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正常大鼠及给予四氯化碳一小时后肝细胞钙的细胞内分布。

The intracellular distribution of liver cell calcium in normal rats and one hour after administration of carbon tetrachloride.

作者信息

Kröner H

出版信息

Biochem Pharmacol. 1982 Mar 15;31(6):1069-73. doi: 10.1016/0006-2952(82)90344-6.

DOI:10.1016/0006-2952(82)90344-6
PMID:6805475
Abstract

In order to recognize the significance of elevated liver calcium level in the early phase of carbon tetrachloride intoxication, the subcellular distribution of calcium in liver was investigated one hour after administration of CCl4 intraperitoneally. During preparation of subcellular fractions attempts were made to prevent redistribution of calcium by adding Ruthenium Red and EGTA or LaCl3 to homogenization medium, and by shortening of differential centrifugation to a minimum. The latter caused a loss of purity in sub cellular fractions which was overcome by correction of calcium values from atom absorption spectrometry by means of marker enzyme activity. The calcium levels in normal rat liver were found to be 70 nmoles/g liver wet wt in cytosol, 310 nmoles/g liver in microsomes and about 500 nmoles/g liver in mitochondria. A minor part of the latter fraction may belong to nuclei and plasma membranes. One hour after CCl4 administration calcium levels in cytoplasma were not altered, in microsomes were decreased to 200 nmoles/g liver and in mitochondria were elevated to 2.5 mumoles/g liver. In rats pretreated with vitamin D the whole additional calcium, after carbon tetrachloride application in the range of 9 mumoles/g liver, was sequestrated in mitochondria. In the early phase of carbon tetrachloride intoxication all border membranes of liver cells have to participate in bringing about the reversible increase of liver cell calcium.

摘要

为了认识到四氯化碳中毒早期肝钙水平升高的意义,在腹腔注射四氯化碳1小时后,研究了肝脏中钙的亚细胞分布。在制备亚细胞组分的过程中,尝试通过向匀浆介质中添加钌红、乙二醇双四乙酸(EGTA)或氯化镧,并将差速离心时间缩短至最短,来防止钙的重新分布。后者导致亚细胞组分纯度降低,通过利用标记酶活性对原子吸收光谱法测得的钙值进行校正得以克服。发现正常大鼠肝脏中,胞质溶胶中的钙水平为70纳摩尔/克肝脏湿重,微粒体中为310纳摩尔/克肝脏,线粒体中约为500纳摩尔/克肝脏。后一组分的一小部分可能属于细胞核和质膜。注射四氯化碳1小时后,细胞质中的钙水平未改变,微粒体中的钙水平降至200纳摩尔/克肝脏,线粒体中的钙水平升至2.5微摩尔/克肝脏。在维生素D预处理的大鼠中,四氯化碳注射后,全部额外的钙(在9微摩尔/克肝脏范围内)都被隔离在线粒体中。在四氯化碳中毒的早期阶段,肝细胞的所有边界膜都必须参与导致肝细胞钙的可逆性增加。

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The intracellular distribution of liver cell calcium in normal rats and one hour after administration of carbon tetrachloride.正常大鼠及给予四氯化碳一小时后肝细胞钙的细胞内分布。
Biochem Pharmacol. 1982 Mar 15;31(6):1069-73. doi: 10.1016/0006-2952(82)90344-6.
2
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X-ray microanalysis of calcium, potassium, and phosphorus in liver mitochondria stressed by carbon tetrachloride.四氯化碳应激下肝线粒体中钙、钾和磷的X射线微分析
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Altered calcium homeostasis in carbon tetrachloride exposed rat hepatocytes.四氯化碳暴露大鼠肝细胞中钙稳态的改变
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Carbon tetrachloride-induced release of calcium from isolated hepatocytes.四氯化碳诱导分离的肝细胞释放钙。
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引用本文的文献

1
Potential role of regucalcin as a specific biochemical marker of chronic liver injury with carbon tetrachloride administration in rats.在给大鼠注射四氯化碳的情况下,调钙素作为慢性肝损伤特异性生化标志物的潜在作用。
Mol Cell Biochem. 2002 Dec;241(1-2):61-7. doi: 10.1023/a:1020822610085.
2
Alteration in calcium content and Ca2+-ATPase activity in the liver nuclei of rats orally administered carbon tetrachloride.口服四氯化碳的大鼠肝细胞核中钙含量及Ca2+-ATP酶活性的改变
Mol Cell Biochem. 1998 Aug;185(1-2):153-9. doi: 10.1023/a:1006803610945.
3
Activatory effect of regucalcin on hepatic plasma membrane (Ca(2+)-Mg2+)-ATPase is impaired by liver injury with carbon tetrachloride administration in rats.
大鼠经四氯化碳给药致肝损伤后,钙网蛋白对肝细胞膜(Ca²⁺-Mg²⁺)-ATP酶的激活作用受损。
Mol Cell Biochem. 1996 May 10;158(1):9-16. doi: 10.1007/BF00225877.
4
Ca-efflux, from direct membrane injury by CCl4, is elicited by amphiphilic vehicles in vitro.四氯化碳对细胞膜的直接损伤所引发的钙外流,在体外可由两亲性载体诱导产生。
Experientia. 1993 Oct 15;49(10):854-8. doi: 10.1007/BF01952597.