Hexavalent chromium (Cr(VI)) is a common environmental pollutant. Exposure of Cr(VI) can lead to cell autophagy, but the preventive measures for diminishing Cr(VI)-induced autophagy need further study. COX-2 can be induced by several heavy metals and can lead to endoplasmic reticulum (ER) stress and autophagy; thus, COX-2, ER stress, and autophagy may be related. This study mainly investigated the role of COX-2 in the eIF2α-ATF4 pathway, which is a major pathway in cell autophagy. In this study, Cr(VI) was used as a xenobiotic to determine changes in the parameters of ER stress, autophagy, and COX-2 levels. At the same time, a clear contrast was obtained by assigning positive and negative controls of ER stress and autophagy. The results showed that during Cr(VI) invasion, the parameters of ER stress and autophagy (such as BiP, PERK, p62, LC3-II, and mTOR) were enhanced, similarly to the positive control of ER stress and/or the autophagy controls. Such enhancement is a protective mechanism for cell survival. Additionally, the COX-2 levels increased. Moreover, when COX-2 was inhibited, the PERK level remained high, whereas the LC3-II level decreased. This finding suggests that COX-2 specifically affects the interaction between ER stress and autophagy. Notably, this study reveals that Cr(VI) can induce ER stress and autophagy in DF-1 cells and that COX-2 plays an essential role in the interaction between ER stress and autophagy.

六价铬（Cr（VI））是一种常见的环境污染物。Cr（VI）的暴露可导致细胞自噬，但减少Cr（VI）诱导的自噬的预防措施有待进一步研究。COX-2可由多种重金属诱导，并可能导致内质网（ER）应激和自噬。因此，COX-2，内质网应激和自噬可能是相关的。这项研究主要研究了COX-2在eIF2α-ATF4途径中的作用，eIF2α-ATF4途径是细胞自噬的主要途径。在这项研究中，Cr（VI）被用作一种外源生物，以确定ER应激，自噬和COX-2水平参数的变化。同时，通过分配正向和负向内质网应激和自噬的对照获得了清晰的对比。结果表明，在Cr（VI）入侵过程中，ER应力和自噬参数（例如BiP，PERK，p62，LC3-II，和mTOR）增强，类似于ER应激的阳性对照和/或自噬对照。这种增强是细胞存活的保护机制。此外，COX-2水平增加。此外，当COX-2被抑制时，PERK水平保持较高，而LC3-II水平下降。这一发现表明，COX-2特异性影响内质网应激与自噬之间的相互作用。值得注意的是，这项研究表明Cr（VI）可以诱导DF-1细胞中的内质网应激和自噬，而COX-2在内质网应激和自噬之间的相互作用中起着至关重要的作用。PERK水平保持较高水平，而LC3-II水平下降。这一发现表明，COX-2特异性影响内质网应激与自噬之间的相互作用。值得注意的是，这项研究表明Cr（VI）可以诱导DF-1细胞中的内质网应激和自噬，而COX-2在内质网应激和自噬之间的相互作用中起着至关重要的作用。PERK水平保持较高水平，而LC3-II水平下降。这一发现表明，COX-2特异性影响内质网应激与自噬之间的相互作用。值得注意的是，这项研究表明Cr（VI）可以诱导DF-1细胞中的内质网应激和自噬，而COX-2在内质网应激和自噬之间的相互作用中起着至关重要的作用。