The responses of the developing endocrine system to hormones and drugs

Telegdy, G.

doi:10.1016/0163-7258(80)90030-3

Cited by 3 publications

References 769 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Thyroxine‐induced differential mortality of cleft lip mouse embryos: Dose‐ and time‐response studies of the A/WySn strain

Juriloff

Harris

1985

Teratology

View full text Add to dashboard Cite

Pregnant A/WySn mice, 20 to 30% of whose offspring have spontaneous cleft lip, were treated with thyroxine. Following treatment, cleft lip and normal embryos died, but cleft lip embryos died at a higher rate. The increased liability of cleft lip embryos to thyroxine-induced death was considered as a possible experimental route to identify the basic genetic defect that causes cleft lip. A time-response study indicated that cleft lip embryos responded more than normals following treatment on any of days 7 to 12 of gestation, that there is no sharply defined critical period, and that normal and cleft lip embryos do not differ in time of maximum sensitivity. A dose-response study showed linear responses of normal and cleft lip embryos on a probit-log dose scale, with a common slope and LD50's of 1.9 and 1.3 mg respectively. These dose-response properties indicate that normal and cleft lip embryos are probably killed by the same mechanism, but differ in dosage tolerance. That is, they differ quantitatively, not qualitatively. Thyroxine did not significantly change the cleft lip frequency, and the difference between normal and cleft lip embryos that leads to cleft lip itself is therefore not in the same pathway as that which leads to thyroxine-induced death. A hypothetical example of the defect basic to both pathways is presented.

show abstract

Thyroxine‐induced differential mortality of cleft lip mouse embryos: Dose‐ and time‐response studies of the A/WySn strain

Juriloff

Harris

1985

Teratology

View full text Add to dashboard Cite

show abstract

Prevention of the eye closure defect in lg^Ml/lg^Ml fetal mice by thyroxine

Juriloff

1985

Teratology

View full text Add to dashboard Cite

The open-eye birth defect of mice caused by the lgMl mutation was prevented by prenatal administration of thyroxine (T4) to the pregnant mother. Treatment on days 10 to 11 of gestation was most effective in preventing open-eyes. A contrasting worsening of the defect was seen after treatment on day 14 of gestation. A dose-response relationship for prevention appeared to be present up to a dose of 0.1 mg/mouse, after which 39% of fetuses had both eyes closed compared to 2% in controls. Higher doses appeared to give little or no further increase in beneficial effect. Scanning electron microscopy was used to compare thyroxine-treated and untreated lgMl/lgMl and normal CBA/J day 16 or 17 fetal eyes. Mutant eye closure after thyroxine differed from untreated mutant in the growth of both upper and lower eyelids across the eye and in increased numbers of rounded periderm cells on the advancing lid edges. The underlying epithelial tissue layer appeared to fuse closed. The induced eye closure in the mutant was not normal, however. The periderm cell layer had disorderly fusion at the outer canthus, premature flattening, and failure to fuse in the inner canthus.

show abstract