The interference in endocrine signaling in particular of hypothyroid-pituitary-thyroid axis during embryonic/neonatal development increases the risk of long-lasting immune dysfunctioning. Anticipating that, environmentally realistic exposure of established thyroid disrupting pesticides of dithiocarbamate group mancozeb and phenylpyrazole fipronil was given to mice as individual and as mixtures (MIX-I/MIX-II) during the critical initiation phase of the immune response from postnatal day (PND) 31 till PND 60 (maturation phase). The direct exposure effect was assessed at PND 61 and the persistent effect was assessed at PND 91. Pronounced oxidative stress/genotoxicity in lymphoid organs at even low dose mixture exposure of pesticides (MIX-I/ MIX-II) continued to suppress the immune system till adulthood; might be due to the synergistic/additive action. The oxidative stress/genotoxicity effect was prevented on T4 supplementation to inhibit immunotoxicity as T4 is an immune enhancer and antioxidants. Oxidative stress/genotoxicity is suggested as a mechanism of thyroid disruption mediated immune suppression.

胚胎/新生儿发育过程中内分泌信号的干扰，特别是甲状腺-垂体-甲状腺轴的干扰增加了长期免疫功能障碍的风险。预期在出生后一天（PND）的免疫反应的关键起始阶段，以小鼠的个人和混合物（MIX-I / MIX-II）的形式在环境中实际暴露已确立的破坏甲状腺的二硫代氨基甲酸酯类代森锰锌和苯基吡唑氟虫腈的甲状腺杀虫剂。 ）31至PND 60（成熟阶段）。在PND 61评估了直接暴露效果，在PND 91评估了持久效果。即使在低剂量的农药混合暴露下（MIX-I / MIX-II），淋巴器官的明显氧化应激/遗传毒性仍继续抑制免疫系统直到成年；可能是由于协同/相加作用。由于T4是一种免疫增强剂和抗氧化剂，因此在补充T4时可防止氧化应激/遗传毒性作用，从而抑制免疫毒性。氧化应激/遗传毒性被认为是甲状腺破坏介导的免疫抑制的机制。