Lead-induced alterations of apoptosis and neurotrophic factor mRNA in the developing rat cortex, hippocampus, and cerebellum

Department of Natural Sciences, Fayetteville State University, Fayetteville, NC 28301, USA.
Journal of Biochemical and Molecular Toxicology (Impact Factor: 1.93). 10/2007; 21(5):265-72. DOI: 10.1002/jbt.20191
Source: PubMed


Previous reports have recently shown the prototypic neurotoxicant, lead, to induce apoptosis in the brains of developing organisms. In the current study, timed-pregnant rats were exposed to lead acetate (0.2% in the drinking water) 24 h following birth at postnatal day 1 (PND 1). Dams and pups were continuously exposed to lead through the drinking water of the dam until PND 20. Postnatal exposure in the pups resulted in altered mRNA levels of the following apoptotic and neurotrophic factors: caspase 2 and 3, bax, bcl-x, brain-derived neurotrophic factor (BDNF). Ribonuclease protection assays were conducted to measure the factors simultaneously at the following postnatal time points: 9, 12, 15, 20, 25, days. Our results suggest a brain region- and time-specific response following lead acetate exposure. The region most vulnerable to alterations occurs in the hippocampus with alterations beginning at PND 12, in which caspase 3, bcl-x, BDNF increase with lead exposure. Significant treatment effects were not observed for both the cortex and cerebellum.

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Available from: G. Jean Harry, Oct 04, 2015
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    • "Another study has also indicated that lead produce rod photoreceptor cell apoptosis by opening the mitochondrial permeability transition pore (He et al. 2000a, b). The effects of lead on apoptosis of cells from hippocampus have been reported previously (Han et al. 2007; Chao et al. 2007; Zhang et al. 2004; Niu et al. 2002), but the design of the present study was different. Another important aspect of lead neurotoxicity to investigate is the sensitivity of younger compare to older rats to lead neurotoxicity. "
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