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Effect of separate and combined maternal ingestion of alkali metals on the developing mouse
1Texas Tech University Health Science Center, School of Medicine, Lubbock.
The effect of postnatal maternal ingestion of LiCl, CsCl or both during weaning period on the developing newborn was studied in the albino mouse. Maternal exposure to CsCl alone or in combination with LiCl reduced the weanling body weight from corresponding control which persisted for a subsequent 2 weeks after separation of the offspring from maternal breast feeding. This was compared to a moderate reduction in offspring growth by maternal Li-exposure during alkali metal-free period. Exposure of nursing dams to either alkali metals studied, but not their combination, decreased brain weight of the developing mouse. The maternal Li-exposure caused a marked increase in female but not male offspring spleen weight as compared to a reduction of kidney weight from corresponding controls. Coadministration of CsCl with LiCl negated this sex-dependent Li-mediated changes of the offspring's tissue weights. The maternal Li-treatment caused sex-dependent induction of offspring hepatic aldehyde dehydrogenase but not alcohol dehydrogenase. The results suggest that breast feeding by nursing dams ingesting these alkali metals could cause retarded growth during development. The Cs+ appears to negate some of the changes produced by Li on brain and kidney weights. The interaction between Cs+ and Li+ may prove useful in minimizing some of the neonatal toxicity studied.
The effect of postnatal maternal ingestion of LiCl, CsCl or both during weaning period on the developing newborn was studied in the albino mouse. Maternal exposure to CsCl alone or in combination with LiCl reduced the weanling body weight from corresponding control which persisted for a subsequent 2 weeks after separation of the offspring from maternal breast feeding. This was compared to a moderate reduction in offspring growth by maternal Li-exposure during alkali metal-free period. Exposure of nursing dams to either alkali metals studied, but not their combination, decreased brain weight of the developing mouse. The maternal Li-exposure caused a marked increase in female but not male offspring spleen weight as compared to a reduction of kidney weight from corresponding controls. Coadministration of CsCl with LiCl negated this sex-dependent Li-mediated changes of the offspring's tissue weights. The maternal Li-treatment caused sex-dependent induction of offspring hepatic aldehyde dehydrogenase but not alcohol dehydrogenase. The results suggest that breast feeding by nursing dams ingesting these alkali metals could cause retarded growth during development. The Cs+ appears to negate some of the changes produced by Li on brain and kidney weights. The interaction between Cs+ and Li+ may prove useful in minimizing some of the neonatal toxicity studied.