Tissue phosphatase changes following triamcinolone associated with cleft palate in rats.

@article{Holst1975TissuePC,
  title={Tissue phosphatase changes following triamcinolone associated with cleft palate in rats.},
  author={Patricia A. Holst and Barbara G. Mills},
  journal={Teratology},
  year={1975},
  volume={11 1},
  pages={
          57-63
        },
  url={https://api.semanticscholar.org/CorpusID:23617472}
}
Imbalanced acid phosphatase, beta-glucuronidase, and alkalineosphatase activity compared with protein synthesis at the time of palate closure following triamcinolone in rats is suggested.
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6 Citations

6 Citations

Light and electron microscopic observations on hydrocortisone-induced cleft palate in hamsters.

It appears that the normal process of protein synthesis is inhibited following hydrocortisone administration and that this, in turn, during palatogenesis, disrupts normal cellular differentiation and the integrity of the basal lamina, which are associated with the production of a cleft palate.

Secondary palate development in the domestic duck (Khaki Campbell). An electron microscopic, histochemical, autoradiographic and biochemical study.

Although the morphogenesis of palate in duck, chick and quail is similar, the cytodifferentiation of their MEE is different and a continuation of DNA synthesis in the MEE, unchanged levels of cyclic AMP in the palatal tissues and an absence of programmed cell death during duck palatogenesis distinguish it from the mammalian palate morphogenesis.

In vitro differentiation of the Japanese quail secondary palate.

Results indicated that the medial edge epithelia of quail were capable of full differentiation in vitro from a very early age, and an inverse relationship between the levels of cyclic AMP and the synthesis of DNA in the MEE may exist during secondary palate development, which in turn may regulate the fate of the Mee in birds and mammals.

Current concepts on the mechanisms of normal and abnormal secondary palate formation

Even though cleft palate has been mentioned only in the recent literature, evidence of the deformity far predates the literature, as demonstrated in early Egyptian mummy1.

Analytical Techniques for the Study of Teratogenic Mechanisms

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18 References

Glucocorticoid induction of cleft palate in mice; no correlation with inhibition of mucopolysaccharide synthesis.

The results suggest that the induction of cleft palate by gluco-corticoids is not related to inhibition of mucopolysaccharide synthesis by them but rather to growth inhibition.

Metabolism of -aminopropionitrile and its teratogenic activity in rats.

The data indicate that BAPN itself is teratogenic and that it acts within a narrow period of time on day 15 in producing cleft palate.

Tritiated thymidine labelling of the palatal processes of rat embryos with cleft palate induced by hypervitaminosis A.

Glucocorticoid inhibition of RNA synthesis and the critical period for cleft palate induction in inbred mice.

A comparison was made of the teratogenic effects of triamcinolone (induction of cleft palate) and its ability to inhibit RNA synthesis in the C3H and A/J strains of mice. The “critical period” for…

Phosphatase activity in the limb bones of monkeys (Lagothrix humboldti) with hyperparathyroidism

It seems likely that the parathyroid hypertrophy and rachitic changes were caused by low blood calcium dependent on a low calcium diet and lack of vitamin D, in which the requirements of New World monkeys are reputedly high.

Acid mucopolysaccharide synthesis in the secondary palate of the developing rat at the time of rotation and fusion.

Glucocorticoid inhibition of RNA synthesis responsible for cleft palate in mice: a model.

Support for the model derives from the fact that the palatine shelves rise and fuse 3-4 days after the most sensitive time of administration of steroid; RNA synthesis was markedly inhibited 6-24 hr after its administration; and coadministration of cycloheximide partially reversed the tendency toward cleft palate formation.

Relation of mandible growth to palate closure in mice.

It is concluded that cortisone, 6-aminonicotinamide, and hypervitaminosis-A do not cause cleft palate by reducing the length of the mandible at palate-closure time.

A radioautographic study of deoxyribonucleic acid synthesis in embryonic rat palatal shelf epithelium with reference to the concept of programmed cell death.

Acid phosphatase activity in palates of developing normal and chlorcyclizine treated rodents.