铅暴露对大鼠体内离子浓度及相关PKC信号通路分子的影响

摘要

Objective By observing the change of trace element content of lead poisoning in rats,to clarify the regulation changes of theion-mediated PKC(proteinkinase C) signaling pathway molecules and provide the experimental basis for the toxic effects of lead poisoning and prevention. Methods Rats exposed to different concentrations of lead acetate. Through the detection of trace elements calcium,iron,magnesium,zinc,copper,phosphorus in rats exposed to lead,to explore the impact of ion concentration on the signaling pathway molecule expression of PKC. Results Compared with the control group, concentration of serum Ca2+ ,Fe2+ ,Zn2+ and P3+ concentration were significantly lower in rats exposed to lead (P<0. 05). Rat exposure to lead serum Cu2+ concentration was decreased,but compared with the control group,no significant differences (P> 0. 05). Compared with the control group,serum Mg2+ concentration was significantly higher in rats exposed to lead ( P< 0. 05). Western blot results confirmed that rats exposed to lead signal pathway molecules PKC phosphorylation increased significantly in brain tissue (P<0. 05). Prompted the levels of lead-induced ion changes may activate the expression levels of the PKC signaling pathway molecules. Conclusion Chronic lead exposure can competitively inhibit the absorption and utilization of some metal elements in rats. Metalion levels in lead-induced changes may activate the expression level of the PKC signaling pathway molecules in rats.%目的 通过观察铅暴露大鼠体内不同离子浓度含量的改变,阐明铅通过破坏不同离子浓度在体内各系统的平衡状态,影响离子介导的蛋白激酶C(proteinkinase C,PKC)信号通路分子的调控作用,为探讨铅毒性作用机制的生物途径提供实验依据.方法 80只断乳SD雄性大鼠,按体重随机分为对照,0.1,0.2和0.3 mg/ml醋酸铅(PbC4H6O4·3H2O)浓度组,通过饮水建立大鼠铅暴露模型,利用大鼠血铅浓度确定建模成功;通过观察铅暴露大鼠血中离子Ca2+,Fe2+,Mg2+,Zn2+,Cu2+和P3+浓度的变化以及Western blot验证铅暴露大鼠脑组织离子相关信号通路分子PKC的表达改变,探讨离子浓度变化对铅暴露大鼠脑组织信号通路分子PKC表达的影响.结果 铅暴露大鼠血Zn2+,Fe2+,Ca2+和P3+离子浓度减低,与对照组比较差异有统计学显著性意义(P<0.05);铅暴露大鼠血Cu2+离子浓度减低,与对照组无统计学显著性意义(P>0.05);铅暴露大鼠血Mg2+离子浓度升高,与对照组比较差异有统计学显著性意义(P<0.05);Western blot结果进一步证实铅暴露大鼠脑组织信号通路分子PKC磷酸化增加显著(P<0.05).结论 慢性铅暴露可以竞争性抑制大鼠体内部分离子的吸收和利用,且铅暴露诱导的体内离子浓度改变可活化PKC信号通路分子的表达.