Embryonic developmental toxicity to estuarine fish: Single and co-exposure to EHMC and its phototransformation products in Mugilogobius chulae.

The ecological risks posed by organic ultraviolet filters (OUVFs) and their phototransformation products to estuarine ecosystems remain inadequately characterized. This study investigated the developmental toxicity in the early-life stages of the estuarine fish Mugilogobius chulae when exposed individually and jointly to 2-Ethylhexyl 4-methoxycinnamate (EHMC) and its phototransformation products (2-ethylhexanol (2-EH) and 4-methylbenzaldehyde (4-MBA)). The 120 h no-observed-effect concentration (NOEC) for embryonic malformations was >34435 nM (10000 μg/L) for EHMC, 61429 nM (8000 μg/L) for 2-EH, and 10283 nM (1400 μg/L) for 4-MBA. This indicates that the phototransformation products exhibit greater developmental toxicity than the parent compound EHMC. Notably, co-exposure at environmentally relevant concentrations accelerated embryonic heart rate and hatching (p < 0.05). Gene expression analysis revealed that 2-EH and 4-MBA singularly downregulated the expression of the GDF2, while 2-EH additionally upregulated the expression of BMP4, MATN3, and TBX5 (p < 0.05). In contrast, co-exposure potentiated transcriptional alterations in cardiac development-related genes (TGFβ2, BMP2, BMP4, GDF2, FGF4, WNT3A, TBX5, and NKX2-5; p < 0.05). The individual exposure of 138 nM (EHMC), 307 nM (2-EH), and 294 nM (4-MBA) suppressed superoxide dismutase (SOD) activity. Moreover, 2-EH and 4-MBA additionally inhibiting glutathione S-transferase (GST), resulting in 3.7- and 4.1-fold increases in malondialdehyde (MDA) levels, respectively (p < 0.05). The mixture further exacerbated oxidative imbalance through SOD and GST reduction and catalase (CAT) induction (p < 0.05). These findings underscore the critical need to consider photochemical transformation products in ecological risk assessments of OUVFs in estuarine ecosystems.