PMID- 15182478 OWN - NLM STAT- MEDLINE DCOM- 20050524 LR - 20131121 IS - 0253-9624 (Print) IS - 0253-9624 (Linking) VI - 38 IP - 3 DP - 2004 May TI - [Studies on the effects of lead on the growth and differentiation of hippocampal neural cells as well as the expression of Oct-2]. PG - 151-4 AB - OBJECTIVE: In order to explore the effects of lead on the growth and development of cultured hippocampal neural cells and on the expression of Oct-2, the II subtype POU domain protein. METHODS: Experiment cell model was established using primary culture of hippocampal neural cells from SD rat embryos. Target cells were exposed to lead acetate in the different concentrations, i.e. 10(-1), 10(0), 10(1), 10(2), 10(3) micromol/L, while the control group was given the same quantity of the culture medium. The immunohistochemistry method was utilized to detect the expressions of Neurofilament (NF) and Glial Fibrillary Acidic Protein (GFAP), the markers for neuron and astrocyte, respectively, and the expression of Oct-2 as well. RESULTS: The results showed that 10 micromol/L lead acetate treatment caused diminishing of neuronal cell body and the decreases of both axon lengths and inter-cellular connections. In addition, 1 micromol/L lead acetate significantly increased the number of GFAP-positive cells compared with the control group (P < 0.05). By image analysis system, 1 micromol/L lead acetate treatment was found to induce a statistically significant increase of the positive area rate concerning Oct-2 expression in hippocampal neurons and astrocytes, while both positive area rate and integral density of light of Oct-2 expression were found to increase markedly in the groups treated by 10 micromol/L lead acetate (P < 0.01). CONCLUSIONS: Lead acetate treatment may contribute to the inhibitions of both growth and differentiation of hippocampus neurons, and to the stimulation of glial cell hyperplasia simultaneously. In addition, the CNS impairments caused by lead is partly correlated with the enhancement of Oct-2 expression. FAU - Chen, Jun AU - Chen J AD - Department of Occupational and Environmental Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. FAU - Zhu, Wei-guo AU - Zhu WG FAU - Chen, Qiu-sheng AU - Chen QS FAU - Lu, Ling AU - Lu L FAU - Chen, Xue-min AU - Chen XM LA - chi PT - English Abstract PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - China TA - Zhonghua Yu Fang Yi Xue Za Zhi JT - Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] JID - 7904962 RN - 0 (DNA-Binding Proteins) RN - 0 (Glial Fibrillary Acidic Protein) RN - 0 (Neurofilament Proteins) RN - 0 (Octamer Transcription Factor-2) RN - 0 (Pou2f2 protein, rat) RN - 0 (Transcription Factors) RN - 2P299V784P (Lead) SB - IM MH - Animals MH - Astrocytes/metabolism MH - Cell Division/drug effects MH - Cells, Cultured MH - DNA-Binding Proteins/*biosynthesis/genetics MH - Dose-Response Relationship, Drug MH - Embryo, Mammalian MH - Female MH - Glial Fibrillary Acidic Protein/biosynthesis/genetics MH - Hippocampus/cytology/*metabolism MH - Lead/*toxicity MH - Neurofilament Proteins/biosynthesis/genetics MH - Neurons/cytology/metabolism MH - Octamer Transcription Factor-2 MH - Pregnancy MH - Rats MH - Rats, Sprague-Dawley MH - Transcription Factors/*biosynthesis/genetics EDAT- 2004/06/09 05:00 MHDA- 2005/05/25 09:00 CRDT- 2004/06/09 05:00 PHST- 2004/06/09 05:00 [pubmed] PHST- 2005/05/25 09:00 [medline] PHST- 2004/06/09 05:00 [entrez] PST - ppublish SO - Zhonghua Yu Fang Yi Xue Za Zhi. 2004 May;38(3):151-4.