Disruption of Synaptic Expression Pattern and Age-related DNA oxidation in a Neuronal Model of Lead-induced Toxicity

Publication date: Available online 3 February 2020Source: Environmental Toxicology and PharmacologyAuthor(s): Zuntao Wu, Lin Bai, Yunqi Tu, Lijie Zhang, Yue Ba, Huizhen Zhang, Xing Li, Xuemin Cheng, Wenjie Li, Hui HuangAbstractLead (Pb) is recognized as a potent inducer of synaptic toxicity generally associated with reduced synaptic transmission and increased neuronal fiber excitability, becoming an environmental risk for neurodegenerative processes. Despite numerous toxicological studies on Pb have been directed to the developing brain, attention concerning long-term consequences of pubertal chronic Pb exposure on neuronal activity is still lacking. Thus, we exposed 4-week-old male mice to 0.2% lead acetate solution for one month, then, conducted behavioral tests or extracted brain homogenate from mice prefrontal cortex (PFC) and hippocampus at the age of 4, 13 and 16-month-old respectively. Our results showed that treated mice exhibited an evident increase in latency to reach platform following pubertal Pb exposure and aging. The increase of 8-OHdG revealed evident neural DNA oxidative damage across time upon pubertal Pb exposure. In the hippocampus of lead exposed mice at three age nodes, the expression of brain-derived neurotrophic factor precursor (proBDNF) increased, while that of mature BDNF (mBDNF), cAMP-response element binding protein (CREB) and phosphorylated CREB (pCREB) decreased compared with the control group. Furthermore, the expression of BACE1 protein and ta...
Source: Environmental Toxicology and Pharmacology - Category: Environmental Health Source Type: research