Departments of Surgery, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Eur J Pain. 2011 Aug;15(7):708-15. doi: 10.1016/j.ejpain.2010.12.003. Epub 2011 Jan 22.
Reactive oxygen species (ROS) are known to be involved in the pathophysiology of complex regional pain syndrome type I (CRPS I). Since the mitochondrial respiratory chain is a major source of ROS, we hypothesized that mitochondria play a role in the pathophysiology of CRPS I. The hypothesis was tested by studying mitochondrial energy metabolism in muscle tissue from amputated limbs of CRPS I patients. We observed that mitochondria obtained from CRPS I muscle tissue displayed reduced mitochondrial ATP production and substrate oxidation rates in comparison to control muscle tissue. Moreover, we observed reactive oxygen species evoked damage to mitochondrial proteins and reduced MnSOD levels. It remains to be established if the mitochondrial dysfunction that is apparent at the end-stage of CRPS I is also present in earlier stages of the disease, or are secondary to CRPS I. The observation of a reduced mitochondrial energy production combined with reactive oxygen species induced damage in muscle tissue from CRPS I patients warrants further studies into the involvement of mitochondrial dysfunctioning in the pathophysiology of CRPS I.
活性氧 (ROS) 已知参与 I 型复杂性区域疼痛综合征 (CRPS I) 的病理生理学过程。由于线粒体呼吸链是 ROS 的主要来源，我们假设线粒体在 CRPS I 的病理生理学中起作用。通过研究 CRPS I 患者截肢肢体的肌肉组织中的线粒体能量代谢来检验该假设。我们观察到，与对照肌肉组织相比，从 CRPS I 肌肉组织中获得的线粒体显示出减少的线粒体 ATP 产生和底物氧化速率。此外，我们观察到活性氧引起的线粒体蛋白损伤和 MnSOD 水平降低。CRPS I 终末期明显的线粒体功能障碍是否也存在于疾病的早期阶段，或者是继发于 CRPS I，仍有待确定。观察到 CRPS I 患者的肌肉组织中减少的线粒体能量产生以及活性氧诱导的损伤，这表明线粒体功能障碍在 CRPS I 的病理生理学中的参与值得进一步研究。
