Nencki Institute of Experimental Biology, Warsaw, Poland.
Biochem Biophys Res Commun. 2011 Apr 22;407(4):772-6. doi: 10.1016/j.bbrc.2011.03.098. Epub 2011 Mar 31.
Release of reactive oxygen species (ROS), measured as the sum of hydrogen peroxide (H₂O₂) and superoxide anion radical (O₂·⁻), from respiring rat heart and skeletal muscle mitochondria was significantly decreased by millimolar concentrations of GTP or GDP. Attempts to differentiate between the two forms of ROS showed that the release of O₂·⁻ rather than that of H₂O₂ was affected. Meanwhile, intramitochondrial ROS accumulation, measured by inactivation of aconitase, increased. These results suggest that guanine nucleotides inhibit the release of O₂·⁻ from mitochondria. As these nucleotides are known inhibitors of uncoupling proteins (UCPs), it is proposed that UCPs may function as carriers of O₂·⁻, thus enabling its removal from the matrix compartment.
耗氧状态下，呼吸反应的大鼠心脏和骨骼肌线粒体中活性氧（ROS）的释放（以过氧化氢（H₂O₂）和超氧阴离子自由基（O₂·⁻）的总和来衡量），会被毫摩尔浓度的 GTP 或 GDP 显著抑制。为了区分两种 ROS，研究尝试表明，受到影响的是 O₂·⁻的释放而不是 H₂O₂。同时，通过测定乌头酸酶失活，发现线粒体中 ROS 的积累增加。这些结果表明，鸟嘌呤核苷酸抑制了 O₂·⁻从线粒体中的释放。由于这些核苷酸是解偶联蛋白（UCPs）的已知抑制剂，因此推测 UCPs 可能作为 O₂·⁻的载体，从而使其能够从基质隔室中去除。
