Induction of calcium release from isolated sarcoplasmic reticulum by triphenyltin.
Induction of calcium release from isolated sarcoplasmic reticulum by triphenyltin.
复制标题
三苯基锡诱导分离的肌浆网释放钙。
DOI：
10.1093/oxfordjournals.jbchem.a021725
复制
发表时间：
1997
影响因子：
2.7
通讯作者：
Y. W. Cheng
中科院分区：
文献类型：
--
作者：
J. J. Kang;I. Chen;Y. W. Cheng
在有机锡中毒中发现了一种直接的外周肌病，这被认为是暴露后肌肉无力发展的一个重要因素。在这项研究中，通过使用分离的肌浆网膜囊泡，我们已经表明，三苯基锡剂量依赖性地诱导钙释放的主动和被动加载肌浆网膜囊泡。三苯基锡以钌红敏感和不敏感的方式诱导Ca 2+释放，EC 50值分别为75和270 μ M。三苯基锡对肌浆网Ca ~（2+）摄取和Ca ~（2+）-ATP酶活性也有抑制作用。三苯基锡对表观[3 H]ryanodine结合有双重影响。三苯基锡（0.5-10 μ M）剂量依赖性地增强[3 H]ryanodine结合;然而，[3 H]ryanodine结合随着三苯基锡浓度的增加而减少。结合[3 H]ryanodine的解离由三苯基锡促进。本研究表明，三苯基锡可通过抑制肌浆网Ca ~（2+）-ATP酶和Ca ~（2+）释放通道（Ryanodine受体），分别抑制Ca ~（2+）摄取和诱导Ca ~（2+）释放，从而耗竭骨骼肌内Ca ~（2+）库。这些结果可以部分解释有机锡中毒的肌肉无力的发展，但是，其相关性周围性肌病的发展需要进一步检查。
A direct peripheral myopathy has been found in organotin intoxication and suggested to be a significant factor in the development of muscle weakness following exposure. In this study, by using the isolated sarcoplasmic reticulum membrane vesicles, we have shown that triphenyltin dose-dependently induced Ca2+ release from the actively and passively loaded sarcoplasmic reticulum vesicles. Triphenyltin induced Ca2+ release in ruthenium red-sensitive and insensitive ways with EC50 values of 75 and 270 microM, respectively. The Ca2+-ATPase activity and Ca2+ uptake of sarcoplasmic reticulum were also inhibited by triphenyltin. Triphenyltin exerted dual effects on the apparent [3H]ryanodine binding. Triphenyltin (0.5-10 microM) dose-dependently potentiated the [3H]ryanodine binding; however, the [3H]ryanodine binding decreased as the concentration of triphenyltin increased. The dissociation of bound [3H]ryanodine was facilitated by triphenyltin. The present study suggested that the internal Ca2+ store of skeletal muscle could be depleted by triphenyltin through the inhibition of the Ca2+ uptake and the induction of Ca2+ release by acting on the Ca2+-ATPase and Ca2+ release channel, also known as the ryanodine receptor, of sarcoplasmic reticulum, respectively. These results could partly explain the development of muscle weakness in organotin intoxication; however, their relevance to the development of peripheral myopathy requires further examination.