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• 研究论文 • 上一篇    

爱大霉素和庆大霉素对胞浆Ca2+影响的初步机制

李忠东*, 王建昌, 李培忠   

  1. 1.空军总医院, 北京 100036;
    2.军事医学科学院毒物药物研究所, 北京 100850
  • 收稿日期:2004-09-30 修回日期:2005-05-10 出版日期:2005-06-15 发布日期:2005-06-15
  • 通讯作者: 李忠东*

Possible Mechanism of Effects of Etimicin and Gentamicin on Intracellular Calcium Homeostasis

LI Zhong-dong*, WANG Jian-chang, LI Pei-zhong   

  1. 1.Air Force General Hospital, Beijing 100036, China;
    2.Institute of Toxicology and Pharmacology, Academy of Military Medical Sciences, Beijing 100850, China
  • Received:2004-09-30 Revised:2005-05-10 Online:2005-06-15 Published:2005-06-15
  • Contact: LI Zhong-dong*

摘要: 目的 观察爱大霉素(EM)和庆大霉素(GM)对胞浆Ca22+影响的初步机制。方法 Fura2/AM为探针测定EMGM在不同浓度时对LLCPK1肾上皮细胞浆Ca2+的影响, 同位素示踪法测定EMGM对线粒体Ca2+摄取和内质网Ca2+摄取的影响。结果 EMGM1 mmol·L-1时对胞浆Ca2+浓度无显著影响, P>0.05; 10 mmol·L-1时可使胞浆Ca2+显著上升, P<0.01EMGM1 mmol·L-1时显著促进线粒体Ca2+摄取(P<0.05); 10 mmol·L-1, 二者显著抑制线粒体Ca2+摄取。EMGM>0.34 mmol·L-1时显著抑制内质网Ca2+摄取(P<0.050.01)结论 低浓度EMGM未能引起胞浆Ca2+升高可能与其促进线粒体Ca2+摄取与抑制内质网Ca2+摄取相互平衡有关; 高浓度EMGM引起胞浆Ca2+升高可能与其均抑制线粒体和内质网Ca2+摄取有关。

关键词: 爱大霉素, 爱大霉素, 爱大霉素, 庆大霉素, 庆大霉素, 庆大霉素, 钙离子稳态, 钙离子稳态, 钙离子稳态, 线粒体, 线粒体, 线粒体, 内质网, 内质网, 内质网

Abstract: Aim Intracellular calcium ([Ca2+]i) is mainly regulated by mitochondria and endoplasmic reticula. This study was carried out to ascertain whether the elementary mechanism of the effects of etimicin (EM) and gentamicin (GM) on [Ca2+]i is related to their effects on mitochondrion Ca2+-uptake and endoplasmic reticulum Ca2+-uptake. Methods The effects of GM and EM on [Ca2+]i in LLC-PK1 were determined with a fluorescent probe of Fura-2/AM. The effects of EM and GM on mitochondrion Ca2+-uptake and endoplasmic reticulum Ca2+-uptake were determined by isotope indicator (45Ca2+). Results EM and GM at the concentration of 1 mmol·L-1 had no significant effect on [Ca2+]i i (P > 0.05) and at 10 mmol·L-1 significantly caused [Ca2+]i to increase (P <0.01). EM and GM at 1 mmol·L-1 caused mitochondrion Ca2+-uptake to ascend dramatically (P< 0.05) and at 10 mmol·L-1 caused mitochondrion Ca2+-uptake to descend significantly. EM and GM at more than 0.34 mmol·L-1 significantly inhibited endoplasmic reticulum Ca2+-uptake (P <0.05 or 0.01). Conclusion No variation of [Ca2+]i caused by EM and GM at lower concentrations might relate to the equilibrium of their promotion of mitochondrion Ca2+-uptake with their inhibition of endoplasmic reticulum Ca2+-uptake. The elevation of [Ca2+]i caused by EM and GM at higher concentrations might correlate with their inhibition of mitochondrion Ca2+-uptake and endoplasmic reticulum Ca2+-uptake.

Key words: etimicin, etimicin, gentamicin, gentamicin, Ca2+ homeostasis, Ca2+ homeostasis, mitochondria, mitochondria, endoplasmic reticula, endoplasmic reticula

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