Plant David R, Lynch Gordon S, Williams David A
Department of Physiology, University of Melbourne, Victoria 3010, Australia.
J Physiol. 2002 Mar 15;539(Pt 3):883-91. doi: 10.1113/jphysiol.2001.013369.
The effect of exogenous hydrogen peroxide (H(2)O(2)) on excitation-contraction (E-C) coupling and sarcoplasmic reticulum (SR) function was compared in mechanically skinned slow twitch fibres (prepared from the soleus muscles) and fast twitch fibres (prepared from the extensor digitorum longus; EDL muscles) of adult rats. Equilibration (5 min) with 1 mM H(2)O(2) diminished the ability of the Ca(2+)-depleted SR to reload Ca(2+) in both slow (P < 0.01) and fast twitch fibres (P < 0.05) compared to control. Under conditions when all Ca(2+) uptake was prevented, 1 mM H(2)O(2) increased SR Ca(2+) "leak" in fast twitch fibres by 24 +/- 5 % (P < 0.05), but leak was not altered in slow twitch fibres. Treatment with 1 mM H(2)O(2) also increased the peak force of low [caffeine] contracture by approximately 45% in both fibre types compared to control (P < 0.01), which could be partly reversed following treatment with 10 mM dithiothreitol (DTT). The changes in SR function caused by 1 mM H(2)O(2) were associated with an approximately 65% increase in the peak height of depolarization-induced contractile response (DICR) in slow twitch fibres, compared to control (no H(2)O(2); P < 0.05). In contrast, peak contractile force of fast twitch fibres was not altered by 1 mM H(2)O(2) treatment. Equilibration with 5 mM H(2)O(2) induced a spontaneous force response in both slow and fast twitch fibres, which could be partly reversed by 2 min treatment with 10 mM DTT. Peak DICR was also increased approximately 40% by 5 mM H(2)O(2) in slow twitch fibres compared to control (no H(2)O(2); P < 0.05). Our results indicate that exogenous H(2)O(2) increases depolarization-induced contraction of mechanically skinned slow but not fast twitch fibres. The increase in depolarization-induced contraction in slow twitch fibres might be mediated by an increased SR Ca(2+) release during contraction and/or an increase in Ca(2+) sensitivity.
在成年大鼠的机械去皮肤慢肌纤维(取自比目鱼肌)和快肌纤维(取自趾长伸肌;EDL肌)中,比较了外源性过氧化氢(H₂O₂)对兴奋-收缩(E-C)偶联和肌浆网(SR)功能的影响。与对照组相比,用1 mM H₂O₂平衡(5分钟)后,在慢肌纤维(P < 0.01)和快肌纤维(P < 0.05)中,Ca²⁺耗尽的SR重新加载Ca²⁺的能力均降低。在阻止所有Ca²⁺摄取的条件下,1 mM H₂O₂使快肌纤维中的SR Ca²⁺“泄漏”增加24±5%(P < 0.05),但慢肌纤维中的泄漏未改变。与对照组相比,用1 mM H₂O₂处理还使两种纤维类型中低[咖啡因]挛缩的峰值力增加约45%(P < 0.01),在用10 mM二硫苏糖醇(DTT)处理后,这种增加可部分逆转。1 mM H₂O₂引起的SR功能变化与慢肌纤维中去极化诱导的收缩反应(DICR)峰值高度增加约65%有关,与对照组(无H₂O₂)相比(P < 0.05)。相反,1 mM H₂O₂处理未改变快肌纤维的峰值收缩力。用5 mM H₂O₂平衡在慢肌纤维和快肌纤维中均诱导出自发性力反应,在用10 mM DTT处理2分钟后,这种反应可部分逆转。与对照组(无H₂O₂)相比,5 mM H₂O₂也使慢肌纤维中的峰值DICR增加约40%(P < 0.05)。我们的结果表明,外源性H₂O₂增加了机械去皮肤慢肌纤维而非快肌纤维的去极化诱导收缩。慢肌纤维中去极化诱导收缩的增加可能是由收缩过程中SR Ca²⁺释放增加和/或Ca²⁺敏感性增加介导的。