Embryonic exposure to bisphenol A glycidyl methacrylate induces craniofacial cartilage malformation via NLR signaling pathway in zebrafish.

Bisphenol A (BPA) can combine with glycidyl methacrylate to form bisphenol A glycidyl methacrylate (Bis-GMA). Bis-GMA is an important industrial raw material and a significant component of dental resin materials. Although Bis-GMA is widely utilized, its effects on neural crest cells and the development of embryonic maxillofacial cartilage remain insufficiently reported. This study evaluated the effect of Bis-GMA on cranio-maxillofacial cartilage using zebrafish as a model organism. Six to 120 h after fertilization, zebrafish embryos exposed to 0.8, 1.6 or 2.4 mg/L Bis-GMA presented with craniomaxillofacial dysplasia accompanied by pericardial edema and behavioral abnormalities. Bis-GMA induced oxidative stress overload in zebrafish embryos, and the development of neural crest cells and chondrocytes was also affected. Gene expression analysis revealed that the damage caused by Bis-GMA to cranio-maxillofacial cartilage was related to activation of the NOD-like receptor signaling pathway. These findings indicate that Bis-GMA has developmental toxicity to craniofacial cartilage and may have adverse effects on the human body and other organisms.