Translactational exposure of F1 mouse pups to selenium.

In an investigation of the modulation of certain neonatal xenobiotic-metabolizing enzymes in liver of mouse pups postnatally exposed to selenium through the transmammary route, sodium selenite was administered in drinking water to lactating dams at the dose levels of 1 or 5 ppm from day 1 of lactation and continued daily for 14 or 21 days. The higher dose of selenium was found to increase the hepatic acid-soluble sulfhydryl content significantly after 21 days of treatment in dams, their pups (P < 0.01) and in the 14-day-old male pups (P < 0.05). Cytochrome b5 content decreased in the livers of dams that received 5 ppm selenium (P < 0.01) and in the F1 pups (P < 0.01) translactationally exposed to selenium for 14 days. Cytochrome P-450 content decreased in dams and pups exposed to 5 ppm selenium for 14 days and either dose for 21 days (P < 0.01). Hepatic glutathione S-transferase decreased in the dam that had received 5 ppm selenium for 14 days (P < 0.05) and in the 14-day-old pups (P < 0.01). Glutathione reductase and glutathione peroxidase activities decreased in both dams and pups (P < 0.01). The overall suppression of neonatal hepatic detoxification enzymes demonstrates that selenium may have far-reaching consequences on neonatal growth, development and drug pharmacokinetics.