Delta-aminolevulinate dehydratase activity in mice with hereditary anemia.

Homozygous (f/f) but not heterozygous (f/+) mice of the highly congenic strain, FL/ Re, manifest a severe transitory siderocytic fetal anemia. Adults of both f/f and f/+ genotype manifest decreased hepatic, splenic, and renal levels of triangle up-amino-levulinate dehydratase (ALD) activity compared to homozygous (+/+) mice of the same strain. The degree of augmentation in splenic ALD activity following phenylhydrazine administration is high in +/+, intermediate in f/+, and low in f/f mice. These findings suggest that perhaps a deficiency in the fetal level of ALD may be responsible for the transitory fetal anemia.