Title : Persistent c-fos induction by nicotine in developing rat brain regions: interaction with hypoxia.

Pub. Date : 1999 Jan

PMID : 9890606






6 Functional Relationships(s)
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1 Persistent c-fos induction by nicotine in developing rat brain regions: interaction with hypoxia. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
2 We administered nicotine to pregnant rats throughout gestation and neonatal brains were examined for expression of c-fos, a nuclear transcription factor involved in differentiation and cell death. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
3 The nicotine group showed persistent c-fos overexpression in the forebrain long after termination of exposure; in the brainstem, overexpression was apparent both after birth and at the end of the second postnatal week. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
4 Hypoxia evoked acute stimulation of c-fos with a regional selectivity and ontogenetic profile differing from those of prenatal nicotine and this acute response was reduced by prenatal nicotine treatment. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
5 Persistent c-fos elevation is a harbinger of cell death, a relationship that provides an underlying mechanism for eventual cell deficits that appear after fetal nicotine exposure. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
6 Nicotine"s interference with the acute c-fos stimulation caused by a subsequent episode of hypoxia may indicate a further compromise of cellular repair mechanisms. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus