Dalian Institute of Chemical Physics, Chinese Academy of Sciences, 457 Zhongshan Road, Dalian, Liaoning, PR China.
Toxicol Lett. 2010 May 19;195(1):90-8. doi: 10.1016/j.toxlet.2010.02.004. Epub 2010 Feb 11.
Crotonaldehyde is a widespread environmental pollutant and lipid peroxidation product. Crotonaldehyde is a risk factor for many diseases (e.g., chronic pulmonary inflammation). However, its toxicity and its mechanism of action have not been thoroughly investigated. The purpose of this study is to investigate crotonaldehyde-induced oxidative stress and mechanism of cell death in BEAS-2B cells. Crotonaldehyde caused decreases of intracellular reduced glutathione levels and increases of reactive oxygen species in a dose-dependent manner. Crotonaldehyde induced cell death by apoptosis, and gradually transitioned to necrosis at high dose of crotonaldehyde, as demonstrated by Annexin V-FITC/PI staining and cell morphology analysis. Crotonaldehyde-induced ATP decline observed in the study might partially account for the switch from apoptosis to necrosis. Mitochondria membrane potential, cytochrome c release, caspase-9, and caspase-3/7 activity were investigated, and the results suggest that crotonaldehyde-induced apoptosis was activated in a caspase-dependent way. Collectively, these results demonstrate crotonaldehyde induces cell oxidative stress and caspase-dependent apoptosis.
巴豆醛是一种广泛存在的环境污染物和脂质过氧化产物。巴豆醛是许多疾病（如慢性肺部炎症）的危险因素。然而，其毒性及其作用机制尚未得到彻底研究。本研究旨在探讨巴豆醛诱导的 BEAS-2B 细胞氧化应激和细胞死亡的机制。巴豆醛以剂量依赖性方式降低细胞内还原型谷胱甘肽水平并增加活性氧。巴豆醛诱导细胞凋亡，随着巴豆醛剂量的增加逐渐向坏死转化，这通过 Annexin V-FITC/PI 染色和细胞形态分析得到证实。研究中观察到的巴豆醛诱导的 ATP 下降可能部分解释了从凋亡向坏死的转变。还研究了线粒体膜电位、细胞色素 c 释放、caspase-9 和 caspase-3/7 活性，结果表明巴豆醛诱导的细胞凋亡是 caspase 依赖性的。总之，这些结果表明巴豆醛诱导细胞氧化应激和 caspase 依赖性细胞凋亡。
