[Thrombopenia after acute experimental ingestion of folic acid antagonists].
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Experimental pregnant rats were placed on a transitory folic acid-deficient regimen, i.e. dietary restriction of folic acid plus the teratogen and folic acid antagonist, 9-methyl pteroylglutamic acid; a regimen resulting in multiple congenital skeletal malformations. Controls received a folic acid-supplemented regimen. Accumulation of a primary component of the extracellular matrix, glycosaminoglycans (GAG), was quantitatively evaluated by measuring uronic acid concentrations in fetal limbs. On days 16 and 18 of gestation, fetal limbs were removed, pooled from each litter, and prepared for uronic acid, protein, and DNA quantitation. The treatment results in (1) a decreased rate of protein and DNA accumulation prior to day 16 of gestation, the rate not being affected from day 16 to day 18 of gestation; (2) a trend toward an increased rate of uronic acid accumulation prior to day 16 of gestation, and (3) a decreased rate of uronic acid accumulation from day 16 to day 18 of gestation. Furthermore, our observations confirm our earlier suggestion that there is a decreased rate of accumulation of some nonprotein component(s) in fetal limbs obtained from folic acid-deficient mothers from day 16 to day 18 of gestation.
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