Nowadays, the risk of oral intake of microplastics (MPs) and cadmium (Cd) by poultry is high. In some industrially polluted areas, the chicken feed samples contain 9.60 × 10² ± 1.09 × 10² MPs per kilogram (mean ± std) in wet weight, and the Cd content in chicken feed has been detected to reach up to 5.61 mg/kg. But scholars still focus more on the toxic effects of MPs and Cd on the liver and intestines of aquatic animals. There are few studies that use poultry as research animals and consider these two organs as an integrated system to investigate the toxicity of MPs and Cd on the gut-liver axis and the mechanisms of inflammation. Therefore, in this research, broilers were used as experimental subjects, and experimental models were established by single or combined exposure of MPs (100 mg/L) and Cd (140 mg/kg) to explore the effects of MPs and Cd on the intestinal mucosae and liver of broilers, as well as the mechanisms behind these toxic effects. In this study, the degree of adverse effects (decreased expression of tight junction proteins, changes in intestinal morphology, abundance and diversity of intestinal flora, liver inflammation) caused by the single exposure group was higher than that of the combined exposure group. The results showed that MPs and Cd induced intestinal damage and liver inflammation in broilers by interfering with the TLR4/MyD88/NF-κB pathway and intestinal flora homeostasis. The toxicity of combined exposure was lower than that of single exposure.

Ochratoxin A (OTA), as a mycotoxin, can contaminate a variety of feeds and foods. Existing studies have shown that the main toxicity of OTA to organisms is nephrotoxicity, but the toxic mechanism to other organs is still worthy of further study. Whether OTA causes intestinal damage through the necroptosis pathway mediated by RIPK1/RIPK3/MLKL remains to be elucidated. Astaxanthin (AST), a feed additive with strong antioxidant properties, was used as an antidote to evaluate the alleviation effect on OTA-induced intestinal injury and the underlying mechanism in this research. Chickens are the most sensitive animals to OTA except pigs. Therefore, 70 white-feathered chickens (n = 15) and Chicken Small Intestinal Epithelial Cells (CSIECs) were used as experimental subjects. Experimental models were established by single or combined exposure of OTA (1.0 mg/kg on chickens for 21 d; 2 μM on CSIEC for 24 h) and AST (100 mg/kg on chickens for 21 d; 40 μM on CSIEC for 24 h). In this study, AST significantly ameliorated OTA-induced intestinal damage by restoring the expression of tight junction proteins (Occludin-1, Claudin-1, and ZO-1), attenuating severe histopathological alterations, mitigating the inflammatory response (elevated pro-inflammatory cytokines and reduced anti-inflammatory mediators), and suppressing necroptosis through downregulation of RIPK1, RIPK3 and MLKL expression. Combined evidence from animal experiments and cell culture experiments demonstrated that AST alleviated the necroptosis and inflammation caused by OTA in CSIECs and the intestine of chickens through the RIPK1/RIPK3/MLKL signaling pathway, thereby reducing the damage caused by OTA.