This work aimed to elucidate whether maternal lithium chloride (LiCl) exposure disturbs the thyroid–cerebral axis in neonatal albino rats. 50 mg of LiCl/kg b.wt. is orally given for pregnant Wistar rats from gestational day (GD) 1 to lactation day (LD) 28. The maternal administration of LiCl induced follicular dilatation and degeneration, hyperplasia, lumen obliteration and colloid vacuolation in the maternal and neonatal thyroid gland at postnatal days (PNDs) 14, 21 and 28. Neuronal degeneration (spongiform), gliosis, nuclear pyknosis, perivascular oedema, and meningeal hyperaemia were observed in the neonatal cerebral cortex of the maternal LiCl-treated group at examined PNDs. This disturbance appears to depend on intensification in the neonatal cerebral malondialdehyde (MDA), nitric oxide (NO), and hydrogen peroxide (H₂O₂) levels, and attenuation in the glutathione (GSH), total thiol (t-SH), catalase (CAT), and superoxide dismutase (SOD) levels. In the neonatal cerebrum, the fold change in the relative mRNA expression of deiodinases (DII and DIII) increased significantly at PNDs 21 and 14, respectively, in the maternal LiCl-treated group. These data suggest that maternal LiCl may perturb the thyroid–cerebrum axis generating neonatal neurodevelopmental disorder.

中文翻译：

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母体 LiCl 暴露会破坏新生白化大鼠的甲状腺 - 脑轴

这项工作旨在阐明母体氯化锂 (LiCl) 暴露是否会扰乱新生白化病大鼠的甲状腺 - 脑轴。50 mg LiCl/kg b.wt。从妊娠日 (GD) 1 到哺乳日 (LD) 28 为怀孕的 Wistar 大鼠口服给药。母体施用 LiCl 可在产后几天诱导母体和新生儿甲状腺中的卵泡扩张和变性、增生、管腔闭塞和胶体空泡形成(PND) 14、21 和 28。在检查的 PND 中，在母体 LiCl 治疗组的新生儿大脑皮层中观察到神经元变性（海绵状）、神经胶质增生、核固缩、血管周围水肿和脑膜充血。这种干扰似乎取决于新生儿大脑丙二醛 (MDA)、一氧化氮 (NO) 和过氧化氢 (H ₂O ₂ ) 水平，以及谷胱甘肽 (GSH)、总硫醇 (t-SH)、过氧化氢酶 (CAT) 和超氧化物歧化酶 (SOD) 水平的衰减。在新生儿大脑中，在母体 LiCl 处理组中，脱碘酶（DII 和 DIII）的相对 mRNA 表达的倍数变化分别在 PND 21 和 14 显着增加。这些数据表明，母体 LiCl 可能会扰乱甲状腺 - 大脑轴，从而产生新生儿神经发育障碍。