Bisphenol A (BPA) is widely used to harden plastics and polycarbonates and causes serious toxic effects in multiple organs, including the intestines. Selenium, as an essential nutrient element for humans and animals, exhibits a predominant effect in various physiological processes. Selenium nanoparticles have attracted more and more attention due to their outstanding biological activity and biosafety. We prepared chitosan-coated selenium nanoparticles (SeNPs) and further compared the protective effects, and investigated the underlying mechanism of SeNPs and inorganic selenium (Na₂SeO₃) on BPA-induced toxicity in porcine intestinal epithelial cells (IPEC-J2). The particle size, zeta potential, and microstructure of SeNPs were detected by using a nano-selenium particle size meter and a transmission electron microscope. IPEC-J2 cells were exposed to BPA alone or simultaneously exposed to BPA and SeNPs or Na₂SeO₃. The CCK8 assay was performed to screen the optimal concentration of BPA exposure and the optimal concentration of SeNPs and Na₂SeO₃ treatment. The apoptosis rate was detected by flow cytometry. Real-time PCR and Western blot methods were used to analyze the mRNA and protein expression of factors related to tight junctions, apoptosis, inflammatory responses and endoplasmic reticulum stress. Increased death and morphological damage were observed after BPA exposure, and these increases were attenuated by SeNPs and Na₂SeO₃ treatment. BPA exposure disturbed the tight junction function involved with decreased expression of tight junction protein Zonula occludens 1 (ZO-1), occludin, and claudin-1 proteins. Proinflammatory response mediated by the transcription factor nuclear factor-k-gene binding (NF-κB), such as elevated levels of interleukin-1β(IL-1β), interleukin-6 (IL-6), interferon-γ (IFN-γ), interleukin-17 (IL-17), and tumor necrosis factor-α (TNF-α) expression was induced at 6 and 24 h after BPA exposure. BPA exposure also disturbed the oxidant/antioxidant status and led to oxidative stress. IPEC-J2 cell apoptosis was induced by BPA exposure, as indicated by increased BCL-2-associated X protein (Bax), caspase 3, caspase 8, and caspase 9 expression and decreased B-cell lymphoma-2 (Bcl-2) and Bcl-xl expression. BPA exposure activated the endoplasmic reticulum stress (ERS) mediated by the receptor protein kinase receptor-like endoplasmic reticulum kinase (PERK), Inositol requiring enzyme 1 (IRE1α), and activating transcription factor 6 (ATF6). We found that treatment with SeNPs and Na₂SeO₃ can alleviate the intestinal damage caused by BPA. SeNPs were superior to Na₂SeO₃ and counteracted BPA-induced tight junction function injury, proinflammatory response, oxidative stress, apoptosis, and ERS stress. Our findings suggest that SeNPs protect intestinal epithelial cells from BPA-induced damage, partly through inhibiting ER stress activation and subsequently attenuating proinflammatory responses and oxidative stress and suppressing apoptosis, thus enhancing the intestinal epithelial barrier function. Our data indicate that selenium nanoparticles may represent an effective and reliable tool for preventing BPA toxicity in animals and humans.

As environmental pollutants, polybrominated diphenyl ethers (PBDEs) can have toxic effects on living organisms and has a bioaccumulative effect. Low doses of selenium nanoparticles (SeNPs) can exert antioxidant, anti-inflammatory and anti-toxin functions on the organism. This experiment evaluated SeNPs' ability to prevent chicken's intestinal damage from decabromodiphenyl ether (BDE-209) exposure. Sixty layer chickens were separated into four groups at randomly and equally: Control group, SeNPs group (1 mg/kg SeNPs), BDE-209 group (400 mg/kg BDE-209), and BDE-209 +SeNPs group (400 mg/kg BDE-209 and 1 mg/kg SeNPs), for 42 days. The results showed that BDE-209 increased MDA content, decreased the activities of T-SOD, T-AOC, GSH and iNOS, up-regulated the expression of TNF-α, RIPK1, RIPK3 and MLKL, promoted the production of inflammatory factors, reduced the levels of tight junction proteins (Claudin-1, Occludin, ZO-1). SeNPs attenuated intestinal oxidative stress, necroptosis, inflammation and intestinal barrier damage caused by BDE-209. This protective effect is associated with the MAPK/NF-κB signaling pathway. Moreover, SeNPs restores flora alpha and beta diversity, improves intestinal flora composition and its abundance. It shifts the dysbiosis of intestinal flora caused by BDE-209 to normal. Overall, SeNPs can alleviate BDE-209-induced intestinal barrier damage and intestinal flora disorders, which are associated with intestinal oxidative stress, necroptosis and inflammation.

Zearalenone (ZEA) is the most common fungal toxin contaminating livestock and poultry feeding, especially in pigs, causing severe toxic effects and economic losses. However, the mechanism of ZEA damage to the intestine is unknown. We constructed an in vitro model of ZEA toxicity in a porcine small intestinal epithelial cell (IPEC-J2) line. ZEA causes severe oxidative stress in porcine small intestine cells, such as the production of ROS and a significant decrease in the levels of antioxidant enzymes GSH, CAT, SOD, and T-AOC. ZEA also caused apoptosis in porcine small intestine cells, resulting in a significant reduction in protein and/or mRNA expression of apoptosis-related pathway factors such as P53, caspase 3, caspase 9, Bax, and Cyt-c, which in turn caused a significant decrease in protein and/or mRNA expression of inflammatory-related factors such as IL-1β, IL-2, Cox-2, NF-κD, NLRP3, IL-6, and IL -18, which in turn caused a significant increase in protein and/or mRNA expression levels. The final results suggest that ZEA can cause a severe toxic response in porcine small intestine cells, with oxidative stress, apoptotic cell death and inflammatory damage.