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Terbuthylazine (TBA), a triazine herbicide, is extensively employed in agriculture for its wide range of effectiveness. However, prolonged utilization of TBA can pose a potential hazard to animals and human health. Here, a total of 180 broiler chickens (Gallus gallus) were stochastically assigned to three groups (control group, 0.4 mg/kg TBA group, and 4 mg/kg TBA group) for investigating the impact of TBA on cardiotoxicity. The results revealed that TBA exposure resulted in pathological alterations in the myocardium. Moreover, TBA exposure activated cGAS-STING pathway and markedly elevated the mRNA and protein expression levels of innate immune response (cGAS, STING, TBK1, and IRF3) in myocardium. Additionally, NF-κB signal was also activated under TBA exposure, which was characterized by the increasing mRNA expression levels of NF-κB, IKKα and the protein expression levels of p-NF-κB/NF-κB, IKKα, p-IκBα/IκBα in the TBA treatment groups. Meanwhile, the expression of pro-inflammatory cytokines (TNF-α and IL-1β) were also significantly increased. In summary, our findings suggested that cGAS-STING/NF-κB pathway functionated in the innate immune response and inflammation in myocardium brought on by TBA exposure, which provided new insights into the TBA toxicology. [Display omitted] • TBA induced pathological damage in chicken myocardium. • The innate immune response and inflammation were activated by TBA. • cGAS-STING and NF-κB pathway mediated innate immune response under TBA exposure. [ABSTRACT FROM AUTHOR]

Terbuthylazine (TBA) is one of the most commonly used and effective herbicides. However, due to its affinity for soil organic matter and water solubility, TBA can lead to biological health concerns. This study exposed broilers to TBA (0 mg/kg bw, 0.4 mg/kg bw, 4 mg/kg bw) for 28 days. The results showed significant pathological damage in broiler myocardial tissue, such as widening of the interstitial space, rupture of muscle fibers, and deposition of myocardial collagen fibers. In addition, Under the 0.4 mg/kg bw TBA exposure, myocardial oxidative stress was observed in broilers, which was accompanied by the activation of Nrf2/HO-1 pathway and the increased protein and mRNA levels of NQO1, NOX2 and SOD2 antioxidant enzymes. However, Nrf2/HO-1 protein and mRNA levels were reversed at 4 mg/kg bw TBA exposure. Meanwhile, the Nrf2/HO-1 mediated antioxidant defense was impaired. In contrast with the low dose, the protein and gene expression levels of NQO1, NOX2, and SOD2 were reduced in 4 mg/kg bw TBA group. The expression of GPX4 and SLC7A11 was significantly downregulated at both protein and mRNA levels. Beyond that, ACSL4 expression was significantly up-regulated, and the protein result was consistent with the mRNA expression, demonstrating the occurrence of ferroptosis. In general, TBA exposure activated the Nrf2/HO-1 pathway, resulting in ferroptosis. This study links ferroptosis to the Nrf2/HO-1 pathway, providing new insights into the potential role of TBA in myocardial toxicity. [Display omitted] • TBA exposure damages the myocardium of broiler chickens. • TBA induces oxidative stress and ferroptosis in broiler myocardium. • Low-dose exposure to TBA activated the Nrf2/HO-1 pathway. • An imbalance in redox occurs when exposed to a high dose of TBA. [ABSTRACT FROM AUTHOR]