Nitrite induces endoplasmic reticulum stress and associates apoptosis of liver cells in grass carp (Ctenopharyngodon idella)

Nitrite pollution is one of the most frequently reported problems in aquaculture. However, little is known for its toxic mechanisms. The present study was conducted to investigate the effects of nitrite on antioxidant capacity, ER stress (Endoplasmic Reticulum stress) and apoptosis in grass carp (Ctenopharyngodon idella). Fish were exposed to nitrite (0, 8, 25, 50 mg L-1) for 96 h, the genes expression, histological section and antioxidant enzyme activity were assayed. The results show that the expression of ER stress marker gene grp78 was significantly upregulated in liver, the expression of PERK pathway genes perk, eif-2 alpha, atf4 and chop have changed, the superoxide dismutase (SOD) activity decreased while the catalase (CAT) activity increased significantly in serum, fish liver shows severe damage in nitrite exposure. Grass carp liver cells (L8824) were incubated in nitrite solution (0, 2.5, 10, 100 mg L-1) for 24 h. Significant decrease in cell viability and apoptosis were observed in the treatment, the expression of ER stress marker gene grp78 was up-regulated, moreover the PERK pathway genes perk, eif-2 alpha, atf4 and chop were up-regulated in 2.5 mg L-1 and 10 mg L-1. The expression of the proapoptotic gene bax was significantly up-regulated, and the expression of the inhibitory gene bcl-2 was significantly down-regulated, therefore the ratio of bax/bcl-2 was up-regulated. These results indicate that in the nitrite-induced acute liver injury of grass carp, ER stress response may activate antioxidant system as a protection.