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.
D000740:Anemia / Q000235:genetics* / Q000378:metabolism*; D000818:Animals; D005260:Female; D005315:Fetal Diseases / Q000378:metabolism; D006400:Hematocrit; D006410:Hematopoiesis; D006836:Hydro-Lyases / Q000378:metabolism*; D066298:In Vitro Techniques; D007501:Iron / Q000378:metabolism; D007668:Kidney / Q000201:enzymology*; D008099:Liver / Q000201:enzymology*; D051379:Mice; D009929:Organ Size; D010659:Phenylhydrazines / Q000494:pharmacology; D011247:Pregnancy; D011270:Pregnancy, Animal; D013154:Spleen / Q000201:enzymology*
D010659:Phenylhydrazines; D007501:Iron; D006836:Hydro-Lyases