Cai Sophia, Kim Min Woo, Chen Pan
Albert Einstein College of Medicine Volunteer Program, Bronx, NY, USA.
Rye High School, Rye, NY, USA.
J Neurobiol Physiol. 2022;4(1):4-8.
Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases. Taken together, to study the molecular programs of integrating ER stress with mitochondrial dysfunction should be an important area of future research for appreciating the mechanisms of as well as developing strategies and targets for metal-induced neurological diseases.
尽管人体需要必需金属离子，但当接触到人体无法承受的金属浓度时，就会发生神经毒性。对于在工业中重要的非必需金属而言，这些元素即使在低浓度下也具有引起神经毒性的特性。当这种神经毒性长期发展时，它会导致各种神经退行性疾病，如阿尔茨海默病和帕金森病。因此，关于神经毒性与金属代谢之间关系的研究正在积极开展，最近的一些研究表明，金属诱导的神经毒性机制主要涉及内质网（ER）应激和线粒体功能障碍。因此，本综述旨在总结此类证据的一些实例，并在试图通过内质网应激和线粒体功能障碍来解决金属诱导的神经毒性问题时提出新的问题，这两个重要主题涉及金属在神经退行性疾病中的作用。综上所述，研究整合内质网应激与线粒体功能障碍的分子程序应该是未来研究的一个重要领域，以便了解金属诱导的神经疾病的机制，并制定相关策略和靶点。
