The present study evaluated the effects of 3 supplemental levels of dietary genistein ingested during the late laying period (66-73 wk) of laying hens. A total of 384 Hy-Line brown hens (66 wk old) were randomly divided into 4 groups (6 replicates of 16 hens in each group), the basal diet group (CON), and groups for the basal diet supplemented with 80, 120, and 400 mg/kg of genistein, G1, G2, and G3, respectively. The results of the present study showed an increased laying rate in groups G2 and G3 (linear, P < 0.01), and decreased feed-egg ratios (linear, P < 0.05) and broken egg rate (P < 0.01) in all genistein-treated groups compared with the CON group. Moreover, the G2 group showed an increase in eggshell strength and ratio (linear, P < 0.05), whereas all genistein-treated groups saw a decrease in the L* value (linear, P < 0.01) and an increase in the a* value (linear, P < 0.05) compared with the CON group. Additionally, all genistein-treated groups had an increase in the total antioxidant capacity of plasma (linear, P < 0.05), along with reduced plasma, ovarian, and yolk malondialdehyde levels (linear, P < 0.05), compared with the CON group. The G2 group had an increase in both the superoxide dismutase activity of plasma (P < 0.01) and the total antioxidant capacity of the ovaries (linear, P < 0.05), compared with the CON group. The G3 group had an increase in both the glutathione peroxidase concentration of plasma (linear, P < 0.05) and the total antioxidant capacity of the ovaries (linear, P < 0.01), compared with the CON group. The transcript levels of nuclear factor erythroid 2-related factor 2, superoxide dismutase 1, and catalase were increased in all of the genistein-treated groups (P < 0.05) compared with the CON group, whereas heme oxygenase 1 and glutamate-cysteine ligase modifier subunit were increased only in the G2 group (P < 0.05). In conclusion, supplementation with 120 mg/kg dietary genistein had the best effect on improving the laying rate, eggshell quality, and antioxidant capacity in Hy-Line brown hens during the late laying period.

Microplastics (MPs), environmental pollutants resulting from the degradation of plastic products and industrial processes, have become ubiquitous in global ecosystems. MPs can enter the human body through ingestion, inhalation, and dermal contact subsequently accumulating in vital tissues such as the liver, lungs, blood, and placenta. This review systematically evaluates the metabolic fate of MPs in humans, emphasizing their translocation across biological barriers and organ-specific deposition. We elaborated on the direct damage of MPs on the intestinal mucosal barrier and while simultaneously remodelling the gut microbiota, and focuses on the regulatory role of gut microbiota in the process of MPs-induced human health damage. Ingestion of MPs induces mechanical damage to the intestinal mucosa, epithelial cell apoptosis, and inflammation. It also alters gut microbial composition, that most notably increasing Firmicutes while decreasing Bacteroidetes and Actinobacteria, as well as disrupts metabolite production, including short-chain fatty acids and bile acids. These microbiota-mediated changes propagate via the gut-liver or gut-brain axis, contributing to obesity, cardiovascular diseases, neurological disorders, and reproductive impairments. This review clarifies the potential mechanism of MPs affecting human health through gut microbiota, and clearly identifies gut microbiota regulation as a potential therapeutic strategy to mitigate MP-induced diseases, and provides practical guidance for reducing MP-related health risks.