Indoor pollution with cooking oil fumes (COF) as one of the main components is closely related to ocular surface disorders. However, as the most abundant aldehyde in COF, the toxicity of trans, trans-2,4-decadienal (tt-DDE) on human cornea has not been explored before. In the present study, we observed a time- and dose-dependent cytotoxicity induced by tt-DDE in human corneal epithelial (HCE) cells, as evidenced by decreased cell viability, altered cell morphology, and increased proportion of apoptotic cells. Exposure to tt-DDE also led to an increase in reactive oxygen species (ROS) production, MMP loss, and a decrease in intracellular ATP levels. In addition, after exposure to tt-DDE, the expression of endoplasmic reticulum (ER) stress-related proteins (Bip, pIRE1, XBP1, pPERK, peIF2α, ATF4, and CHOP) increased, indicating that ER stress was activated. Moreover, pretreatment of HCE cells with two ER stress inhibitors (200 nM ISRIB or 1 mM 4-PBA) effectively attenuated oxidative stress induced by tt-DDE. These results suggested that tt-DDE could cause damage to HCE cells by triggering oxidative stress and ER stress. Furthermore, regulation of ER stress can be considered as a potential protective method for tt-DDE-induced ocular surface disorders.

使用食用油烟（COF）作为主要成分的室内污染与眼表疾病密切相关。然而，作为COF中最丰富的醛，反式，反式2,4-癸二烯醛（tt-DDE）对人角膜的毒性尚未得到探索。在本研究中，我们观察到tt-DDE在人角膜上皮（HCE）细胞中诱导的时间依赖性和剂量依赖性细胞毒性，表现为细胞活力降低，细胞形态改变和凋亡细胞比例增加。暴露于tt-DDE也会导致活性氧（ROS）产生增加，MMP丢失以及细胞内ATP水平降低。此外，暴露于tt-DDE后，内质网（ER）应激相关蛋白（Bip，pIRE1，XBP1，pPERK，peIF2α，ATF4和CHOP）的表达增加，表示已激活ER应力。此外，用两种ER应激抑制剂（200 nM ISRIB或1 mM 4-PBA）预处理HCE细胞可有效减轻tt-DDE诱导的氧化应激。这些结果表明，tt-DDE可能通过触发氧化应激和ER应激而导致HCE细胞损伤。此外，ER应力的调节可以被认为是由tt-DDE引起的眼表疾病的潜在保护方法。