Mitochondrion: a sensitive target for Pb exposure

• Published in: Journal of toxicological sciences Vol. 46; no. 8; pp. 345 - 358
• Main Authors: Han, Qing, Zhu, Gaochun, Chen, Hui, Zhang, Wei, Guo, JingChong, Zhu, Qian, Xia, YongLi
• Format: Journal Article
• Language: English
• Published: Japan The Japanese Society of Toxicology 2021; Japan Science and Technology Agency
• Subjects: Apoptosis; Apoptosis - drug effects; Autophagy; Autophagy - drug effects; Calcium (intracellular); Calcium (mitochondrial); Calcium - metabolism; Calcium homeostasis; Child; Child, Preschool; Children; Damage; Environmental Exposure - adverse effects; Environmental Pollutants - adverse effects; Environmental Pollutants - toxicity; Eukaryotes; Exposure; Female; Food contamination; Germination; Homeostasis; Homeostasis - drug effects; Humans; Inflammation; Inflammation - chemically induced; Intelligence; Lead; Lead - adverse effects; Lead - toxicity; Male; Membrane permeability; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondria - pathology; Mitochondrial Permeability Transition Pore; Organelles; Oxidative stress; Oxidative Stress - drug effects; Pb exposure; Phagocytosis; Pregnancy; Toxicity; Oxidative stress; Inflammation; Pb exposure; Mitochondrial permeability transition pore; Autophagy; Calcium homeostasis
• ISSN: 0388-1350; 1880-3989; 1880-3989
• DOI: 10.2131/jts.46.345

Pb exposure is a worldwide environmental contamination issue which has been of concern to more and more people. Exposure to environmental Pb and its compounds through food and respiratory routes causes toxic damage to the digestive, respiratory, cardiovascular and nervous systems, etc. Children and pregnant women are particularly vulnerable to Pb. Pb exposure significantly destroys children’s learning ability, intelligence and perception ability. Mitochondria are involved in various life processes of eukaryotes and are one of the most sensitive organelles to various injuries. There is no doubt that Pb-induced mitochondrial damage can widely affect various physiological processes and cause great harm. In this review, we summarized the toxic effects of Pb on mitochondria which led to various pathological processes. Pb induces mitochondrial dysfunction leading to the increased level of oxidative stress. In addition, Pb leads to cell apoptosis via mitochondrial permeability transition pore (MPTP) opening. Also, Pb can stimulate the development of mitochondria-mediated inflammatory responses. Furthermore, Pb triggers the germination of autophagy via the mitochondrial pathway and induces mitochondrial dysfunction, disturbing intracellular calcium homeostasis. In a word, we discussed the effects of Pb exposure on mitochondria, hoping to provide some references for further research and better therapeutic options for Pb exposure.