TBBPA caused multiple intestinal injuries via ROS/NF-κB signal in common carp.

Abstract

Tetrabromobisphenol A (TBBPA) is an aquatic environment's prevalent pollutant, posing a great threat to the health of aquatic animals. The intestine is a key organ for nutrient absorption as well as an important barrier to prevent pollutants from invading the body of fish. Exploring the effects of pollutants on the intestine is of great significance for maintaining fish health. Therefore, the purpose of this study was to assess the toxic effects of TBBPA on the intestine of Cyprinus carpio L. (common carp) by establishing models of common carp and primary intestinal epithelial cells exposed to TBBPA. Histological observation revealed that TBBPA exposure led to damage in the intestinal mucosa and breakage of intestinal villi. Detection of oxidative stress levels showed that TBBPA increased the levels of ROS and MDA, and decreased the activity of SOD, CAT, GSH-PX, and T-AOC in intestinal tissue and cells. Observation of inflammatory factor levels revealed that TBBPA upregulated the mRNA levels of inflammatory factors (IL-6, TNF-α, IL-1β, NF-κB p65 and IκBα). ELISA and western blotting results were consistent with the mRNA results. Moreover, TBBPA induced cell death, as evidenced by TUNEL staining and flow cytometry and confirmed by increasing levels of Bax, Cas-3, Cyt C, RIP1, RIP3, and MLKL, together with decreasing the levels of Bcl-2. TBBPA also destroyed the intestinal tight junction by reducing the mRNA and protein levels of claudin-1, ZO-1, and occludin. In summary, this study reveals that TBBPA caused intestinal injuries, inducing oxidative stress, inflammation, cell death, and tight junction disruption via ROS/NF-κB signal in common carp.