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猪心线粒体中能量相关的钙离子积累的研究——镁离子的作用。

Studies on the energy-linked Ca2+ accumulation in pig heart mitochondria - role of Mg2'ons.

作者信息

Vial C, Otokore A, Goldschmidt D, Gautheron D C

出版信息

Biochimie. 1978;60(2):159-69. doi: 10.1016/s0300-9084(78)80749-4.

DOI:10.1016/s0300-9084(78)80749-4
PMID:667169
Abstract

Comparative intracellular distribution of Ca2+, Mg2+ and adenine nucleotides has been studied in pig heart by differential centrifugation or fractional extraction and has shown that Mg2+ and ATP are associated mainly with soluble fractions whereas Ca2+ and ADP are more tightly bound to subcellular structures. Ca2+ accumulation and Ca2+ stimulated respiration were studied in pig heart mitochondria under different energetic conditions in the absence or presence of phosphate. Ca2+ concentrations of about 1200 nmoles/mg protein inhibit Ca2+ accumulation, site I substrate oxidation and induce an efflux of mitochondrial Mg2+. These deleterious effects of Ca2+ on respiration occur even in the absence of phosphate or oxidizable substrate; they are completely prevented by ruthenium red only, and partially prevented by the addition of M2+ to the medium. The kinetics of Ca2+ uptake become of the sigmoidal type when Mg2+ is present. This cation strongly inhibits the rate of Ca2+ uptake in the presence of added phosphate and decreases the affinity of Ca2+ for its transport system. In the absence of phosphate, Mg2+ has no effect on Ca2+ uptake. The possible physiological implications of these findings are discussed

摘要

通过差速离心或分级提取研究了猪心脏中Ca2+、Mg2+和腺嘌呤核苷酸的细胞内分布比较,结果表明Mg2+和ATP主要与可溶性部分相关,而Ca2+和ADP与亚细胞结构结合更紧密。在有无磷酸盐存在的不同能量条件下,研究了猪心脏线粒体中的Ca2+积累和Ca2+刺激的呼吸作用。约1200纳摩尔/毫克蛋白质的Ca2+浓度会抑制Ca2+积累、位点I底物氧化,并导致线粒体Mg2+外流。即使在没有磷酸盐或可氧化底物的情况下,Ca2+对呼吸作用的这些有害影响依然存在;只有钌红能完全阻止这些影响,向培养基中添加M2+可部分阻止这些影响。当存在Mg2+时,Ca2+摄取动力学呈S形。在添加磷酸盐的情况下,这种阳离子强烈抑制Ca2+摄取速率,并降低Ca2+对其转运系统的亲和力。在没有磷酸盐的情况下,Mg2+对Ca2+摄取没有影响。讨论了这些发现可能的生理意义。

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1
Studies on the energy-linked Ca2+ accumulation in pig heart mitochondria - role of Mg2'ons.猪心线粒体中能量相关的钙离子积累的研究——镁离子的作用。
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Am J Physiol. 1981 Nov;241(5):H672-8. doi: 10.1152/ajpheart.1981.241.5.H672.

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J Bioenerg Biomembr. 1998 Dec;30(6):511-32. doi: 10.1023/a:1020576315771.
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J Bioenerg Biomembr. 1981 Aug;13(3-4):133-9. doi: 10.1007/BF00763835.