McCall K E, Duncan C J
Department of Zoology, School of Life Sciences, University of Liverpool, UK.
Pathobiology. 1995;63(5):278-82. doi: 10.1159/000163961.
Exposure of the isolated mouse soleus preparation to 1.0 mM phenazine methosulphate (PMS) caused (i) a slow and modest release of creatine kinase (CK) that was exacerbated by removal of extracellular Ca2+, (ii) a specific type of ultrastructural damage, namely a characteristic spacing of the myofibrils, (iii) swelling of the mitochondria, indicating a modest rise in [Ca2+]i, and (iv) swelling of the sarcoplasmic reticulum (SR). It is suggested that PMS (i) activates a sarcolemma oxidoreductase which synergistically interacts with raised [Ca2+]i to cause modest CK efflux and (ii) activates an oxidoreductase on the SR, thereby generating electrons which directly modify the integrity and organisation of the contractile apparatus.
将分离的小鼠比目鱼肌制剂暴露于1.0 mM吩嗪硫酸甲酯(PMS)会导致:(i)肌酸激酶(CK)缓慢且适度释放,去除细胞外Ca2+会加剧这种释放;(ii)一种特定类型的超微结构损伤,即肌原纤维的特征性间距;(iii)线粒体肿胀,表明细胞内Ca2+浓度适度升高;(iv)肌浆网(SR)肿胀。有人提出,PMS(i)激活一种肌膜氧化还原酶,该酶与升高的细胞内Ca2+协同相互作用,导致适度的CK外流;(ii)激活SR上的氧化还原酶,从而产生电子,直接改变收缩装置的完整性和组织。