Strazdauskas Arvydas, Trumbeckaite Sonata, Jakstas Valdas, Kamarauskaite Justina, Ivanauskas Liudas, Baniene Rasa
Laboratory of Biochemistry, Neuroscience Institute, Lithuanian University of Health Sciences, LT-50162 Kaunas, Lithuania.
Department of Biochemistry, Medical Academy, Lithuanian University of Health Sciences, LT-50161 Kaunas, Lithuania.
Biology (Basel). 2022 Mar 31;11(4):541. doi: 10.3390/biology11040541.
Cardiolipin is a mitochondrial phospholipid that plays a significant role in mitochondrial bioenergetics. Cardiolipin is oxidized under conditions like oxidative stress that occurs during ischemia/reperfusion; however, it is known that even during ischemia, many reactive oxygen species are generated. Our aim was to analyze the effect of in vivo ischemia on cardiolipin oxidation. Adult male Wistar rats were anesthetized; then, their abdomens were opened, and microvascular clips were placed on renal arteries for 30, 40 or 60 min, causing ischemia. After ischemia, kidneys were harvested, mitochondria were isolated, and lipids were extracted for chromatographic and mass spectrometric analysis of tetralinoleoyl cardiolipin and its oxidation products. Chromatographic and mass spectrometric analysis revealed a 47%, 68% and 74% decrease in tetralinoleoyl cardiolipin after 30 min, 40 min and 60 min of renal ischemia, respectively (p < 0.05). Eight different cardiolipin oxidation products with up to eight additional oxygens were identified in rat kidney mitochondria. A total of 40 min of ischemia caused an average of a 6.9-fold increase in all oxidized cardiolipin forms. We present evidence that renal ischemia in vivo alone induces tetralinoleoyl cardiolipin oxidation and depletion in rat kidney mitochondria.
心磷脂是一种线粒体磷脂，在线粒体生物能量学中发挥着重要作用。在缺血/再灌注期间发生的氧化应激等条件下，心磷脂会被氧化；然而，已知即使在缺血期间，也会产生许多活性氧。我们的目的是分析体内缺血对心磷脂氧化的影响。将成年雄性Wistar大鼠麻醉；然后，打开它们的腹部，将微血管夹夹在肾动脉上30、40或60分钟，造成缺血。缺血后，采集肾脏，分离线粒体，并提取脂质，用于对四亚油酰基心磷脂及其氧化产物进行色谱和质谱分析。色谱和质谱分析显示，肾缺血30分钟、40分钟和60分钟后，四亚油酰基心磷脂分别减少了47%、68%和74%（p<0.05）。在大鼠肾脏线粒体中鉴定出了8种不同的心磷脂氧化产物，最多带有8个额外的氧原子。总共40分钟的缺血导致所有氧化形式的心磷脂平均增加了6.9倍。我们提供的证据表明，仅体内肾缺血就会诱导大鼠肾脏线粒体中的四亚油酰基心磷脂氧化和消耗。
