Cadmium activated oxidative stress and endoplasmic reticulum stress pathway promote apoptosis in the common carp (Cyprinus carpio L.) brain

Cadmium (Cd) is one of the main heavy metal water pollutants that seriously endangers fish health. The aim of this study was to investigate the effects of Cd on oxidative stress, endoplasmic reticulum stress (ER-stress) and apoptosis in the common carp (Cyprinus carpio L.) brain. A total of 360 carp (9.93 ± 0.52 g) were exposed to 0, 1, 2, 4 mg/L Cd for 56 days, and oxidative stress ER-stress and apoptosis related indicators detected by RT-qPCR, Western blot, TUNEL, and immunofluorescence. Cd affected MDA, SOD, CAT and GSH-PX levels in serum, the mRNA expression of CAT, SOD, Keap1, Nrf2, Bcl-2, Bax, Caspase3, Caspase9, grp78, ATF4 and ATF6 in brain tissue, and protein expression levels of Bax, Bcl-2, grp78 and ATF6 in brain tissue, indicating that Cd could induce oxidative stress, activate ER-stress and promote apoptosis. To further explore the relationship between Cd-induced apoptosis and ER-stress, ER-stress inhibitors (TUDCA) and agonists (TM) were added under Cd exposure to detect ER-stress (ATF6 and grp78) and apoptosis related indicators (Bax and Bcl-2 ). ER-stress inhibition alleviated Cd-induced apoptosis, while ER-stress activation promoted Cd-induced apoptosis. Basically, Cd induced oxidative stress, and activated ER-stress promoted brain tissue apoptosis, which provides valuable information and a fresh perspective for further research into Cd-induced brain injury in fish.