In the present study, effects of cis-9,10-epoxy stearic acid (ESA) generated by the thermal oxidation of oleic acid on HepG2 cells, including cytotoxicity, apoptosis, and oxidative stress, were investigated. Our results revealed that ESA decreased the cell viability and induced cell death. Cell cycle analysis with propidium iodide staining showed that ESA induced cell cycle arrest at the G0/G1 phase in HepG2 cells. Cell apoptosis analysis with annexin V and propidium iodide staining demonstrated that ESA induced HepG2 cell apoptotic events in a dose- and time-dependent manner; the apoptosis of cells after treated with 500 μM ESA for 12, 24, and 48 h was 32.16, 38.70, and 65.80%, respectively. Furthermore, ESA treatment to HepG2 cells resulted in an increase in reactive oxygen species and malondialdehyde (from 0.84 ± 0.02 to 8.90 ± 0.50 nmol/mg of protein) levels and a reduction in antioxidant enzyme activity, including superoxide dismutase (from 1.34 ± 0.27 to 0.10 ± 0.007 units/mg of protein), catalase (from 100.04 ± 5.05 to 20.09 ± 3.00 units/mg of protein), and glutathione peroxidase (from 120.44 ± 7.62 to 35.84 ± 5.99 milliunits/mg of protein). These findings provide critical information on the effects of ESA on HepG2 cells, particularly cytotoxicity and oxidative stress, which is important for the evaluation of the biosafety of the oxidative product of oleic acid.

中文翻译：

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环氧硬脂酸（一种来自油酸的氧化产物）在HepG2细胞中诱导细胞毒性，氧化应激和凋亡。

在本研究中，顺式作用研究了油酸在HepG2细胞上热氧化生成的-9,10-环氧硬脂酸（ESA），包括细胞毒性，细胞凋亡和氧化应激。我们的结果表明，ESA降低了细胞活力并诱导了细胞死亡。碘化丙啶染色的细胞周期分析表明，ESA诱导的HepG2细胞在G0 / G1期停滞。膜联蛋白V和碘化丙锭染色的细胞凋亡分析表明，ESA以剂量和时间依赖性方式诱导HepG2细胞凋亡事件。500μMESA处理12、24和48 h后，细胞凋亡分别为32.16、38.70和65.80％。此外，ESA对HepG2细胞的处理导致活性氧和丙二醛含量从0.84±0.02增加到8.90±0。50 nmol / mg蛋白质）水平降低，抗氧化酶活性降低，包括超氧化物歧化酶（从1.34±0.27到0.10±0.007单位/ mg蛋白质），过氧化氢酶（从100.04±5.05到20.09±3.00单位/ mg蛋白质） ）和谷胱甘肽过氧化物酶（从120.44±7.62到35.84±5.99毫单位/毫克蛋白质）。这些发现提供了有关ESA对HepG2细胞的影响的关键信息，特别是细胞毒性和氧化应激，这对于评估油酸氧化产物的生物安全性很重要。