Dimethylnitrosamine demethylase activity in fetal, suckling, and maternal mouse liver and its transplacental and transmammary induction by polychlorinated biphenyls.
Oxidative demethylation of dimethylnitrosamine (DMN) was detectable with liver homogenate preparations from fetal mice (noninbred Swiss) by day 16 of gestation; this activity increased to adult levels by postnatal day 7. Treatment of pregnant mice with a mixture of polychlorinated biphenyls (PCB's), 500 mg Aroclor 1254/kg, on the last day of gestation caused a large elevation in DMN demethylase activity in the livers of their sucklings, relative to the normal ontogenic increase, reaching a maximum at postnatal day 21. Foster nursing experiments showed that this inductive effect was due primarily to lactational delivery of the PCB]s. DMN demethylase activity in the maternal livers was significantly lower than normal during pregnancy. The mothers' livers were also less responsive to DMN demethylase induction by PCB's during the last 5 days of gestation in comparison with the response earlier in pregnancy or just after delivery. In the livers of the mothers, induced activity resulting from treatment with PCB's on day 19 of gestation reached a maximum on postnatal days 4-7 and declined to normal levels by the time of weaning.[1]References
- Dimethylnitrosamine demethylase activity in fetal, suckling, and maternal mouse liver and its transplacental and transmammary induction by polychlorinated biphenyls. Jannetti, R.A., Anderson, L.M. J. Natl. Cancer Inst. (1981) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
