Aldehyde reductase (AKR1A1) is a carbonyl detoxification protein in toxic aldehyde removal. In the present study, the full-length cDNA of yellow catfish AKR1A1 (TfAKR1A1) was cloned. As expected, yellow catfish AKR1A1 showed similarities with that of other species. Subsequently, prokaryotic expression vector was constructed and recombinant TfAKR1A1 (rTfAKR1A1) was successfully induced and purified. rTfAKR1A1 exhibited reductive activity to many aldehydes and ketones. To determine whether TfAKR1A1 could confer stress tolerance in vitro, the viability of control and TfAKR1A1 expression E. coli under abiotic stress was compared by spot assay. Results showed that the recombinant strain had better stress resistance under cadmium, hydrogen peroxide, and DL-glyceraldehyde stress. Then, effects of an intraperitoneal injection of rTfAKR1A1 protein on cadmium-induced oxidative stress were evaluated. Results displayed that TfAKR1A1 and Nrf2 expression levels were significantly decreased, CAT and SOD expression levels were significantly increased, BCL-2 and IL-10 expression levels were significantly increased, and caspase3a, NF-κB, and IL-1β expression levels were significantly decreased in protein-injection group. Furthermore, oxidative stress indexes in livers under different protein injection doses were examined by ELISA. Results showed that CAT, SOD, and GSH-Px activities were upregulated, ROS and T-AOC contents were also improved, while MDA content was significantly decreased both in lower and middle dose injection groups. Finally, liver pathological section analysis was performed. Results displayed that liver injury degree in protein-injected groups was lower than that of PBS group under cadmium stress. These results suggested that TfAKR1A1 played important roles in response to cadmium stress in yellow catfish.
Keywords: AKR1A1; Cadmium stress; Histopathology; Oxidative damage; Tachysurus fulvidraco.
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