Acute deltamethrin exposure induces oxidative stress, triggers endoplasmic reticulum stress, and impairs hypoxic resistance of crucian carp

Abstract

Deltamethrin (Del) has been widely used for effectively controlling ectoparasites of crucian carp and was also strictly prohibited in a hypoxic environment. A previous study indicated that Del exposure causes gill injury in Carassius auratus, which is associated with oxidative stress and endoplasmic reticulum stress (ER stress), but the precise mechanism is not well understood. Here, crucian carp were exposed to Del (0.61, 1.22, 2.44, 4.88 μg/L) for 24 h and then subjected to acute hypoxia challenge (1.0 mg/L) for 24 h. The results revealed that acute exposure to Del notably increased MDA content but markedly decreased CAT activities. Moreover, the T-AOC and SOD activities first increased and then decreased in the 4.88 μg/L Del group. Likewise, the mRNA levels of Nrf2 signaling and its target genes (ho-1, mt, sod, cat, and gpx1) were significantly downregulated in the high concentration exposure groups, while the mRNA levels of keap1 showed the opposite change trend. Meanwhile, Del exposure evoked the PERK-ATF4-CHOP and IRE1 signaling pathways and triggered ER stress in a dose-dependent manner in crucian carp. Importantly, we found that Del exposure significantly decreased the survival rate of crucian carp after hypoxia challenge by reducing oxygen uptake, modifying energy metabolism, and promoting lactate accumulation. Additionally, Del exposure aggravated gill damage and apoptosis under hypoxic stress, which was confirmed by histological assays. Collectively, we inferred that acute exposure to deltamethrin induces oxidative stress and ER stress and impairs hypoxic resistance of crucian carp.