The crosstalk between autophagy and apoptosis mechanism of hemocytes in Chlamys farreri under B[a]P exposure in vitro

Abstract

The impact of polycyclic aromatic hydrocarbons (PAHs) on the immune function of marine animals has garnered significant attention. C. farrei is frequently exposed to pollutants and has only innate immunity. To delve more deeply into the immunotoxicity mechanism of PAHs in C. farrei, its hemocytes were cultured in vitro as they were the primary drivers of immune activities. The autophagy and apoptosis of hemocytes are essential components of the immune response. The exposure of pollutant, autophagy and apoptosis of immune cells are often disrupted, leading to immunodeficiency. In aquatic animals, the mechanism of autophagy and apoptosis in hemocytes remains unclear, and the crosstalk between the two needs to be further investigated. To evaluate the mechanism of autophagy and apoptosis of hemocytes in vitro, 0 μM, 1 μM, 2.5 μM or 5 μM Benzopyrene (B[a]p) was chosen. Experimental results demonstrated that B[a]P triggered autophagosome formation, but also caused significant damage to lysosomes, resulting in a compromised autophagic flux. B[a]P causes an increase in apoptosis levels in hemocytes of C. farreri by affecting the transcriptional level of AIF. To further explore the crosstalk mechanism between the two, activator and inhibitor of autophagy were used. After adding autophagy activator or inhibitor, the present results indicated that Lysosomal function determined the patency of autophagic flux. When massive autophagosomes accumulate, it leads to a much higher rate of apoptosis through caspase-dependent apoptotic pathway. Lysosomal damage further leads to apoptosis and inhibit autophagy. In the B[a]P-treated group, immunological parameters were markedly decreased due to autophagy and apoptosis of hemocytes. The immunotoxicity mechanism of B[a]P in C. farreri hemocytes was investigated in present study, which enriched the immunotoxicity network.