PDF(Pubmed)
Abstract：
Heavy metals are encountered in nature, and are used in several human endeavors, including in dental fillings. It is well known that the safety of metals depends on their chemical form, as well as the dose and route through which biological systems are exposed to them. Here, we used the Nauphoeta cinerea model to examine the mechanism by which salts of the heavy metals used in dental fillings - silver and mercury - exert their neurotoxicity. Nymphs exposed to heavy metals presented with reduced motor and exploratory abilities as they spent more time immobile, especially in the periphery of a novel object, and covered less distance compared with control nymphs. Exposure to AgNO3 and HgCl2 also exacerbated levels of oxidative stress markers (MDA & ROS) and the neurotransmitter regulators - AChE and MAO, while reducing antioxidant activity markers, both in biochemical (thiol & GST) and RT-qPCR (TRX, GST, SOD, Catalase) examinations, in neural tissues of the cockroach. The observed disruptions in neurolocomotor control, synaptic transmission and redox balance explain how heavy metal salts may predispose organisms to neurological disorders.
摘要：
重金属在自然界中遇到，并用于多种人类活动，包括牙齿填充物。众所周知，金属的安全性取决于它们的化学形态，以及生物系统暴露于它们的剂量和途径。这里,我们使用Nauphoetacinerea模型来检查牙科填充物中使用的重金属盐-银和汞-发挥其神经毒性的机制。若虫暴露在重金属中，由于花费更多时间不动，因此运动和探索能力降低，尤其是在一个新物体的外围，与对照若虫相比，覆盖的距离更短。暴露于AgNO3和HgCl2也加剧了氧化应激标志物（MDA和ROS）和神经递质调节因子-AChE和MAO的水平，同时减少抗氧化活性标志物，在生物化学(硫醇和GST)和RT-qPCR(TRX，GST,SOD,过氧化氢酶)检查，蟑螂的神经组织。观察到的神经运动控制中断，突触传递和氧化还原平衡解释了重金属盐如何使生物体易患神经系统疾病。
