Exogenous Ca mitigates the toxic effects of TiO nanoparticles on phagocytosis, cell viability, and apoptosis in haemocytes of a marine bivalve mollusk, Tegillarca granosa.

Phagocytosis suppression induced by nanoparticles (NPs) exposure is increasingly reported in marine species. However, the mechanisms underlying this impact remain poorly understood. In order to improve our present understanding of the immunotoxicity of NPs, acute (96 h) TiO NP exposure and rescue trials via exogenous supply of Ca were performed in the blood clam, Tegillarca granosa. The results show that the phagocytosis rate, cell viability, and intracellular Ca concentration of haemocytes were significantly suppressed, whereas the intracellular ROS concentration of haemocytes significantly increased upon nTiO exposure. Exposure to nTiO also led to the significant downregulation of Caspase-3, Caspase-6, apoptosis regulator Bcl-2, Bcl-2-associated X, calmodulin kinase II, and calmodulin kinase kinase II. Furthermore, the toxic impacts of nTiO were partially mitigated by the addition of exogenous Ca, as indicated by the recovery tendency in almost all the measured parameters. The present study indicates that Ca signaling could be one of the key pathways through which nTiO attacks phagocytosis.