Department of Cardiology, The First Affiliated Hospital of China Medical University, 155 Nanjing Bei Street Heping District, Shenyang 110001, Liaoning, China.
Cell Biochem Biophys. 2011 Sep;61(1):131-6. doi: 10.1007/s12013-011-9169-5.
Acrolein, an unsaturated aldehyde, is an environmental toxin known to inhibit mitochondrial electron transport chain in brain and induce lipid peroxidation and apoptosis. However, the nature of the effects of acrolein on cardiac function and myocardium is not known. The objective of this study is to examine whether acrolein induces apoptosis in cardiomyocytes and alters cytosolic calcium concentration and the intracellular oxygen free-radical levels. Adult mouse cardiomyocytes exposed to 1 μmol/l of acrolein showed a marked increase in the intracellular oxygen free-radicals and calcium concentration, by 12- and 2-fold, respectively, compared to the resting value. Moreover, the cardiomyocyte viability decreased significantly in a dose-dependent manner by treatment with 25, 50, and 100 μmol/l of acrolein compared to controls. Morphological changes and DNA laddering typical of apoptosis were found in acrolein-exposed cardiomyocytes. Our finding suggested that acrolein caused apoptotic death of adult mice cardiomyocytes by increasing intracellular oxygen free-radicals and calcium concentration.
丙烯醛，一种不饱和醛，是一种环境毒素，已知它会抑制大脑中线粒体电子传递链，并诱导脂质过氧化和细胞凋亡。然而，丙烯醛对心脏功能和心肌的影响性质尚不清楚。本研究的目的是研究丙烯醛是否会诱导心肌细胞凋亡，并改变胞质钙离子浓度和细胞内氧自由基水平。与静息值相比，暴露于 1 μmol/l 丙烯醛的成年小鼠心肌细胞的胞内氧自由基和钙离子浓度分别增加了 12 倍和 2 倍。此外，与对照组相比，用 25、50 和 100 μmol/l 的丙烯醛处理可显著降低心肌细胞活力，呈剂量依赖性。在丙烯醛暴露的心肌细胞中发现了典型的凋亡形态变化和 DNA 梯状带。我们的研究结果表明，丙烯醛通过增加细胞内氧自由基和钙离子浓度导致成年小鼠心肌细胞凋亡死亡。
