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Transient induction of the mitochondrial permeability transition by uncoupler plus a Ca(2+)-specific chelator.

作者信息

Igbavboa U, Pfeiffer D R

机构信息

Hormel Institute, University of Minnesota, Austin 55912.

出版信息

Biochim Biophys Acta. 1991 Sep 13;1059(3):339-47. doi: 10.1016/s0005-2728(05)80219-1.

DOI:10.1016/s0005-2728(05)80219-1
PMID:1716985
Abstract

Determinations of aqueous space volumes, swelling and Mg2+ release experiments demonstrate that EGTA plus uncoupler causes the permeability transition in Ca(2+)-loaded mitochondria. Extramitochondrial Mg2+ is required to obtain this effect. Changes in transition-dependent parameters are smaller and more varied when induced by EGTA plus uncoupler than when induced by Ruthenium red plus uncoupler, although inhibitor-sensitive experiments show that the same basic mechanism is involved in both cases. Measurements of sucrose trapping and sucrose or inulin accessible space, after changes in transition-dependent parameters are complete, indicate that rapid reversal occurs when the transition is induced by EGTA plus uncoupler, explaining why limited responses are obtained. Data support the hypothesis that an external divalent cation binding site regulates activity of the mitochondrial Ca2+ uniporter.

摘要

相似文献

1
Transient induction of the mitochondrial permeability transition by uncoupler plus a Ca(2+)-specific chelator.
Biochim Biophys Acta. 1991 Sep 13;1059(3):339-47. doi: 10.1016/s0005-2728(05)80219-1.
2
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Reoxygenation-induced mitochondrial damage is caused by the Ca2+-dependent mitochondrial inner membrane permeability transition.复氧诱导的线粒体损伤是由钙离子依赖性线粒体内膜通透性转变引起的。
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Inhibition of the mitochondrial Ca2+ uniporter by pure and impure ruthenium red.
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