The molecular mechanism of ferroptosis in the Pacific oyster Crassostrea gigas under Erastin treatment or high temperature stress

Abstract

Ferroptosis is an iron- and lipotoxicity-dependent form of programmed cell death, and it is distinct from apoptosis, pyroptosis, and autophagy. In the present study, the hemocytes were found to be shrunken under Erastin treatment or high temperature stress. The mitochondrial atrophy, crest loss and fracture were observed in hemocytes under high temperature stress. In addition, the fluorescence intensity of mitochondrial probe JC-1 monomers increased significantly in hemocytes under high temperature stress. Hemocytes were found to be wrinkled under ultrastructure and the contents of LPO, ROS and GSH increased significantly under Erastin treatment or high temperature stress. The band intensity of CgVDAC2 also decreased under Erastin treatment or high temperature stress. The mRNA expressions of genes involved in enhancing the antioxidation system as well as genes involved in promoting the iron metabolism all decreased significantly under Erastin treatment or high temperature stress. Those of genes involved in impairing the antioxidation system, genes involved in inhibiting the iron metabolism, as well as genes involved in reducing the lipid peroxidation all increased significantly under Erastin treatment or high temperature stress. These results indicated that Erastin could activate the three key ferroptotic signaling pathways in oyster and the activation mechanism of ferroptosis in oyster under high temperature stress was similar with that under Erastin treatment.