Zacks Michele A, Wen Jian-Jun, Vyatkina Galina, Bhatia Vandanajay, Garg Nisha
Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
An Acad Bras Cienc. 2005 Dec;77(4):695-715. doi: 10.1590/s0001-37652005000400009. Epub 2005 Nov 29.
There is growing evidence to suggest that chagasic myocardia are exposed to sustained oxidative stress-induced injuries that may contribute to disease progression. Pathogen invasion- and replication-mediated cellular injuries and immune-mediated cytotoxic reactions are the common source of reactive oxygen species (ROS) in infectious etiologies. However, our understanding of the source and role of oxidative stress in chagasic cardiomyopathy (CCM) remains incomplete. In this review, we discuss the evidence for increased oxidative stress in chagasic disease, with emphasis on mitochondrial abnormalities, electron transport chain dysfunction and its role in sustaining oxidative stress in myocardium. We discuss the literature reporting the consequences of sustained oxidative stress in CCM pathogenesis.
越来越多的证据表明,恰加斯病性心肌病患者的心肌会受到持续的氧化应激诱导损伤,这可能会促进疾病进展。病原体入侵和复制介导的细胞损伤以及免疫介导的细胞毒性反应是感染性病因中活性氧(ROS)的常见来源。然而,我们对恰加斯病性心肌病(CCM)中氧化应激的来源和作用的理解仍然不完整。在这篇综述中,我们讨论了恰加斯病中氧化应激增加的证据,重点是线粒体异常、电子传递链功能障碍及其在维持心肌氧化应激中的作用。我们还讨论了报道持续氧化应激在CCM发病机制中后果的文献。