Lithium and the neonate: developmental and metabolic aspects.

The interrelationship between lithium salts, which has been used in clinical trials of alcoholism, and ethanol, which evoke fetal alcohol syndrome by chronic use, was studied. This was made by evaluating the effect of prenatal and postnatal exposure to LiCl on ethanol and acetaldehyde metabolizing enzymes in the newborn mouse. The three Li-treatment regimens made consisted of acute and short-term prenatal exposure to LiCl in addition to postnatal exposure until weaning of the neonates. The weaned mice were then kept on water for a subsequent two weeks prior to sacrifice. The effects of LiCl, given in drinking fluid, on body weight, selected organ weights, hepatic alcohol dehydrogenase, aldehyde dehydrogenase and heart lactate dehydrogenase of the offspring were determined. Prenatal and postnatal ingestion of LiCl by the nursing mother resulted in decreased brain weight of offspring from both sexes. Concomitantly, there was a reduction in female but not male kidney weight. A marked decrease in the testis weight also occurred. The Li-treatment induced both neonatal hepatic alcohol dehydrogenase and heart lactate dehydrogenase in both sexes. Conversely, an inhibition of hepatic mitochondrial aldehyde dehydrogenase, for the enzyme with the apparent high Km, was determined in the male offspring. Maternal postnatal ingestion of LiCl decreased brain and spleen weights from corresponding control of neonatal male and female, respectively. This Li-treatment also induced hepatic neonatal alcohol dehydrogenase in both sexes. The results suggest that maternal ingestion of LiCl may interfere in brain development.(ABSTRACT TRUNCATED AT 250 WORDS)