Deoxynivalenol leads to endoplasmic reticulum stress-mediated apoptosis via the IRE1/JNK/CHOP pathways in porcine embryos

• Published in: Food and chemical toxicology Vol. 188; p. 114633
• Main Authors: Kim, Ye-Won, Yang, Seul-Gi, Seo, Byoung-Boo, Koo, Deog-Bon, Park, Hyo-Jin
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.2024
• Subjects: Deoxynivalenol; Endoplasmic reticulum stress; Porcine embryo; Tauroursodeoxycholic acid; Unfolded protein response; Tauroursodeoxycholic acid; Deoxynivalenol; Porcine embryo; Endoplasmic reticulum stress; Unfolded protein response
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2024.114633

The cytotoxic mycotoxin deoxynivalenol (DON) reportedly has adverse effects on oocyte maturation and embryonic development in pigs. Recently, the interplay between cell apoptosis and endoplasmic reticulum (ER) stress has garnered increasing attention in embryogenesis. However, the involvement of the inositol-requiring enzyme 1 (IRE1)/c-jun N-terminal kinase (JNK)/C/EBP homologous protein (CHOP) pathways of unfolded protein response (UPR) signaling in DON-induced apoptosis in porcine embryos remains unknown. In this study, we revealed that exposure to DON (0.25 μM) substantially decreased cell viability until the blastocyst stage in porcine embryos, concomitant with initiation of cell apoptosis through the IRE1/JNK/CHOP pathways in response to ER stress. Quantitative PCR confirmed that UPR signaling-related transcription factors were upregulated in DON-treated porcine blastocysts. Western blot analysis showed that IRE1/JNK/CHOP signaling was activated in DON-exposed porcine embryos, indicating that ER stress-associated apoptosis was instigated. The ER stress inhibitor tauroursodeoxycholic acid protected against DON-induced ER stress in porcine embryos, indicating that the toxic effects of DON on early developmental competence of porcine embryos can be prevented. In conclusion, DON exposure impairs the developmental ability of porcine embryos by inducing ER stress-mediated apoptosis via IRE1/JNK/CHOP signaling. •DON exposure reduces the developmental capacity of porcine blastocysts.•DON exposure decreases ER-phagy.•0.1 μM DON induces the IRE1 pathway due to Ca2+ imbalance.•0.25 μM DON triggers the JNK/CHOP pathways by increasing mitochondrial Ca2+.•TUDCA protects ER stress on development of DON-exposed porcine embryos.