Biochemical indices, histological observations and transcriptome sequencing reveal the response mechanism of largemouth bass (Micropterus salmoides) to transport stress

In this study, transport conditions were simulated to investigate changes in intestinal tissue structure, oxidative stress, apoptosis and transcriptome levels during transport stress of largemouth bass (Micropterus salmoides). The results showed that the serum cortisol and lactic acid levels in largemouth bass significantly increased with increasing transport time, and the glucose content peaked after 8 h of transport. After 8 h and 12 h, the Reactive oxygen species, superoxide dismutase, malondialdehyde, and lipid peroxide contents in the intestine were significantly higher than those in the control group and the stressed group at 4 h. Additionally, more of the mucous membrane of intestinal tissue was exfoliated, resulting in edema, and the intestinal villi height and density significantly decreased. The differentially expressed genes were further analyzed after 0 h, 8 h, and 12 h of transport stress. There were significant differences in genes associated with the p53 signaling pathway (igfbp1a, ccnb1, cdk1, and igfbp6b) and apoptosis (bcl2l11, parp3, pik3r1, fadd, aifm1, and lmnb1). Combined with the increasing amount of apoptotic cells after stress, these results indicated that transport stress had a substantial effect on intestinal cell apoptosis. The intestinal antioxidant activity and tissue structure of the stressed groups recovered to the pre-stress level after 7 d of recovery from 8 h of transport; however, these parameters did not return to pre-stress levels after 7 d of recovery from 12 h of transport. This finding further demonstrated that long-term transport stress induced apoptosis and tissue damage in the largemouth bass intestine through p53 signaling.