Thallium (Tl) is one of the most toxic heavy metals and is found ubiquitously in the earth's crust. To investigate the cellular responses to and against Tl cytotoxicity, we conducted DNA microarray analysis using three human cell lines of different origins: SH-SY5Y (neuroblast-derived), HEK293T (embryonic kidney-derived), and Huh-7 (hepatoma-derived) cells. All of the ten genes that showed the highest inductions in Huh-7 cells treated with 60 µM Tl2SO4 for 72 hours are metallothionein (MT) genes. The induction of the MT genes appears specific to Huh-7 cells; increases of 50-140-fold in the ten MT genes were observed in Huh-7 cells, while the increases were less than 4-fold in HEK293T and SH-SY5Y cells by microarray analysis. Investigation of the pathway responsible for Tl2SO4-induced MT expression in Huh-7 cells revealed that the RNA interference-mediated forced downregulation of MTF1 transcription factor resulted in the suppression of Tl2SO4-induced MT gene expressions, but not Tl2SO4-induced cell death, suggesting that MTF1-mediated MT gene expression is insufficient to protect Huh-7 cells against death by Tl2SO4. In contrast, the knockdown of nrf1 worsened Tl2SO4-induced cell death without suppressing MT gene expressions. These results indicate that MT gene induction in response to Tl2SO4 is mediated at least in part by MTF1 in Huh-7 cells. Nevertheless, MT gene induction through MTF1 seems insufficient to prevent the cell death caused by Tl2SO4. Nrf1 appears to be involved in protection against Tl2SO4 toxicity through mechanisms other than MT gene induction.

Thallium (Tl) is one of the most toxic heavy metals, associated with accidental poisoning and homicide. It causes acute and chronic systemic diseases, including gastrointestinal and cardiovascular diseases and kidney failure. However, few studies have investigated the mechanism by which Tl induces acute kidney injury (AKI). This study investigated the toxic effects of Tl on the histology and function of rat kidneys using biochemical and histopathological assays after intraperitoneal thallium sulfate administration (30 mg/kg). Five days post-administration, rats exhibited severely compromised kidney function. Low-vacuum scanning electron microscopy revealed excessive calcium (Ca) deposition in the outer medulla of Tl-loaded rats, particularly in the medullary thick ascending limb (mTAL) of the loop of Henle. Tl accumulated in the mTAL, accompanied by mitochondrial dysfunction in this segment. Tl-loaded rats showed reduced expression of kidney transporters and channels responsible for Ca2+ reabsorption in the mTAL. Pre-administration of the Na-K-Cl cotransporter 2 (NKCC2) inhibitor furosemide alleviated Tl accumulation and mitochondrial abnormalities in the mTAL. These findings suggest that Tl nephrotoxicity is associated with preferential Tl reabsorption in the mTAL via NKCC2, leading to mTAL mitochondrial dysfunction and disrupted Ca2+ reabsorption, culminating in mTAL-predominant Ca crystal deposition and AKI. These findings on the mechanism of Tl nephrotoxicity may contribute to the development of novel therapeutic approaches to counter Tl poisoning. Moreover, the observation of characteristic Ca crystal deposition in the outer medulla provides new insights into diagnostic challenges in Tl intoxication.

Thallium (Tl) is one of the most toxic metals and its historic use in homicides has led it to be known as "the poisoner's poison." This review summarizes the methods for identifying Tl and determining its concentrations in biological samples in recently reported poisoning cases, as well as the toxicokinetics, toxicological effects, toxicity mechanisms, and detoxication methods of Tl. Recent findings regarding Tl neurotoxicological pathways and toxicological effects of Tl during pregnancy are also presented. Confirmation of elevated Tl concentrations in blood, urine, or hair is indispensable for diagnosing Tl poisoning. The kidneys show the highest Tl concentration within 24 h after ingestion, while the brain shows the highest concentration thereafter. Tl has a very slow excretion rate due to its large distribution volume. Following acute exposure, gastrointestinal symptoms are observed at an early stage, and neurological dysfunction is observed later: Tl causes the most severe damage in the central nervous system. Alopecia and Mees' lines in the nails are observed within 1 month after Tl poisoning. The toxicological mechanism of Tl is considered to be interference of vital potassium-dependent processes with Tl+ because its ionic radius is similar to that of K+, as well as inhibition of enzyme reactions by the binding of Tl to -SH groups, which disturbs vital metabolic processes. Tl toxicity is also related to reactive oxygen species generation and mitochondrial dysfunction. Prussian blue is the most effective antidote, and metallothionein alone or in combination with Prussian blue was recently reported to have cytoprotective effects after Tl exposure. Because Tl poisoning cases are still reported, early determination of Tl in biological samples and treatment with an antidote are essential.

Ferric hexacyanoferrate, Fe4 [Fe(CN)6]3 · xH2O, known as Prussian blue (PB), has proven its effectiveness as an antidote in cases of accidental poisoning or poisoning caused by radioactive materials such as cesium (Cs) and thallium (Tl); which due to their solubility in water, when absorbed by the human body, cause serious damage to vital organs. The local development of a drug with PB as an active ingredient arises as a response to the civil and military needs established within the Ministry's pharmacy request for national defense. This fact contemplates the circumstances related to public health protection in the nuclear, radiological, biological and chemical (NRBQ) of the emergency institutions in health and national security. In this paper and by using various analytical techniques, the characterization of the locally synthesized PB with pharmaceutical quality has been described, as a first step to predict its behavior in the preparation of a drug that contains it as an active ingredient. The research findings demonstrate that locally synthesized PB is suitable for use in oral dosage forms, enabling the local development of drug formulations incorporating PB, thus being able to potentially become a main resource in the treatment of Cs and Tl poisoning in any accidental or intended of the population. This development opens up the possibility of creating drug formulations that incorporate PB at a local level, making it a potentially significant resource in the treatment of Cs and Tl poisoning. The ability to locally produce and utilize PB in oral dosage forms could be crucial in addressing cases of accidental or intentional exposure within the population. This advancement not only contributes to the scientific understanding of PB but also holds promising implications for practical applications in public health and emergency situations.

A method for determining thallium in water samples via solid sampling high-resolution continuum source graphite furnace atomic absorption spectrometry (SS HR-CS GF AAS) after preconcentration using chromatographic filter paper as a solid support was proposed. The effects of pH, stirring time, and sample volume in the analyte preconcentration step were studied. The presence of potential interferences in the sample and the type of masking agent were also examined. In the proposed procedure, the sample was placed in contact with the solid phase in a polypropylene tube, and after stirring for 3 min, thallium determination was performed via HR-CS GF AAS directly on chromatographic filter paper. A preconcentration factor of 55, a precision of 9.4% (n = 10; 10 μg L-1), a limit of detection of 0.018 μg L-1, and a limit of quantification of 0.059 μg L-1 were achieved. Analyte addition and recovery tests were performed, and the results ranged from 91% to 110%. The accuracy of the method was evaluated by analyzing a water reference material. The procedure was used to determine thallium in water samples collected in Barreiras, Bahia, Brazil. The results were compared with those obtained using inductively coupled plasma‒mass spectrometry (ICP‒MS). Thallium concentrations in the analyzed samples ranged from <0.059 to 0.80 μg L-1.

Hypertension is a key risk factor for cardiovascular disease (CVD). Thallium is a highly toxic metal that exists in all aspects of our lives and can cause damage to human health. The aim of this study was to identify the potential correlation between urinary thallium (U-Tl) and hypertension in American youth aged 8-17 years. The National Health and Nutritional Examination Survey (NHANES) database was mined for cross-sectional information on 2295 American children and adolescents aged 8-17 years. Inductively coupled plasma mass spectrometry (ICP-MS) was utilized to measure U-Tl levels, and the results were categorized into four quartiles (Q1-Q4). Logistic generalized linear models and unweighted restricted cubic spline (RCS) regression were used to investigate the relationship between U-Tl and hypertension. After adjusting for covariates, the odds ratios (ORs) at 95% confidence intervals (CIs) for hypertension prevalence in the 2nd, 3rd, and 4th quartiles were 0.43 (0.22-0.81), 0.54 (0.29-0.99), and 0.43 (0.22-0.81), when compared to the lowest quartile (P for trend = 0.024). RCS plot showed a negative linear correlation between log2-transformed U-Tl levels and hypertension (P for non-linearity = 0.869). Subgroup analysis based on sex indicated a statistically significant link between U-Tl and hypertension in male (P < 0.05). There is a negative linear relationship between U-Tl and hypertension in American children and adolescents aged 8-17 years with low thallium exposure. Due to the nature of cross-sectional studies, further studies are necessary to validate our conclusions and elucidate possible mechanisms.

This review analyzes the causes and consequences of apoptosis resulting from oxidative stress that occurs in mitochondria and cells exposed to the toxic effects of different-valence heavy metals (Ag+, Tl+, Hg2+, Cd2+, Pb2+, Al3+, Ga3+, In3+, As3+, Sb3+, Cr6+, and U6+). The problems of the relationship between the integration of these toxic metals into molecular mechanisms with the subsequent development of pathophysiological processes and the appearance of diseases caused by the accumulation of these metals in the body are also addressed in this review. Such apoptosis is characterized by a reduction in cell viability, the activation of caspase-3 and caspase-9, the expression of pro-apoptotic genes (Bax and Bcl-2), and the activation of protein kinases (ERK, JNK, p53, and p38) by mitogens. Moreover, the oxidative stress manifests as the mitochondrial permeability transition pore (MPTP) opening, mitochondrial swelling, an increase in the production of reactive oxygen species (ROS) and H2O2, lipid peroxidation, cytochrome c release, a decline in the inner mitochondrial membrane potential (ΔΨmito), a decrease in ATP synthesis, and reduced glutathione and oxygen consumption as well as cytoplasm and matrix calcium overload due to Ca2+ release from the endoplasmic reticulum (ER). The apoptosis and respiratory dysfunction induced by these metals are discussed regarding their interaction with cellular and mitochondrial thiol groups and Fe2+ metabolism disturbance. Similarities and differences in the toxic effects of Tl+ from those of other heavy metals under review are discussed. Similarities may be due to the increase in the cytoplasmic calcium concentration induced by Tl+ and these metals. One difference discussed is the failure to decrease Tl+ toxicity through metallothionein-dependent mechanisms. Another difference could be the decrease in reduced glutathione in the matrix due to the reversible oxidation of Tl+ to Tl3+ near the centers of ROS generation in the respiratory chain. The latter may explain why thallium toxicity to humans turned out to be higher than the toxicity of mercury, lead, cadmium, copper, and zinc.

The effects of the exposure of proliferating MDCK cells to thallium [Tl(I) or Tl(III)] on cell viability and proliferation were investigated. Although Tl stopped cell proliferation, the viability was >95%. After 3h, two autophagy markers (SQSTM-1 expression and LC3β localization) were altered, and at 48h increased expression of SQSTM-1 (60%) and beclin-1 (50-100%) were found. At 24h, the expression of endoplasmic reticulum (ER) stress markers ATF-6 and IRE-1 were increased in 100% and 150%, respectively, accompanied by XBP-1 splicing and nuclear translocation. At 48h, major ultrastructure abnormalities were found, including ER enlargement and cytoplasmic vacuolation which was not prevented by protein synthesis inhibition. Increased PHB (85% and 40% for Tl(I) and Tl(III), respectively) and decreased β-tubulin (45%) expression were found which may be related to the promotion of paraptosis. In summary, Tl(I) and Tl(III) promoted ER stress and probably paraptosis in MDCK cells, impairing their proliferation.

After the use of thallium as rat poison was banned, the knowledge about the severe and treacherous course of poisonings with this toxic metal has widely been lost. In the present case, the male victim sustained two insidious poisoning attacks in 2017 and 2020 by the perpetrator, his female life partner. In the first poisoning episode, he suffered from increasing heavy pain of the abdomen, stinging pain of both legs, persistent obstipation, hyperesthesia, and, after about 2 weeks, tuft-wise loss of hair as typical symptoms of the thallium poisoning. Within 7 weeks, he was successively examined in six hospitals with a wide variety of diagnostic methods, but a conclusive explanation of the complaints was not found. The possibility of a metal intoxication was then suggested by the perpetrator who privately arranged the analysis of a blood sample with the result of 175 µg/l thallium. Although a criminal poisoning was assumed, the perpetrator was not identified. After the victim left the perpetrator, she subtly executed a second poisoning attack with thallium sulfate (blood level 1230 µg/l after 1 day, urine level 4760 µg/l after 10 days, and hair concentrations 3.26-0.49 from proximal to distal in 9 segments). The perpetrator was sentenced to 10.5 years imprisonment for grievous bodily harm and attempted murder. Because of the behavior of the perpetrator, a Munchausen by proxy syndrome was discussed as a motivation of the first poisoning but was excluded by the psychiatric expert because of a missing antisocial personality disorder.

Heavy metal ions are one of the main sources of water pollution. Most heavy metal ions are carcinogens that pose a threat to both ecological balance and human health. With the increasing demand for heavy metal detection, electrochemical detection is favorable due to its high sensitivity and efficiency. Here, after discussing the pollution sources and toxicities of Hg(ii), Cd(ii), As(iii), Pb(ii), UO₂(ii), Tl(i), Cr(vi), Ag(i), and Cu(ii), we review a variety of recent electrochemical methods for detecting heavy metal ions. Compared with traditional methods, electrochemical methods are portable, fast, and cost-effective, and they can be adapted to various on-site inspection sites. Our review shows that the electrochemical detection of heavy metal ions is a very promising strategy that has attracted widespread attention and can be applied in agriculture, life science, clinical diagnosis, and analysis.

Thallium (Tl) and uranium (U) contaminants pose serious threats to the ecological environment and human health. In this research, a cost-effective feroxyhite (δ-FeOOH) dispersed with sodium dodecyl sulfonate (SDS) was prepared and a series of experiments were optimized to explore the removal mechanism of Tl⁺ and UO₂²⁺ from the effluent. The SDS/δ-FeOOH exhibited highly dispersed colloidal particles and showed significantly enhanced adsorption performance on the removal of Tl and U in the presence of H₂O₂ and pH of 7.0. Equilibrium uptakes of 99.5% and 99.7% were rapidly achieved for Tl⁺ and UO₂²⁺ within 10 min, respectively. The Freundlich isotherm model fitted well with the adsorption data of Tl and U. The maximum isotherm sorption capacity of SDS/δ-FeOOH for Tl⁺ and UO₂²⁺ was 182.9 and 359.6 mg/g, respectively. The sorption of Tl followed the pseudo-second-order kinetic model, whereas the sorption of U followed the pseudo-first-order kinetic model. The uptake of Tl and U by SDS/δ-FeOOH was notably inhibited at Na⁺, K⁺ concentrations over 5.0 mM, and a high content of dissolved organic matter (over 0.5 mg/L). The mechanistic study revealed that ion exchange, precipitation, and surface complexation were main mechanisms for the removal of Tl and U. The findings of this study indicate that stabilizer dispersion may serve as an effective strategy to facilitate the treatment of wastewater containing Tl and U by using δ-FeOOH.

Thallium (Tl), a ubiquitous environmental toxicant, can cross the placental barrier during pregnancy. However, the effects of prenatal Tl exposure on placental function are currently unclear. Based on the Ma'anshan Birth Cohort study, we examined whether long-term prenatal Tl exposure was associated with placental inflammation. Tl concentrations were quantified in serum samples (n = 7050) from 2515 pregnancy during each trimester, placental inflammatory cytokine mRNA expression was assessed in 2519 placenta tissues. Geometric mean values of serum Tl concentrations were 63.57, 63.63 and 48.71 ng/L for the first, second and third trimesters, respectively. After adjustment for potential confounders, serum Tl concentration was positively associated with CD68 (β: 0.30; 95% CI: 0.05, 0.56) in the first trimester and TNF-α (β: 0.12; 95% CI: 0.01, 0.23), IL-6 (β: 0.15; 95% CI: 0.05, 0.25) and CD68 (β: 0.25; 95% CI: 0.10, 0.39) in the third trimester, however was negatively associated with IL-4 (β: -0.21; 95% CI: -0.41, -0.01) and CD206 (β: -0.23; 95% CI: -0.45, -0.02) in the first trimester. Repeated measures analysis showed that TNF-α, IL-6 and CD68 increased by 0.11 (95% CI: 0.01, 0.21), 0.12 (0.15, 95% CI: 0.05, 0.25), 0.22 (95% CI: 0.10, 0.39), respectively, with each 1ln-transformed Tl increase in total samples. Gender-specific analyses revealed that these associations were largely driven by male offspring. In addition, immunohistochemistry revealed that nuclear NF-κB p65 expression increased in placenta tissue. The results of this prospective cohort study provide longitudinal evidence that prenatal Tl exposure induces a placental inflammatory response in the Chinese population.

Thallium (TI) is one of the most toxic heavy metals and priority pollutant metals. The emerging TI environmental pollution worldwide has posed a great threat to human health. However, based on the World Health Organization (WHO), the risk and severity of adverse health effects of TI in the range of 5-500 μg/L are uncertain. Moreover, evidence regarding the adverse impacts of TI on children's health is still insufficient. Herein, we aim to investigate the early adverse effects of TI on children's health and provide references for the WHO to establish stricter safety limits of TI. From 2015 to 2019, urinary TI and many clinical laboratory parameters related to blood routine, hepatic, renal, myocardial, coagulation function and serum electrolyte were measured in six children aged 1-9 years. The urinary TI concentration ranged from 13.4 μg/L to 60.1 μg/L with a mean of 36.1 μg/L and a median of 34.8 μg/L in six children in 2015. Although only four children felt a little poor appetite, several laboratory abnormalities indicated early damage in liver, renal, and myocardial functions in all children in 2015. After treatment and following up for four years, although the children's TI concentration decreased below 5 μg/L, their liver and renal functions did not completely recover, and their myocardial function worsened. Results indicated that impaired liver, renal, and myocardial functions were closely associated with elevated urinary TI concentration in children. Considering the increasing use of TI in high-technology industries and emerging TI environmental-contamination zones worldwide, establishing stricter safety limits of TI and paying more attention to the adverse health effects of TI on children are urgently required. SUMMARY: We found that a relatively low concentration of thallium (13.4 μg/L to 60.1 μg/L) impaired liver, renal, and myocardial function in six children. After treatment and following up these children for four years, although their urinary TI concentration decreased below 5 μg/L, their liver and renal functions did not completely recover, and their myocardial function worsened.

The banning of the heavy metal thallium (Tl) in many Countries, because of its toxicity, led to a remarkable reduction of the number of cases of poisoning both accidental and homicidal forcing us to better study the pharmacokinetics of this poison using new technologies. The Authors, in this work, are reporting the case of a collective thallium toxicosis caused by voluntary adulteration of an infusion with thallium sulfate, occurred in 8 members of the same familial nucleus; the administration of Prussian Blu resulted to be ineffective for 3 of these members that died at a later time. The most peculiar aspects of this rare manner of poisoning are discussed; the analytical procedures used, Inductively Coupled Plasma Mass Spectrometry (ICP-MS) in particular, resulted to be fundamental in the forensic diagnosis process of acute poisoning cause by thallium.

The interaction among various soil minerals can significantly impact on the environmental geochemical process of contaminants. Therefore, this study investigated the effects of interaction between vermiculite (VER) and manganese dioxide (MnO₂) on the migration and transformation of Tl(I). The VER exhibited typical layered structure and MnO₂ possessed a flower-like structure with serious reunion phenomenon, while the production of interaction between vermiculite and manganese dioxide, labeled VER-MnO₂, illustrated as fish scales evenly spread over a large sheet, suggesting that MnO₂ could triumphantly be anchored on the VER and the aggregation of MnO₂ was prevented. Compared with the pure MnO₂, VER acted as template substrate contributed the higher specific surface area (298.18 m²·g^-1) and the oxidation degree of Mn. VER-MnO₂ showed the highest fixation capacity (144.29 mg·g^-1) than other two materials in the order VER-MnO₂ > MnO₂ > VER, and there was no risk derived from Mn dissolution. The influence mechanism of VER-MnO₂ on Tl(I) migration and transformation lied in immobilization, ion exchange and oxidization. Fixed-bed column immobilization experiments showed that VER-MnO₂ could purify drinking water contaminated by Tl (20 μg·L^-1) and the effective breakthrough volumes were 900 bed volumes until reaching the maximum limits allowed in drinking water (0.1 μg·L^-1). VER-MnO₂ excellently catches Tl to prevent groundwater pollution. This study provides a theoretical guidance for environmental fate and restoration of soil heavy metal pollution.

Thallium (Tl) is a cumulative high toxicant in the environment, but few longitudinal studies have investigated the respiratory impairment of Tl exposure.

This study aimed to evaluate the effect of Tl and its interaction with smoking on lung function decline, and explore the potential mechanisms.

The baseline and follow-up lung functions were measured from a prospective cohort study of 1243 workers, who were followed from 2010 to 2014. Their baseline urinary levels of Tl were determined. We also measured the plasma C-reactive protein (CRP) and urinary 8-iso-prostaglandin-F2α (8-iso-PGF2α) in a randomly selected subcohort of 474 subjects.

The results showed that a 2-fold increase in urinary Tl was associated with 29.81 mL (95%CI: 3.83-55.80) increased decline in forced expiratory volume in 1 s (FEV₁). The effect was more pronounced among heavy-smokers (≥15 pack-years) [β(95%CI) = 56.42 mL (9.66-103.19)]. In particular, compared to never-smokers with low Tl, heavy-smokers with high Tl had a separate 158.44 mL (95%CI: 54.88-262.00) and 4.58% (95%CI: 1.40-7.76) increased declines in FEV₁ and percentage of predicted (ppFEV₁), respectively. There was a significant interaction between Tl and smoking intensity on ppFEV₁ decline (P_int = 0.034). More importantly, the increasing level of urinary Tl was correlated with elevated CRP and 8-iso-PGF2α.

Our prospective cohort study identified that exposure to high Tl had a deleterious effect on lung function, and this effect may be enhanced by tobacco smoking. Increased inflammation may partly contribute to the joint effects of Tl and smoking on impaired lung function, but the biological mechanisms need further explorations.

α4/7-Conotoxin LvIA is an isoform-selective inhibitor of the α3β2 nicotinic acetylcholine receptor. An efficient strategy for the synthesis of this toxin is critical to advancing its utility as a probe for receptor function and as a potential pharmaceutical lead target. On-resin methods for peptide synthesis offer potential synthetic advantages; however, strategies for on-resin formation of multiple disulfides have historically been low-yielding. Here, we harness the reactivity of the Allocam protecting group and employ 3-amino acid spacer strategy to synthesize α4/7-conotoxin LvIA via three different on-resin strategies, each of which results in an isolated yield higher than prior fully on-resin approaches.

Heavy metals pose significant morbidity and mortality threats to humans in connection with both acute and chronic exposure. The often-delayed manifestations of some toxic effects and the wide-spectrum of symptoms caused by heavy metal poisoning may perplex the clinical diagnosis and, when involved in crimes, complicate the forensic investigation. To investigate the original intoxication process of a thallium poisoning case, which occurred in China more than two decades ago, laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS) was used to analyze several hairs of the victim from before, during and after the poisoning period. Ablation line scans of the entire length of a ∼7cm hair revealed ∼4months of repeated exposure to thallium with increased doses and frequency toward the end, while scan of a ∼0.7cm hair revealed ∼2weeks of constant ingestions of large doses of thallium accompanied by elevated amount of lead. The endogenous origin of thallium was confirmed by the preservation of the same longitudinal distribution profile in the inner part of hair, but the source of lead could not be unambiguously determined due to the intrinsic limitation of hair analysis to distinguish ingested lead from exogenous contaminants. The overall thallium distribution profiles in the analyzed hairs suggested both chronic and acute thallium exposures that correlated well with the sequential presentation of a plethora of symptoms experienced by the victim. Aligning the time-resolved thallium peaks with symptoms also provided clues on possible routes of exposure at different poisoning stages. This work demonstrated the capability of using single hair LA-ICP-MS analysis to reconstitute a prolonged and complicated heavy metal poisoning case, and highlighted the necessity of assessing multiple elements in the medico-legal investigation of suspicious heavy metal poisonings.

There are a number of toxic agents that can cause alopecia. In this review we summarize the known substances that cause alopecia as one of the clinical signs of overdose or toxicity.

A search was conducted using PubMed, EMBASE, and Cochrane for studies describing hair loss of any type as a result of exposure to or ingestion of a toxic agent. The search yielded 856 articles, with 47 studies included in this review.

Agents with the strongest evidence of association to alopecia include thallium, mercury, selenium, and colchicine. Agents with described incidents include boric acid, arsenic, vitamin A, botulinum toxin, Podostroma cornu-damae, and the synthetic opioid MT-45.

Numerous toxic agents have been implicated in alopecia, and the strength of evidence behind each agent varies. Toxic levels of thallium and colchicine have long been established to cause alopecia, as compared to agents such as botulinum toxin A and synthetic recreational drugs which have less literature describing their links to alopecia and will need further investigation to characterize their relationships to hair loss. Knowledge of typical presentations of hair loss will aid in the development of a differential diagnosis for patients presenting with alopecia.

A FeOOH-loaded MnO₂ nano-composite was developed as an emergency material for Tl(I) pollution incident. Structural characterizations showed that FeOOH successfully loaded onto MnO₂, the nanosheet-flower structure and high surface area (191 m² g^-1) of material contributed to the excellent performance for Tl(I) removal. FeOOH-loaded MnO₂ with a Fe/Mn molar ratio of 1:2 exhibited a noticeable enhanced capacity for Tl(I) removal compared to that of pure MnO₂. The outstanding performance for Tl(I) removal involves in extremely high efficiency (achieved equilibrium and drinking water standard within 4 min) and the large maximum adsorption capacity (450 mg g^-1). Both the control-experiment and XPS characterization proved that the removal mechanism of Tl(I) on FeOOH-loaded MnO₂ included adsorption and oxidation: the oxidation of MnO₂ played an important role for Tl(I) removal, and the adsorption of FeOOH loaded on MnO₂ enhanced Tl(I) purification at the same time. In-depth purification of Tl(I) had reach drinking water standards (0.1 μg L^-1) at pH above 7, and there wasn't security risk produced from the dissolution of Mn²⁺ and Fe²⁺. Moreover, the as-prepared material could be utilized as a recyclable adsorbent regenerated by using NaOH-NaClO binary solution. Therefore, the synthesized FeOOH-loaded MnO₂ in this study has the potential to be applied as an emergency material for thallium pollution incident.

Thallium (Tl), lead and steroid exposures were reported as a result of street drug consumption such as heroin and cocaine.

This study aimed to compare the values of qualitative and quantitative assays for detecting Tl as an adulterant in opioid-like compound drug users.

This case-control study was conducted throughout a specified time bracket ranging from May 2015 to November 2015 in Imam Reza Hospital, Mashhad, Iran. In general, urine thallium samples for 100 opioid overdosed subjects with a history of chronic opioid use and 50 non-drug users were studied. Qualitative 24 hours-urinary-thallium-level (QL) and quantitative 24 hours-urinary-thallium-level (QT) were conducted in both groups. Independent-samples t-test and Spearman's Coefficient were applied for analytical purposes. SPSS software 16 was used to conduct statistical analyses with P values less than 0.05 regarded as significant.

A total of 150 cases were studied. Raw opium users accounted for 66% of the cases followed by mixed (28%) and heroin users (6%). Mean (SD) QT level for QL was 26.8 (1) μg/L, while it was 2.3 μg/L (0.4 μg/L) for negative QL, which was far below QL positive cases (p=0.002). The qualitative test showed more accuracy at higher quantitative levels. In all cases, qualitative test was fully sensitive (100%), highly specific (89%) with a positive likelihood ratio (PLR) of 9.1 and a negative likelihood ratio (NLR) of 0.

These results suggest that qualitative assays could be used with confidence in assessing Tl exposure in drug users. Physicians may easily and confidently use Tl qualitative tests in rehabilitation centers, where toxicology laboratories may not be available.

The conformation of adenine nucleotide translocase (ANT) has a profound impact in opening the mitochondrial permeability transition pore (MPTP) in the inner membrane. Fixing the ANT in 'c' conformation by phenylarsine oxide (PAO), tert-butylhydroperoxide (tBHP), and carboxyatractyloside as well as the interaction of 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) with mitochondrial thiols markedly attenuated the ability of ADP to inhibit the MPTP opening. We earlier found (Korotkov and Saris, 2011) that calcium load of rat liver mitochondria in medium containing TlNO3 and KNO3 stimulated the Tl(+)-induced MPTP opening in the inner mitochondrial membrane. The MPTP opening as well as followed increase in swelling, a drop in membrane potential (ΔΨmito), and a decrease in state 3, state 4, and 2,4-dinitrophenol-uncoupled respiration were visibly enhanced in the presence of PAO, tBHP, DIDS, and carboxyatractyloside. However, these effects were markedly inhibited by ADP and membrane-penetrant hydrophobic thiol reagent, N-ethylmaleimide (NEM) which fix the ANT in 'm' conformation. Cyclosporine A additionally potentiated these effects of ADP and NEM. Our data suggest that conformational changes of the ANT may be directly involved in the opening of the Tl(+)-induced MPTP in the inner membrane of Ca(2+)-loaded rat liver mitochondria. Using the Tl(+)-induced MPTP model is discussed in terms finding new transition pore inhibitors and inducers among different chemical and natural compounds.

Thallium (Tl) is a highly toxic heavy metal situated between mercury and lead in the periodic table. While its neighbors have been thoroughly studied for DNA-based sensing, little is known about thallium detection. In this work, in vitro selection of RNA-cleaving DNAzymes is carried out using Tl(3+) as the target metal cofactor. Both normal DNA and phosphorothioate (PS)-modified DNA are tested for this purpose. While no Tl(3+)-dependent DNAzymes are obtained, a DNA oligonucleotide containing a single PS-modified RNA nucleotide is found to cleave by ∼7% by Tl(3+) at the RNA position. The remaining 93% are desulfurized. By hybridization of this PS-modified oligonucleotide with the Tm7 DNAzyme, the cleavage yield increases to ∼40% in the presence of Tl(3+) and Er(3+). Tm7 is an Er(3+)-dependent RNA-cleaving DNAzyme. It cleaves only the normal substrate but is completely inactive using the PS-modified substrate. Tl(3+) desulfurizes the PS substrate to the normal substrate to be cleaved by Tm7 and Er(3+). This system is engineered into a catalytic beacon for Tl(3+) with a detection limit of 1.5 nM, which is below its maximal contamination limit defined by the U.S. Environmental Protection Agency (10 nM).