Caito Samuel W, Aschner Michael
Department of Molecular Pharmacology, Albert Einstein College of Medicine , Bronx, New York.
Antioxid Redox Signal. 2015 Aug 20;23(6):578-95. doi: 10.1089/ars.2015.6289. Epub 2015 Apr 29.
Mitochondria are structurally and biochemically diverse, even within a single type of cell. Protein complexes localized to the inner mitochondrial membrane synthesize ATP by coupling electron transport and oxidative phosphorylation. The organelles produce reactive oxygen species (ROS) from mitochondrial oxygen and ROS can, in turn, alter the function and expression of proteins used for aerobic respiration by post-translational and transcriptional regulation.
New interest is emerging not only into the roles of mitochondria in disease development and progression but also as a target for environmental toxicants.
Dysregulation of respiration has been linked to cell death and is a major contributor to acute neuronal trauma, peripheral diseases, as well as chronic neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease.
Here, we discuss the mechanisms underlying the sensitivity of the mitochondrial respiratory complexes to redox modulation, as well as examine the effects of environmental contaminants that have well-characterized mitochondrial toxicity. The contaminants discussed in this review are some of the most prevalent and potent environmental contaminants that have been linked to neurological dysfunction, altered cellular respiration, and oxidation.
线粒体在结构和生化方面具有多样性，即使在单一类型的细胞内也是如此。定位于线粒体内膜的蛋白质复合物通过耦合电子传递和氧化磷酸化来合成ATP。这些细胞器利用线粒体中的氧产生活性氧（ROS），反过来，ROS可通过翻译后和转录调控改变用于有氧呼吸的蛋白质的功能和表达。
人们不仅对线粒体在疾病发生和发展中的作用重新产生兴趣，而且对其作为环境毒物的靶点也有了新的关注。
呼吸调节异常与细胞死亡有关，是急性神经元损伤、外周疾病以及慢性神经退行性疾病（如帕金森病和阿尔茨海默病）的主要促成因素。
在此，我们讨论线粒体呼吸复合物对氧化还原调节敏感性的潜在机制，并研究具有明确线粒体毒性的环境污染物的影响。本综述中讨论的污染物是一些与神经功能障碍、细胞呼吸改变和氧化相关的最普遍、最具毒性的环境污染物。
