| Lead (Pb) is a heavy metal with neurotoxicity, exists widely in the environment. Children are sensitive to it, and their nervous system development can be interrupted by low-level long-term exposure. Synaptic plasticity is the basis of molecular mechanism of learning memory, exogenous BDNF remediated presynaptic effects of Pb. Nutrition was mentioned as the important modified factor of the lead metabolism and toxicity, so, exploring the role of prevention of lead poision is one of the currently research direction.ObjectivesThe goal of present study is to investigate the protective effect of zinc in lead exposure young mice. The parameters observed included the mouse blood and hippocampal lead and zinc level, hippocampal BDNF mRNA expression, and the mouse spatial learning memory performance.MethodsFifty Kunming mice, weighed18-22g, were randomly divided into five groups: the control group (C), Pb exposured group (Pb), low dose zinc intervention group (L), medium dose zinc intervention group (M), high dose zinc intervention group (H). Under the same feeding condition, the mice were provided with distilled water,1.0g/L lead acetate,0.2g/L zinc acetate+1.0g/L lead acetate,0.4g/L zinc acetate+1.0g/L lead acetate, and0.6g/L zinc acetate+1.0g/L lead acetate for8weeks. The animals were weighed weekly. After eight weeks feeding, Morris water maze (MWM) test was employed for evaluating the spatial learning memory ability in the mice. Then, the mice blood was drawn from orbital sinus. Their brain was dissected and the hippocampus was isolated. The lead levels in blood and hippocampus were analyzed by graphite furnace atomic absorption spectrometry. The zinc levels in blood and hippocampus were analyzed by polarization zeeman atomic absorption spectrometry. The expression level of hippocampal BDNF mRNA was quantified by RT-PCR method.ResultsMice body weight in Pb group was lower than that in the C group (P<0.05), while the M group was higher than that in Pb group (P<0.05) at sixth weeks. The Pb and L groups were markedly lower than that in C group (P<0.05), while the M and H groups was significantly higher than that in Pb group (P<0.05) at seventh weeks. The Pb and L groups were lower than the C group (P<0.01), while the M and H group was higher than the Pb group (P<0.01, P<0.05) at eighth weeks. MWM test showed that the escape latency was significantly increased in Pb and L groups (P<0.01), while the M and H groups showed shorter escape latency than Pb group (P<0.05) and L group (P<0.01).The blood and hippocampal lead levels were significantly higher in Pb, L, M and H groups than that in C group (P<0.01). The blood lead level was lower in M, H group than that in Pb group (P<0.01). The hippocampal lead levels were lower in L, M and H groups than that in Pb groups (P<0.01). The blood and hippocampal zinc levels were significantly lower in Pb group than that in C group (P<0.01). The blood zinc level was lower in C group than that in M and H group (P<0.01). The hippocampal zinc levels were lower in C group than that in L, M and H groups (P<0.01).The expression levels of hippocampal BDNF mRNA in Pb was the lowest, and in C was the highest, while the expression levels were higher in M and H groups than that in Pb group (P<0.01).ConclusionChronic lead exposure could elevate blood and hippocampal lead level, influence body weight gain, and cause defect of learning and memory in young mice. The lead exposure could decrease hippocampal BDNF mRNA expression. To some degree, zinc could partially reverse above adverse impacts caused by lead exposure and improve body growth and brain function in mice. |
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