Effects of hydrazine and its derivatives on the development of intestinal brush border enzymes

Pregnant hamsters were exposed by intubation to a single oral dose of hydrazine hydrate (260 mg/kg) or 1,2-dimethylhydrazine dihydrochloride (150 mg/kg) as a neutralized solution on Day 12 of gestation (4 days before birth). Similarly, doses of methylazoxymethanol acetate (340 and 85 mg/kg) were given and found to be lethal to the dams within a 24- to 48-hr period. Groups of these animals ( N = 3) were sacrificed 1 or 2 days before birth and 3 or 4, 10, 17, 24 or 25, and 53 or 60 days after birth to evaluate the development of intestinal brush border enzymes. lactase, sucrase, and alkaline phosphatase, as compared to the enzyme development in control animals. The results indicate that exposure to hydrazine diminished neonatal lactase activity, elevated postnatal and young adult sucrase activity, and elevated the neonatal and postnatal activity of alkaline phosphatase. In contrast, after prenatal exposure to 1,2-dimethylhydrazine, the postnatal level of sucrase activity and all levels of alkaline phosphatase activity were elevated. There was no significant effect of 1,2-dimethylhydrazine on the development of lactase activity. A screen for teratogenic effects revealed no incidence of cleft palate formation in the offspring. While there are no apparent teratogenic events, biochemical alterations reveal more subtle effects of these environmental toxins on this developing organ system.