NDLI: In utero analysis of sister chromatid exchange: alterations in suscptibility to mutagenic damage as a function of fetal cell type and gestational age.

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Isolation and structure of pro-somatostatin: a putative somatostatin precursor from pig hypothalamus.

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Urotensin II: a somatostatin-like peptide in the caudal neurosecretory system of fishes.

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Identification of folate binding protein of mitochondria as dimethylglycine dehydrogenase.

Intermediate filaments of baby hamster kidney (BHK-21) cells and bovine epidermal keratinocytes have similar ultrastructures and subunit domain structures.

Reactivity of reverse transcriptase toward (s4U,U)n copolymers and spin-labeled nucleic acid lattices.

Chemical probes for higher-order structure in RNA.

Fidelity of structure representation in electron micrographs of negatively stained protein molecules.

Synthesis of new proteins associated with the induction of interferon in human fibroblast cells.

Liver tumors distinguished by immunofluorescence microscopy with antibodies to proteins of intermediate-sized filaments.

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Coordinate regulation of two estrogen-dependent genes in avian liver.

Direct spectroscopic studies of cation translocation by Torpedo acetylcholine receptor on a time scale of physiological relevance.

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In utero analysis of sister chromatid exchange: alterations in suscptibility to mutagenic damage as a function of fetal cell type and gestational age.

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In utero analysis of sister chromatid exchange: alterations in suscptibility to mutagenic damage as a function of fetal cell type and gestational age.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kram, D. Senula, G. C. Schneider, E. L. Bynum, G. D. Bickings, C. K.
Abstract	Frequencies of baseline and cyclophosphamide-induced sister chromatid exchanges (SCE) were measured in mouse maternal and fetal cells between days 11 and 19 of gestation. Baseline levels of SCE did not vary as a function of gestational age in either the mother or fetus. Cyclophosphamide-induced SCE frequencies remained constant in maternal cells but declined dramatically in the fetus throughout the latter half of development. Because cyclophosphamide is a metabolically activated mutagen, a direct-acting drug, mitomycin C, was given on days 11 and 15 to determine if the decline in induced SCE levels seen with gestational results from alterations in activating enzymes. A similar decline in mitomycin C-induced SCE levels was noted in fetal tissues as a function of gestational age. Dose-response curves to cyclophosphamide performed on day 13 of gestation showed increases in SCE as a function of cyclophosphamide concentration in both the mother and the fetus. When mutagen-induced SCE levels were compared in different fetal organs, the direct-acting drugs (mitomycin C and daunomycin) were found to induce similar levels in all tissues. Cyclophosphamide, which is metabolically activated, induced higher SCE levels in fetal liver than in lung or gut. Whereas cyclophosphamide induced similar SCE levels in fetal and maternal cells on day 13 of gestation, daunomycin produced fetal SCE levels that were approximately 50% of maternal levels. Simultaneous measurement of the distribution of [14C]cyclophosphamide and [3H]daunomycin in maternal and fetal cells revealed that the lower SCE induction by daunomycin was probably due to decreased ability to cross the placental barrier.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	8
Volume Number	77
Language	English
Publisher	National Academy of Sciences
Publisher Date	1980-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Carcinogens Pharmacology Crossing Over, Genetic Drug Effects Mutagens Pregnancy, Animal Sister Chromatid Exchange Animals Cyclophosphamide Daunorubicin Gestational Age Maternal-Fetal Exchange Mice Mitomycins Pregnancy Tissue Distribution Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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