Cytotoxicity induced by abamectin in hepatopancreas cells of Chinese mitten crab, Eriocheir sinensis: An in vitro assay

Toxic effects of abamectin on non-target aquatic organisms have been well documented due to its extensive use in both agricultural and aquacultural areas. However, knowledge of the abamectin induced cytotoxicity in crustacean hepatopancreas is still incomplete. In this study, we investigated the cytotoxic effects of abamectin on hepatopancreas cells of Chinese mitten crab, Eriocheir sinensis by an in vitro assay. The results showed that abamectin inhibited cell viability with elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels in a dose-dependent manner. Increased olive tail moment (OTM) values and 8-hydroxy-2 & PRIME;-deoxyguanosine (8-OHdG) contents indicate the DNA damage under abamectin exposure. The up-regulation of the typical apoptosis-related protein BCL2-associated X protein (Bax) and the down-regulation of B cell leukemia/lymphoma 2 (Bcl-2) demonstrate apoptosis in hepatopancreas cells. Meanwhile, the activities of both caspase-3 and caspase9 were increased, indicating caspase-mediated apoptosis. In addition, qRT-PCR results showed the up-regulation of antioxidant genes superoxide dismutase (SOD) and catalase (CAT). The mRNA expression of Cap 'n & PRIME; Collar isoform-C (CncC) and c-Jun NH2-terminal kinases (JNK) was also significantly increased, implying the involvement of the Nrf2/MAPK pathway in the antioxidative response. The alteration of innate immune-associated genes Tolllike receptor (TLR) and myeloid differentiation primary response gene 88 (Myd88) also indicates the influence of abamectin on immune status. In summary, the present study reveals the cytotoxicity of abamectin on hepatopancreas cells of E. sinensis and this in vitro cell culture model could be used for further assessment of pesticide toxicity.

Automated summary

This study investigated the cytotoxic effects of abamectin on hepatopancreas cells of Chinese mitten crab. The results showed that abamectin inhibited cell viability and caused oxidative stress, DNA damage, and apoptosis. It also induced changes in antioxidant response and immune status.