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Maternally-mediated developmental lithium toxicity in the mouse

F S Messiha1

  • 1Texas Tech University Health Sciences Center, School of Medicine, Lubbock 74930.

General Pharmacology
|January 1, 1993
PubMed
Summary

Maternal lithium chloride (LiCl) exposure during pregnancy and breastfeeding causes developmental toxicity in mouse offspring. Female offspring showed greater sensitivity to organ weight changes, with specific enzyme alterations observed in both sexes.

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Area of Science:

  • Toxicology
  • Developmental Biology
  • Pharmacology

Background:

  • Lithium salts are widely used therapeutically but can cross the placenta.
  • Maternal medication use during pregnancy and lactation necessitates understanding potential offspring toxicity.

Purpose of the Study:

  • To investigate maternally-mediated developmental toxicity of lithium chloride (LiCl) in mice offspring.
  • To determine the influence of offspring gender and maternal LiCl intake duration on toxicity.

Main Methods:

  • Mice dams were administered LiCl (1 mEq) from preconception through weaning.
  • Offspring were assessed for organ weight changes and specific enzyme activities (hepatic alcohol dehydrogenase, heart lactate dehydrogenase, liver aldehyde dehydrogenase).

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Main Results:

  • Female offspring exhibited greater sensitivity to organ weight changes compared to males.
  • Maternal LiCl intake induced hepatic alcohol dehydrogenase and heart lactate dehydrogenase in both sexes.
  • Liver aldehyde dehydrogenase induction occurred only following postnatal LiCl exposure.

Conclusions:

  • Maternal exposure to lithium salts during gestation and lactation can lead to developmental toxicity in offspring.
  • Breastfeeding plays a role in the transmission of LiCl-induced developmental effects.
  • Gender-specific sensitivities and enzyme alterations highlight the complex impact of in utero and lactational LiCl exposure.