Inhibition of cortisone-induced cleft palate in mice by cobaltous chloride

Kasirsky, Gilbert; Gautieri, Ronald F.; Mann, David E.

doi:10.1002/jps.2600561024

Cited by 17 publications

(2 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The malformations of Xenopus embryos that were induced by Co2+ included craniofacial, ocular, and skeletal anomalies, similar to those previously noted in Co2+-exposed chick and mouse embryos [19][20][21][22]. The present authors are loath to extrapolate Incidence of the malformation in surviving tadpoles (%I from observations in Xenopus, a non-mammalian species, to suggest that Co2+ may represent a teratogenic risk for human embryos, since teratogenesis assays of Co2+ have yielded essentially negative results in rats and hamsters [ 15-181.…”

Section: Discussionsupporting

confidence: 77%

“…Cobalt salts gave negative or equivocal results in bacterial mutagenesis assays [ 1 1-131, but crystalline cobalt sulfide gave strongly positive results in a mammalian mutagenesis assay-in vitro morphological transformation of Syrian hamster embryo cells [14,15]. Teratogenesis tests of cobalt salts were negative in rats and hamsters [ 16- 18 J , but positive in mice and chickens [19][20][21][22]; cobalt chloride caused cleft palate and delayed skeletal ossification in mouse embryos [ 19,201 and ocular and skeletal anomalies in chick embryos [21,22].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Teratogenicity of cobalt chloride in Xenopus laevis, assayed by the FETAX procedure

Plowman

Peracha

Hopfer

et al. 1991

Teratog Carcinog Mutagen

View full text Add to dashboard Cite

The teratogenicity of cobalt chloride (CoCl2) was tested by the FETAX (Frog Embryo Teratogenesis Assay: Xenopus) procedure in the South African frog, Xenopus laevis. In five assays, beginning at 5 h post-fertilization, groups of Xenopus embryos were incubated for 96 h in media that contained CoCl2 at concentrations ranging from 1.8 x 10(-6) to 1.8 x 10(-2) mol/L; control groups were incubated in the same medium without added CoCl2. At 101 h post-fertilization, surviving embryos were counted, fixed in formalin, and examined by microscopy to score malformations and measure head-to-tail lengths. In control embryos, survival was greater than or equal to 95% and malformations were less than or equal to 5%. Malformations were found in greater than 99% of embryos exposed to Co2+ levels greater than or equal to 56 mumol/L. Co2+)-exposed embryos showed a concentration-related pattern of malformations, comprising gut malrotation, ocular anomalies, kinked tail, craniofacial dysplasia, cardiac deformities, and dermal blisters. Other concentration-dependent abnormalities, not categorized as malformations, included stunted growth, edema, ventral distention, and hypopigmentation. The median embryolethal concentration (LC50) of CoCl2 was 10.4 (SE +/- 0.4) mmol/L; the median teratogenic concentration (EC50) was 25 (SE +/- 2) mumol/L; the teratogenic index (TI = LC50/EC50) was 416 (SE +/- 13), indicating that CoCl2 is a potent teratogen for Xenopus laevis.

show abstract

Section: Discussionsupporting

confidence: 77%