Thallium Toxicity: General Issues, Neurological Symptoms, and Neurotoxic Mechanisms

Abstract

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.

Thallium toxicity due to audultered infusion with thallium sulfate in eight members belonging to the same family nucleus: Autopsy findings and ICP-MS analysis (inductively coupled plasma mass spectrometry) in a triple homicide

“…Acute intoxication from thallium (the lethal dose in men is estimated to be between 8 and 12 mg/kg; the lethal plasmatic concentration is considered to be between 0.5 and 11 mcg/mL) is an exceptional and often rare condition [9] and is one of the most rare and complex situations studied [10]: in the biological processes, thallium acts in a way similar to potassium but with an affinity 10 times higher, replacing this latter substance in a series of enzymatic complexes, especially mitochondrial, that need this substance as an activator and ending up being damaged [11]. In fact, the immediate administration of thallium, via any way of administration, generates lethal effects caused by a complete upsetting of important processes with a mechanism that has not yet been clarified [12].…”

Hair Loss: Evidence to Thallium Poisoning

“…The major clinical manifestation of thallium poisoning includes gastrointestinal reaction and multiple peripheral neuropathy. It is also characterized by hair loss [ 10 ], which usually occurs within 2-3 weeks after the poisoning [ 11 ]. In the six months of follow-up, our case demonstrated the whole process of the hair change after thallium poisoning.…”

Metallothionein alone or in combination with Prussian blue attenuates acute thallium systemic toxicity in rats.

“…The mechanism of thallium toxicity is based upon the inhibition of enzymes speci c of the glycolysis, Krebs cycle and oxidative phosphorylation. Those inhibitions produce a depletion of the levels of ATP in the cells [24]. Tl has a high a nity for the sulfhydryl groups of amino acids such as cysteine and methionine.…”