Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methylmercury (MeHg: 5 mg Hg/kg maternal body weight) in 0.13 M NaCl, 0.01 M NaH2PO4-Na2HPO4, pH 7.4 (PBS) administered to gravid CFW mice on day 12, hour 6 (12(6)) of gestation induced a high incidence of cleft palate in fetuses examined on days 15(6) (72%), 16(6) (62%) and 17(6) (40%). Palate closure (100%) in PBS control animals occurred by 14(10). One day post MeHg administration, total fetal protein was decreased 22% while DNA content was unaltered. Protein was maximally decreased (28%) on 14(6) and, thereafter, returned toward control levels. Alterations in DNA content followed a similar pattern; but the maximal decrease (32%) occurred on 15(6). The rate of fetal protein synthesis was depressed 5% at 12(9) and between 20% to 26% from this time to 13(6) (end of observation). The agreement between the calculated decrease in protein synthesis (19%) and the measured decrease in protein content (22%) suggests that a reduction in protein synthesis is responsible for the decreased fetal protein content. Placental blood flow and fetal water space, measured with 3H--H2O at 12(18), were not affected by MeHg treatment. However, fetal free amino acid concentrations at 12(18) were generally decreased (alanine, 23.0%; valine, 9.7%; methionine, 22.6%; isoleucine, 12.0%; leucine, 18.2%) while uptake of the non-metabolizable amino acid, 14C-cycloleucine, was decreased 23%. From this, it is concluded that the growth inhibitory effects of MeHg are related, at least in part, to impaired placental/fetal transfer of amino acids.
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PMID:Effects of methyl mercury on murine fetal amino acid uptake, protein synthesis and palate closure. 92 35

DNA methylation is an epigenetical mechanism that plays crucial roles in cellular differentiation and tissue development in embryogenesis. The aim of the present study was to determine the effects of a demethylating agent, 5-azacytidine, on testicular development during embryonal life in mouse. Ten pregnant mice were administered 5-azacytidine (5-azaC) (i.p. 2 mg/kg of agent dissolved in 0.1 mg/ml PBS) during 8th (Group 1), 11th (Group 2), 14th (Group 3) and 18th (Group 4) days of pregnancy periods and male siblings of these animals were obtained (experimental groups) whereas the control group animals received no treatment and siblings of this group were also obtained. Testicular tissues from all groups were taken 20 days after birth and examined at the light and electron microscopical levels. All pregnancies were terminated in Group 1 animals, therefore no observations could be done in this group. While Group 2 and 3 siblings showed distinctive kongenital abnormalities such as; anancephaly, growth failure, cleft palate, extremity abnormalities, supernumerary ribs and whirled shaped-tails, no such abnormalities were observed in Group 4 when compared to the control group. Microscopical examination of testicular tissues in groups 2 and 3 demonstrated cellular disintegration of spermatocytes in seminiferous tubules. In addition, cytoplasmic vacuoles and thickening of the basement membrane were also evident in both groups 2 and 3. Apoptotic-like cells were seen especially in group 2 and rarely in group 3. There were no structural alterations in group 4 animals, except a decreased number of spermatocytes in seminiferous tubules when compared to the control group, possibly indicating the completion of embryogenesis in this group. In conclusion, it could be suggested that the demethylating agent 5-azacytidine may trigger an unknown gene reactivation during early embryogenesis possibly affecting the cell and tissue differentiation in developing mammalian embryos.
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PMID:Effects of a DNA demethylating agent--5-azacytidine--on testicular morphology during mouse embryo development. 1040 45