Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology

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.