Kang J J, Liu S H, Chen I L, Cheng Y W, Lin-Shiau S Y
Institute of Toxicology, College of Medicine, National Taiwan University, Section 1, Taipei.
Pharmacol Toxicol. 1998 Jan;82(1):23-7. doi: 10.1111/j.1600-0773.1998.tb01393.x.
Effects of organotins, including triethyltin and tributyltin, on skeletal muscle were studied with diaphragm and isolated sarcoplasmic reticulum membrane vesicles. Triethyltin induced muscle contracture in mouse diaphragm while tributyltin had comparatively less potency and efficacy in inducing the muscle contracture. The contracture induced by tributyltin was inhibited when the diaphragm was pretreated with low Ca2+ medium or caffeine while the contracture induced by triethyltin persisted in the Ca2+-free medium but was inhibited by pretreatment of caffeine. Pretreatment of dithiothreitol blocked the contracture induced by tributyltin but not that by triethyltin. Triethyltin dose-dependently induced Ca2+ release from sarcoplasmic reticulum vesicles and inhibited the Ca2+-ATPase activity. These results suggested that triethyltin induced contracture in mouse diaphragm was mainly by induction of Ca2+ release and inhibition of Ca2+ uptake of the internal Ca2+ storage site the sarcoplasmic reticulum, while the tributyltin induced contracture might be due to enhancement of extracellular Ca2+ influx which further induce the release of internal Ca2+ through the Ca2+-induced Ca2+ release mechanism.
利用膈肌和分离的肌浆网膜囊泡研究了包括三乙锡和三丁锡在内的有机锡对骨骼肌的影响。三乙锡可诱导小鼠膈肌肌肉挛缩,而三丁锡诱导肌肉挛缩的效力和效能相对较低。当膈肌用低钙培养基或咖啡因预处理时,三丁锡诱导的挛缩受到抑制,而三乙锡诱导的挛缩在无钙培养基中持续存在,但咖啡因预处理可抑制该挛缩。二硫苏糖醇预处理可阻断三丁锡诱导的挛缩,但不能阻断三乙锡诱导的挛缩。三乙锡剂量依赖性地诱导肌浆网囊泡释放Ca2+并抑制Ca2+-ATP酶活性。这些结果表明,三乙锡诱导小鼠膈肌挛缩主要是通过诱导Ca2+释放和抑制肌浆网这个细胞内Ca2+储存位点的Ca2+摄取,而三丁锡诱导的挛缩可能是由于细胞外Ca2+内流增强,进而通过Ca2+诱导的Ca2+释放机制诱导细胞内Ca2+释放。