What is it about?

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.

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Why is it important?

The maternal administration of 50 mg of LiCl/kg. b.wt. caused thyroid dysgenesis in maternal rats and their neonates. Also, this administration induced some histological alterations in the neonatal cerebral cortex, imbalanced the neonatal cerebral prooxidant/antioxidant system, and disrupted the relative mRNA expression of deiodinases II & III. Thus, maternal LiCl exposure perturbed thyroid-cerebral hemostasis during the postnatal period.

Perspectives

Two conclusions can be drawn from these results: (1) Maternal administration of LiCl caused thyroid dysgenesis in neonates and disrupted THs metabolism (deiodinases II & III) in the neonatal cerebrum. (2) This administration appeared to disturb the prooxidant and antioxidant axis, and cerebral development. This disruption may perturb thyroid-cerebral hemostasis during the postnatal period (Fig. 5). Thus, the possible detrimental effects of LiCl on the developing thyroid-brain axis are immensely complex, an observation that may also be of significance to human life. Additional experimental studies need to be carried out to recognize this issue.

Full Professor Ahmed R. G.
Division of Anatomy and Embryology, Zoology department, Faculty of Science, Beni-Suef University, Egypt.

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This page is a summary of: Maternal LiCl exposure disrupts thyroid‐cerebral axis in neonatal albino rats, International Journal of Developmental Neuroscience, September 2021, Wiley,
DOI: 10.1002/jdn.10151.
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