP AND WITH ATRACTYLOSIDE.线粒体的内源性二磷酸腺苷,作为氧化磷酸化的早期磷酸受体,通过用碳-14标记的二磷酸腺苷、三磷酸腺苷及用苍术苷进行动力学研究得以揭示。
Biochem Biophys Res Commun. 1965 Jan 18;18:174-9. doi: 10.1016/0006-291x(65)90736-9.
8
BIOLOGICAL OXIDOREDUCTIONS.生物氧化还原反应
Annu Rev Biochem. 1964;33:729-90. doi: 10.1146/annurev.bi.33.070164.003501.
9
THYROIDAL IODIDE ACCUMULATION AND LOSS IN VITRO.甲状腺碘在体外的摄取与丢失
Endocrinology. 1965 Mar;76:441-53. doi: 10.1210/endo-76-3-441.
10
[ACTION OF THYROTROPIC HORMONE ON THE ENERGY METABOLISM OF THYROID TISSUE: I. IN VITRO EFFECTS OF THE HORMONE].[促甲状腺激素对甲状腺组织能量代谢的作用:I. 该激素的体外效应]
Bull Soc Chim Biol (Paris). 1964;46:1131-44.

线粒体抑制剂对甲状腺切片呼吸及碘化物能量依赖性摄取的影响。

Influence of mitochondrial inhibitors on the respiration and energy-dependent uptake of iodide by thyroid slices.

作者信息

Tyler D D, Gonze J, Lamy F, Dumont J E

出版信息

Biochem J. 1968 Jan;106(1):123-33. doi: 10.1042/bj1060123.

DOI:10.1042/bj1060123
PMID:4238489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1198477/
Abstract

The influence of mitochondrial inhibitors, including oligomycin, antimycin and rotenone, on the iodide and oxygen uptake and the nucleotide content of incubated sheep thyroid slices was investigated. Each inhibitor strongly suppressed both iodide and oxygen uptake, and decreased the nucleoside triphosphate content of the slices. In most cases the addition of glucose or mitochondrial substrates restored iodide uptake in inhibitor-treated slices. Inhibitor concentrations sufficient to inhibit iodide uptake strongly had only slight effects on the thyroidal Na(+)+K(+)-activated adenosine triphosphatase. It is concluded that the inhibitors produce their effects by the inhibition in vivo of mitochondrial oxidative phosphorylation. ATP synthesis appears to be essential for iodide uptake to occur, and the high-energy intermediates (or energized state) of oxidative phosphorylation cannot be used to energize the uptake process. To a limited extent glycolytic ATP synthesis can support iodide uptake, which is therefore not exclusively dependent on aerobic metabolism. The mechanism of energy-linked iodide uptake is discussed.

摘要

研究了包括寡霉素、抗霉素和鱼藤酮在内的线粒体抑制剂对孵育的绵羊甲状腺切片的碘摄取、氧摄取及核苷酸含量的影响。每种抑制剂均强烈抑制碘摄取和氧摄取,并降低切片中核苷三磷酸的含量。在大多数情况下,添加葡萄糖或线粒体底物可恢复抑制剂处理切片中的碘摄取。足以强烈抑制碘摄取的抑制剂浓度对甲状腺钠钾激活的三磷酸腺苷酶仅有轻微影响。得出的结论是,抑制剂通过在体内抑制线粒体氧化磷酸化发挥作用。ATP合成似乎是碘摄取发生所必需的,氧化磷酸化的高能中间体(或活跃状态)不能用于为摄取过程供能。糖酵解ATP合成在有限程度上可支持碘摄取,因此碘摄取并非完全依赖有氧代谢。文中讨论了能量关联碘摄取的机制。