Disease relevance of Maternal-Fetal Exchange

• After transplacental exposure to N-ethyl-N-nitrosourea (25 mg/kg BW) brain tumors developed in 18% (7/39) of GFAP-Y236delta transgenic p53-/- mice, while in p53+/- mice the incidence was 28% (11/40) (P>0.3) [1].
• Subsequently sex-specificity in isoniazid tumorigenicity was also studied as well as the effect of vitamin B complex or protein deficiency, and of transplacental exposure of Swiss strain embryos to isoniazid [2].
• The activated neu gene was detected in tumors of the nervous system that arose in mice following transplacental exposure to N-ethyl-N-nitrosourea [3].
• BACKGROUND: Oligodendrogliomas respond to nitrosourea-based chemotherapy and are induced in rats following transplacental exposure to ethylnitrosourea, observations suggesting that neoplastic and normal cells of the oligodendrocyte lineage are "sensitive" to nitrosoureas [4].

High impact information on Maternal-Fetal Exchange

• Increased incidence of mammary tumors in rats after direct or transplacental exposure to 3-hydroxyxanthine [5].
• Transplacental exposure of rats to a single dose of the direct acting carcinogen methylnitrosourea (MNU) results in the induction of a variety of neoplasias of neuroectodermal, epithelial, and mesenchymal origin [6].
• Relationship between in utero development of the mouse liver and tumor development following transplacental exposure to ethylnitrosourea [7].
• Effects of transplacental exposure to diethylstilbestrol on carcinogenic susceptibility during postnatal life in hamster progeny [8].
• We found that recurrent, transplacental exposure of mouse embryos to cocaine from embryonic day 8 to 15 decreases tangential neuronal migration and results in deficits in GABAergic neuronal populations in the embryonic cerebral wall [9].

Biological context of Maternal-Fetal Exchange

• In order to examine the transforming potential of the K-fgf gene in the nervous system, we combined retrovirus-mediated transfer of the K-fgf oncogene with a single transplacental exposure of the donor animals to the neurotropic carcinogen N-ethyl-N-nitrosourea (NEU) [10].
• Evaluation of DNA damage induced by norfloxacin in liver and kidney of adult rats and in fetal tissues after transplacental exposure [11].
• Transplacental exposure to the DNA alkylating agent N-methyl-N-nitrosourea on day 16 of gestation in CD-1 albino mice induces a degeneration of the retina, the severity of which depends upon the dosage level of the drug [12].
• Chromosome analysis of experimental rat glial tumor(1)--correlation of chromosome changes between glial tumors and fetal brain tissue of rats after a transplacental exposure to ethylnitrosourea [13].

Anatomical context of Maternal-Fetal Exchange

• Because prior work with mice had revealed remarkable inhibition of central nervous system (CNS) tumor by chronic Toxoplasma infection, the effect of immunomodulation produced by this obligate intracellular parasite was studied in rats which developed CNS tumors following transplacental exposure to the chemical carcinogen ethylnitrosourea [14].
• The level of clastogenic damage in mice following in vivo adult and transplacental exposure to benzidine, heliotrine, monocrotaline and urethane was compared using the micronucleus (MN) assays of polychromatic erythrocytes (PCE) found in mouse adult bone marrow and foetal liver [15].
• Trophoblast lining the area of maternal-fetal exchange, the labyrinth, on the other hand, maintained a constitutive lower level of IGF-II expression throughout late pregnancy [16].
• The binding of 7,12-dimethylbenz[a]anthracene to mammary gland macromolecules in the hamster:effects of Enovid feeding or transplacental exposure to diethylstilboestrol [17].

Associations of Maternal-Fetal Exchange with chemical compounds

• We experimentally induced LGH in brains of rat pups by transplacental exposure to methylmercury [18].
• Enhanced expression of limb malformations and axial skeleton alterations in legless mutants by transplacental exposure to retinoic acid [19].
• Neonatal effects of transplacental exposure to polychlorinated biphenyls (PCBs) and dichlorodiphenyl dichloroethene (DDE) were examined in a study of 912 infants [20].
• Maternal-fetal exchange during protein malnutrition in the rat. Placental transfer of alpha-amino isobutyric acid [21].
• Maternal-fetal exchange during protein malnutrition in the rat. Placental transfer of glucose and a nonmetabolizable glucose analog [22].

Gene context of Maternal-Fetal Exchange

• Ethoxyresorufin O-deethylase (EROD) and 1-chloro-2,4-dinitrobenzene assays were performed to evaluate whether transplacental exposure to IQ results in the induction of fetal Cyp1a1 and GST, respectively, in lung and liver tissues [23].
• Tissue-specific activating mutations of Ha- and Ki-ras oncogenes in skin, lung, and liver tumors induced in mice following transplacental exposure to DMBA [24].
• We hypothesized that nestin would be a sensitive marker of early neoplasia after transplacental exposure of rats to ethylnitrosourea (ENU) [25].
• Transplacental exposure to indole-3-carbinol induces sex-specific expression of CYP1A1 and CYP1B1 in the liver of Fischer 344 neonatal rats [26].
• The cyclooxygenase inhibitor ibuprofen and the FLAP inhibitor MK886 inhibit pancreatic carcinogenesis induced in hamsters by transplacental exposure to ethanol and the tobacco carcinogen NNK [27].

References