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钠、代谢抑制剂和三磷酸腺苷对L细胞中钙运动的影响。

Effect of Na, metabolic inhibitors and ATP on Ca movements in L cells.

作者信息

Lamb J F, Lindsay R

出版信息

J Physiol. 1971 Nov;218(3):691-708. doi: 10.1113/jphysiol.1971.sp009640.

Abstract
  1. The Ca movements in normal and ;ghost' L cells have been examined; all measurements were made using (45)Ca.2. Normal cells have a Ca concentration of about 1 m-mole/l. of cell volume, and exchange Ca in a complex way but with great rapidity; the time taken for the initial Ca(*) content to fall to half was less than 2 min.3. Poisoning normal cells with DNP 10(-3)M + IAA 10(-4)M causes a marked reduction in the Ca efflux, no change in Ca influx and an increase in total Ca.4. Variation in internal or external Na concentration does not alter the Ca fluxes or concentrations. Application of cyanide or ouabain and alteration of external K concentration had no effect on the Ca fluxes.5. The sulphydryl reagents, ethacrynic acid and N-ethylmaleimide (NEM), have a rapid and marked effect on reducing the Ca efflux.6. L cell ghosts previously poisoned with DNP+IAA have a low Ca efflux. When ATP or CTP is incorporated into such cells the Ca efflux becomes normal.7. An extra amount of phosphate is produced by L cell ghosts when pumping Ca. This is equivalent to the splitting of 1.8 moles of ATP per mole of Ca pumped.8. It is concluded that L cells have a Ca pump driven by ATP, and that Na has no effect on Ca movements in these cells.
摘要
  1. 已对正常L细胞和“空壳”L细胞中的钙运动进行了检测;所有测量均使用(45)钙进行。

  2. 正常细胞的钙浓度约为每细胞体积1毫摩尔/升,以复杂方式但快速地交换钙;初始钙(*)含量降至一半所需时间不到2分钟。

  3. 用10(-3)M的二硝基苯酚(DNP)+10(-4)M的吲哚乙酸(IAA)毒害正常细胞会导致钙外流显著减少,钙内流无变化,总钙增加。

  4. 细胞内或细胞外钠浓度的变化不会改变钙通量或浓度。应用氰化物或哇巴因以及改变细胞外钾浓度对钙通量无影响。

  5. 巯基试剂、依他尼酸和N-乙基马来酰亚胺(NEM)对减少钙外流有快速且显著的作用。

  6. 先前用DNP+IAA毒害的L细胞空壳钙外流较低。当将ATP或CTP掺入此类细胞时,钙外流恢复正常。

  7. L细胞空壳在泵出钙时会产生额外的磷酸盐。这相当于每泵出1摩尔钙消耗1.8摩尔ATP。

  8. 得出的结论是,L细胞有一个由ATP驱动的钙泵,并且钠对这些细胞中的钙运动没有影响。

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Studies on the colorimetric determination of phosphate.磷的比色测定研究。
Biochem J. 1938 Feb;32(2):286-94. doi: 10.1042/bj0320286.
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J Physiol. 1969 Feb;200(2):431-58. doi: 10.1113/jphysiol.1969.sp008702.

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