Osorio-Rico Laura, Santamaria Abel, Galván-Arzate Sonia
Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía, Insurgentes Sur 3877, Mexico City, 14269, Mexico.
Laboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía, Insurgentes Sur 3877, Mexico City, 14269, Mexico.
Adv Neurobiol. 2017;18:345-353. doi: 10.1007/978-3-319-60189-2_17.
Thallium (Tl) is a ubiquitous natural trace metal considered as the most toxic among heavy metals. The ionic ratio of Tl is similar to that of potassium (K), therefore accounting for the replacement of the latter during enzymatic reactions. The principal organelle damaged after Tl exposure is mitochondria. Studies on the mechanisms of Tl include intrinsic pathways altered and changes in antiapoptotic and proapoptotic proteins, cytochrome c, and caspases. Oxidative damage pathways increase after Tl exposure to produce reactive oxygen species (ROS), changes in physical properties of the cell membrane caused by lipid peroxidation, and concomitant activation of antioxidant mechanisms. These processes are likely to account for the neurotoxic effects of the metal. In humans, Tl is absorbed through the skin and mucous membranes and then is widely distributed throughout the body to be accumulated in bones, renal medulla, liver, and the Central Nervous System. Given the growing relevance of Tl intoxication, in recent years there is a notorious increase in the number of reports attending Tl pollution in different countries. In this sense, the neurological symptoms produced by Tl and its neurotoxic effects are gaining attention as they represent a serious health problem all over the world. Through this review, we present an update to general information about Tl toxicity, making emphasis on some recent data about Tl neurotoxicity, as a field requiring attention at the clinical and preclinical levels.
铊（Tl）是一种普遍存在的天然痕量金属，被认为是重金属中毒性最强的。铊的离子比例与钾（K）相似，因此在酶促反应中会取代后者。铊暴露后受损的主要细胞器是线粒体。关于铊作用机制的研究包括内在途径的改变以及抗凋亡和促凋亡蛋白、细胞色素c和半胱天冬酶的变化。铊暴露后氧化损伤途径增加，产生活性氧（ROS），脂质过氧化导致细胞膜物理性质改变，并伴随抗氧化机制的激活。这些过程可能是该金属神经毒性作用的原因。在人类中，铊通过皮肤和粘膜吸收，然后广泛分布于全身，在骨骼、肾髓质、肝脏和中枢神经系统中蓄积。鉴于铊中毒的相关性日益增加，近年来不同国家有关铊污染的报告数量显著增加。从这个意义上说，铊产生的神经症状及其神经毒性作用正受到关注，因为它们在全球范围内都是一个严重的健康问题。通过本综述，我们提供了关于铊毒性的一般信息更新，重点介绍了一些关于铊神经毒性的最新数据，这是一个在临床和临床前水平都需要关注的领域。
