The increasing environmental release of nano-titanium dioxide (nTiO₂) due to its widespread industrial application raises concerns about its potential effects on aquatic ecosystems, particularly marine organisms. Fertilization, a critical reproductive process for broadcast-spawning bivalves, is highly sensitive to environmental pollutants. In the present investigation, we explored the effects of nTiO₂ at environmentally relevant concentrations on oocyte quality and the fertilization process in the economically important marine bivalve Tegillarca granosa. nTiO₂ exposure significantly reduced fertilization success and sperm–egg fusion efficiency, while markedly increasing polyspermy incidence. Mechanistically, nTiO₂ triggered oxidative stress in oocytes, elevating ROS and MDA levels and causing structural damage to the oocyte membrane. Moreover, nTiO₂ exposure disrupted cellular energy metabolism by inhibiting PK and PFK activities, depleting ATP content, and reducing MMP. Additionally, nTiO₂ exposure impaired Ca²⁺ homeostasis by suppressing Ca²⁺-ATPase activity, which reduced intracellular Ca²⁺ levels. These cellular disruptions collectively compromised the cortical reaction by inhibiting cortical granule exocytosis and microfilament migration. Our findings suggest that nTiO₂-induced oxidative stress, coupled with an imbalance in energy and Ca²⁺ homeostasis, impairs the cortical reaction and fertilization capacity in T. granosa. This study provides valuable insights into the mechanistic pathway underlying the reproductive toxicity of nTiO₂ in marine invertebrates, offering a basis for evaluating the ecological risks associated with the presence of nanomaterials in marine environments.

Polybrominated biphenyls (PBBs) are metabolically transformed into monohydroxylated PBBs (OH-PBBs) in the environment and living organisms. Although OH-PBBs pose a significant health threat to organisms, little is known about the immunotoxicity of OH-PBBs. Therefore, the objectives of this study were to validate BB-80 and OH-BB-80 induced immunotoxicity and to explore the associated pathway mechanisms. Early development of zebrafish (Danio rerio) larvae was inhibited by 10 μg/L BB-80 and OH-BB-80, as indicated by negative changes in developmental indices. BB-80 and OH-BB-80 induced oxidative stress, significantly up-regulated reactive oxygen species (ROS) and reactive nitrogen species (RNS), and activated the antioxidant enzyme system at 10 μg/L. The mRNA expression levels of inflammatory cytokines and inflammatory chemokines were up-regulated, indicative of the onset of inflammation in zebrafish after BB-80 and OH-BB-80 exposure. In addition, downregulation of toll-like receptor 4 (TLR4), MyD88, and NF-κB pathway-related genes was observed, suggesting that BB-80 and OH-BB-80 target the TLR/NF-κB signaling pathway. Molecular docking data showed that BB-80 and OH-BB-80 bound stably to TLR4. Taken together, BB-80 and OH-BB-80 mediate immunotoxicity and early developmental suppression associated with the TLR4/NF-κB signaling pathway. Our results further the understanding of BB-80- and OH-BB-80-induced immunotoxicity, highlighting the need for toxicological studies to examine the toxic effects of the transformation products of PBBs.