Early-life glyphosate exposure impairs intestinal antioxidant status and induces growth retardation in post-hatched chicks.

Glyphosate is the most popular herbicide used worldwide. This study aimed to investigate the toxicological effects of early-life glyphosate exposure on the growth performance, intestinal digestive function, and antioxidant capacity of post-hatch layer chicks. During the embryonic incubation period, the eggs were treated with glyphosate. Samples were collected on the day of hatching (day 0) and seven days post-hatching (day 7). The results showed that glyphosate exposure reduced hatchability and body weight on day 7, while also decreasing average daily gain (ADG) and increasing the feed-to-gain ratio (F:G ratio). The villus height in the jejunum and ileum decreased on both day 0 and day 7, and the villus height-to-crypt depth ratio in the jejunum declined on day 7. Additionally, the intestinal digestive and absorptive functions, as well as the intestinal barrier function of the chicks, were also impaired after hatching. Glyphosate also triggered inflammation by upregulating TNF-α, IL-1β, and IL-6 mRNA levels and activating the NF-κB signaling pathway. Antioxidant capacity was initially enhanced on day 0, as evidenced by increased T-SOD activity and elevated MDA levels. However, it significantly declined by day 7, with reduced activities of T-SOD and GSH-px, as well as decreased expression of Nrf2 pathway proteins (Nrf2, NQO1, HO1). These findings demonstrate that early-life glyphosate exposure induces intestinal oxidative stress during later stages of growth, impairing intestinal digestion and absorption function, ultimately reducing growth performance. In this process, excessive oxidative stress induced by glyphosate exposure activates the Nrf2 and NF-κB signaling pathways. Our study provides experimental data and a reference for assessing risks of early-life glyphosate exposure-induced developmental disorders.