The mechanism of Mitogen-Activated Protein Kinases to mediate apoptosis and immunotoxicity induced by Benzo[a]pyrene on hemocytes of scallop Chlamys farreri in vitro.

Benzo [a]pyrene (B [a]P) has received widespread attention for serious pollution in the sea, which may reduce immunity and lead to the outbreak of disease in bivalves. However, the mechanism of immunotoxicity induced by B [a]P in bivalves was still unclear. Previous studies have found that Mitogen-Activated Protein Kinases (MAPKs) including three classic pathways (ERK, p38 and JNK) play an important role in mediating this process. Thus, in order to explore the mechanism of immunotoxicity induced by B [a]P in scallop Chlamys farreri, hemocytes were treated with PD98059 (ERK inhibitor), SB203580 (p38 inhibitor) and SP600125 (JNK inhibitor) for 1 h and then incubation with B [a]P for 24 h at 1 µg/mL. Indexes including oxidative damage, apoptotic rate, and immune indicators were detected in the present study. The results showed that the increase of Reactive Oxygen Species (ROS) and DNA damage induced by B [a]P was inhibited with PD98059 and SB203580. Besides, lysosomal membrane stability (LMS) damage was promoted by PD98059, while it was opposite when treated with SB203580. Moreover, the ascended apoptosis rate induced by B [a]P was increased significantly after treatment with PD98059, but it was remarkably attenuated by SB203580 and SP600125. However, the opposite pattern was showed in phagocytosis compared with apoptosis rate in all of three inhibitors. In addition, antibacterial activity and bacteriolytic activity were enhanced by SB203580 while inhibited by PD98059. Therefore, these results showed that MAPKs directly or indirectly mediate the decrease of oxidative damage, apoptosis and immune defense ability of C. farreri hemocytes, which suggesting ERK/p38/JNK pathways have different functions in the apoptosis and immunity of C. farreri hemocytes after B [a]P exposure. In conclusion, this study intended to enrich the theoretical basis for immunotoxicology of bivalves exposed to pollutants.