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叔丁基过氧化氢(tBHP)诱导大鼠肝线粒体在体外肿胀。

tBHP induced in vitro swelling of rat liver mitochondria.

作者信息

Kakkar P, Mehrotra S, Viswanathan P N

机构信息

Ecotoxicology Section, Industrial Toxicology Research Centre, Lucknow, India.

出版信息

Mol Cell Biochem. 1996 Jan 12;154(1):39-45. doi: 10.1007/BF00248459.

DOI:10.1007/BF00248459
PMID:8717415
Abstract

Tert-butyl hydroperoxide induced swelling of freshly isolated rat liver mitochondria was inhibited by butylated hydroxytoluene, butylated hydroxyanisole and alpha-tocopherol by acting at the initial phase. EDTA was more effective than EGTA in reducing the initial swelling and so were desferal and bipyrridyl. Spermine, an allosteric activator of calcium uptake, enhanced swelling whereas lanthanum and ruthenium red, the Ca2+ uniport blockers, reduced it. Inhibition of phospholipase A2 by dibucaine and Ca2+ activated proteases by antipain and leupeptin also reduced t-BHP induced swelling. The data indicate that peroxidative mitochondrial swelling involves an iron mediated initial rapid phase and a subsequent calcium dependent propagation phase.

摘要

叔丁基过氧化氢诱导的新鲜分离大鼠肝线粒体肿胀在初始阶段可被丁基化羟基甲苯、丁基化羟基茴香醚和α-生育酚抑制。乙二胺四乙酸(EDTA)在减轻初始肿胀方面比乙二醇双四乙酸(EGTA)更有效,去铁胺和联吡啶也是如此。精胺是钙摄取的变构激活剂,可增强肿胀,而镧和钌红是Ca2+单向转运体阻滞剂,可减轻肿胀。丁卡因对磷脂酶A2的抑制以及抗痛素和亮抑蛋白酶肽对Ca2+激活蛋白酶的抑制也可减轻叔丁基过氧化氢诱导的肿胀。数据表明,过氧化线粒体肿胀涉及铁介导的初始快速阶段和随后的钙依赖性传播阶段。

相似文献

1
tBHP induced in vitro swelling of rat liver mitochondria.叔丁基过氧化氢(tBHP)诱导大鼠肝线粒体在体外肿胀。
Mol Cell Biochem. 1996 Jan 12;154(1):39-45. doi: 10.1007/BF00248459.
2
The calcium sensor ruthenium red can act as a Fenton-type reagent.钙传感器钌红可作为一种芬顿型试剂。
Arch Biochem Biophys. 1996 Apr 15;328(2):239-44. doi: 10.1006/abbi.1996.0169.
3
Ruthenium red-catalyzed degradation of peroxides can prevent mitochondrial oxidative damage induced by either tert-butyl hydroperoxide or inorganic phosphate.钌红催化的过氧化物降解可预防由叔丁基过氧化氢或无机磷酸盐诱导的线粒体氧化损伤。
Arch Biochem Biophys. 1998 Jan 15;349(2):275-80. doi: 10.1006/abbi.1997.0450.
4
Relationships between Ca2+ release, Ca2+ cycling, and Ca2+-mediated permeability changes in mitochondria.线粒体中钙离子释放、钙离子循环与钙离子介导的通透性变化之间的关系。
J Biol Chem. 1985 Oct 15;260(23):12416-25.
5
Permeabilization of the inner mitochondrial membrane by Ca2+ ions is stimulated by t-butyl hydroperoxide and mediated by reactive oxygen species generated by mitochondria.叔丁基过氧化氢可刺激Ca2+离子引起线粒体内膜通透性增加,且这一过程由线粒体产生的活性氧介导。
Free Radic Biol Med. 1995 Mar;18(3):479-86. doi: 10.1016/0891-5849(94)00166-h.
6
Increased permeability of mitochondria during Ca2+ release induced by t-butyl hydroperoxide or oxalacetate. the effect of ruthenium red.叔丁基过氧化氢或草酰乙酸诱导的Ca2+释放过程中线粒体通透性增加。钌红的作用。
J Biol Chem. 1982 Jun 25;257(12):7161-71.
7
Effects of the general anaesthetic Propofol on the Ca2(+)-induced permeabilization of rat liver mitochondria.
FEBS Lett. 1991 Feb 11;279(1):45-8. doi: 10.1016/0014-5793(91)80246-y.
8
[Effect of antioxidants and complexons on mitochondrial swelling induced by thyroxine].
Biull Eksp Biol Med. 1977 Oct;84(10):426-8.
9
Permeability pathways of Ca2+ efflux from mitochondria: H+ specificity and reversibility of the permeability defect.线粒体中Ca2+外流的通透性途径:H+特异性与通透性缺陷的可逆性。
Adv Exp Med Biol. 1988;232:15-23. doi: 10.1007/978-1-4757-0007-7_2.
10
EGTA inhibits reverse uniport-dependent Ca2+ release from uncoupled mitochondria. Possible regulation of the Ca2+ uniporter by a Ca2+ binding site on the cytoplasmic side of the inner membrane.乙二醇双(2-氨基乙基醚)四乙酸(EGTA)抑制从解偶联线粒体中通过反向单向运输依赖的Ca2+释放。内膜细胞质侧的Ca2+结合位点可能对Ca2+单向运输体有调节作用。
J Biol Chem. 1988 Jan 25;263(3):1405-12.

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Alteration in mitochondrial thiol enhances calcium ion dependent membrane permeability transition and dysfunction in vitro: a cross-talk between mtThiol, Ca(2+), and ROS.线粒体巯基的改变增强了钙离子依赖的膜通透性转换和体外功能障碍:mtThiol、Ca(2+) 和 ROS 之间的串扰。
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