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在混合重金属(银和汞)暴露下,Nauphoeta cinerea 的神经行为、神经递质和氧化还原修饰。

Neurobehavioral, neurotransmitter and redox modifications in Nauphoeta cinerea under mixed heavy metal (silver and mercury) exposure.

机构信息

Division of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

Division of Translational Research and Technology Innovation, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

出版信息

BMC Res Notes. 2024 Jul 5;17(1):188. doi: 10.1186/s13104-024-06852-2.

DOI:10.1186/s13104-024-06852-2
PMID:38970085
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11227235/
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 AgNO and HgCl 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

重金属存在于自然界中,并被应用于人类的多项活动中,包括在补牙材料中。众所周知,金属的安全性取决于其化学形态,以及生物系统暴露于金属的剂量和途径。在这里,我们使用 Nauphoeta cinerea 模型来研究用于补牙的重金属盐(银和汞)发挥其神经毒性的机制。接触重金属的若虫表现出运动和探索能力下降,因为它们静止不动的时间更多,尤其是在新物体的外围,与对照若虫相比,移动的距离更短。暴露于 AgNO 和 HgCl 还加剧了氧化应激标志物(MDA 和 ROS)和神经递质调节剂 - AChE 和 MAO 的水平,同时降低了神经组织中的抗氧化活性标志物,包括生化(硫醇和 GST)和 RT-qPCR(TRX、GST、SOD、Catalase)检测,在蟑螂中。观察到的神经运动控制、突触传递和氧化还原平衡的破坏解释了重金属盐如何使生物体易患神经紊乱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/133a/11227235/ab5df9e8a755/13104_2024_6852_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/133a/11227235/4a29f03cdd08/13104_2024_6852_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/133a/11227235/3aa9c5742a45/13104_2024_6852_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/133a/11227235/ab5df9e8a755/13104_2024_6852_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/133a/11227235/4a29f03cdd08/13104_2024_6852_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/133a/11227235/3aa9c5742a45/13104_2024_6852_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/133a/11227235/ab5df9e8a755/13104_2024_6852_Fig3_HTML.jpg

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