Maternally-mediated neonatal lithium-cesium interaction in the mouse.

The effect of maternal exposure to LiCl, CsCl or both salts in the weaning and developing offspring mice was studied on selected organ weights, hepatic and cardiac dehydrogenase enzymes. The concentration of alkali metal used in maternal drinking fluid during pregnancy and breast-feeding did not produce taste aversion and therefore approximate equal consumption was assured. Maternal exposure to either alkali metal reduced brain and testis weights of the developing offspring mice compared to controls. This suggests a delayed toxic effect on the CNS and endocrine organs. Coadministration of both salts negated this effect. The maternal neonatal Li-mediated increases of weanling spleen weight and the reduction of testis weight of developing offspring mice by Li or Cs were not evident when both alkali metals were given in combination. The combined maternal exposure to both Li and Cs salts also negated the induction of offspring mouse liver alcohol dehydrogenase produced by either alkali metal alone. Likewise, the induction of developing mouse heart lactate dehydrogenase isoenzyme (LDH5) by maternal exposure to LiCl was no more apparent by the combined Li and Cs treatment. These data suggest a Li+-Cs+ interaction in the offspring mouse due to maternal exposure to these alkali metals during pregnancy and breast-feeding periods. The results also suggest that both alkali metals most probably have been delivered to the suckling pups and some of their toxic effect was retarded.