Role of reactive oxygen species on diesel exhaust particle-induced cytotoxicity in rat cardiac myocytes
Role of reactive oxygen species on diesel exhaust particle-induced cytotoxicity in rat cardiac myocytes
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DOI：
10.1080/15287390600631078
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发表时间：
2006-09-15
影响因子：
2.6
通讯作者：
Tsubone, Hirokazu
中科院分区：
文献类型：
--
作者：
Okayama, Yuta;Kuwahara, Masayoshi;Tsubone, Hirokazu
暴露于含有柴油机排气颗粒（DEP）的空气污染与心血管疾病导致的死亡率增加有关，但DEP在细胞水平产生不良心血管效应的机制尚未阐明。本研究探讨了DEP体外诱导的新生大鼠心肌细胞的细胞毒性机制，重点是活性氧（ROS）的作用。DEP提取物（DEPE）以浓度和时间依赖性方式损伤细胞。乳酸脱氢酶活性泄漏到介质中也增加了浓度依赖性的方式后，24小时的DEPE曝光。DEPE诱导的细胞毒性显着降低治疗与超氧化物歧化酶，过氧化氢酶，N-（2-巯基丙酰基）-甘氨酸。此外，超氧化物产生的DEPE和心肌细胞。这些结果表明，ROS，如超氧阴离子，过氧化氢，和羟基自由基参与DEPE诱导的心肌细胞损伤。
Exposure to air pollution containing diesel exhaust particles (DEP) is associated with an increase in mortality rate attributed to cardiovascular diseases, but the mechanisms by which DEP produces adverse cardiovascular effects at the cellular level are not elucidated. This study investigated the cytotoxic mechanisms underlying DEP-induced neonatal rat cardiac myocytes effects in vitro, focusing on the role of reactive oxygen species (ROS). DEP extracts (DEPE) damaged cells in a concentration-and a time-dependent manner. Lactate dehydrogenase activity leaked to medium was also increased in a concentration-dependent manner after 24 h of DEPE exposure. DEPE-induced cytotoxicity was markedly reduced by treatment with superoxide dismutase, catalase, and N-(2-mercaptopropionyl)-glycine. Furthermore, superoxide was produced from both DEPE and myocardial cells. These results suggest that ROS such as superoxide, hydrogen peroxide, and hydroxyl radical are involved in DEPE-induced cardiac cell damage.