Silva Pamelli Maria de Souza, Tanabe Eduardo, Hermoso Aparecida Pinto Munhos, Bersani-Amado Ciomar A, Bracht Adelar, Ishii-Iwamoto Emy L, Salgueiro-Pagadigorria Clairce Luzia
Laboratory of Biological Oxidations, Department of Biochemistry, University of Maringá, Maringá, Brazil.
Cell Biochem Funct. 2008 Jun;26(4):443-50. doi: 10.1002/cbf.1461.
The involvement of the mitochondrial permeability transition pore (PTP) in the responses of mitochondria from adjuvant-induced arthritic rats to Ca(2+) addition was investigated. The respiratory activity, the Ca(2+)-induced osmotic swelling and the electrophoretic (45)Ca(2+) uptake were evaluated in the absence and in the presence of cyclosporin A (CsA), a well-known inhibitor of the mitochondrial PTP. The Ca(2+)-induced mitochondrial permeability transition (MPT) process occurred in mitochondria from arthritic rats even in the presence of a low Ca(2+) concentration. Whereas in the normal condition, the Ca(2+)-induced uncoupling of oxidative phosphorylation and osmotic swelling was observed in the presence of 10 or 20 microM Ca(2+) concentration, in the arthritic condition, these events occurred at 1.0 microM concentration. In addition, mitochondria from arthritic rats presented an impaired ability to accumulate (45)Ca(2+). All these effects were completely prevented by the administration of CsA. The results of the present study suggest that the higher sensitivity of mitochondria from arthritic rats to Ca(2+)-induced MPT may be an important factor in the pathogenesis of the arthritis disease.
研究了线粒体通透性转换孔（PTP）在佐剂诱导的关节炎大鼠线粒体对添加Ca(2+)的反应中的作用。在存在和不存在环孢菌素A（CsA）（一种著名的线粒体PTP抑制剂）的情况下，评估了呼吸活性、Ca(2+)诱导的渗透性肿胀和电泳法（45）Ca(2+)摄取。即使在低Ca(2+)浓度存在的情况下，Ca(2+)诱导的线粒体通透性转换（MPT）过程也发生在关节炎大鼠的线粒体中。在正常情况下，在10或20微摩尔Ca(2+)浓度存在时观察到Ca(2+)诱导的氧化磷酸化解偶联和渗透性肿胀，而在关节炎情况下，这些事件在1.0微摩尔浓度时发生。此外，关节炎大鼠的线粒体积累（45）Ca(2+)的能力受损。给予CsA可完全预防所有这些效应。本研究结果表明，关节炎大鼠线粒体对Ca(2+)诱导的MPT的更高敏感性可能是关节炎疾病发病机制中的一个重要因素。
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