Brain damage caused by the metal accumulation may result in the permanent injuries including severe neurological disorders. Thus, the aim of this study was to determine the medicinal efficacy of broccoli extract in arsenic-induced brain poisoning. Twenty-eight female rats were classified into 4 groups; control, receiving sodium arsenate (As), As + broccoli extract (As + Bc), and (Bc). Then, the Elevated Plus-Maze and pathological-biochemical assessment of the brain tissue were performed. Moreover, the GC-MS was used to explore the quantity and quality of broccoli extract. The catalase had a significant decrease in the As group compared to that of the control group; As + Bc and Bc groups also showed a significant increase compared to that of the As group. Glutathione peroxidase was the lowest in the As group (1.84 ± 0.97) and the highest in the Bc group (5.51 ± 2.31). The Treatment significantly reduced pro-inflammatory cytokines in the As + Bc group. In addition, in terms of behavioral changes, the duration of presence in the open arm was reduced in the As group compared to that of the control group. Besides, the open arm duration increased significantly in the Bc group. Interestingly, there was a significant increase in estrogen and gonadotropin hormones in the Bc group compared to the other groups. Pathological findings showed that the condition of cortical neurons was improved and the surrounding space was reduced in As + Bc compared to that of the As group. In addition, more than 30% of the extract's compounds are made up Phytol,1-isothiocyanate-4-[methylsulfinyl] butane, and γ-Sitosterol. Thereby, the broccoli extract with active substances was highly effective in enhancing the behavioral and pathological parameters switch in rats with arsenic-induced poisoned brains.

Arsenic (AS) is a metalloid element that widely exists and can cause different degrees of liver damage. The molecular mechanism of arsenic-induced liver injury has yet to be fully elucidated. Clinically, glutathione (GSH) is often used as an antidote for heavy metal poisoning and hepatoprotective drugs. However, the hepatoprotective effect of glutathione remains unknown in arsenic-induced liver injury. The regulatory relationship between Foxa2 and XIAP may play an important role in mitochondrial survival and death. Therefore, we took Foxa2-XIAP as the axis to explore the protective mechanism of GSH. In this study, we first established a mouse model of chronic arsenic exposure and examined liver function as reflected by quantitative parameters such as aspartate aminotransferase and alanine aminotransferase. Also, redox parameters in the liver were measured, including malondialdehyde, superoxide dismutase, 8-hydroxy-2'-deoxyguanosin, and glutathione peroxidase. RT-qPCR and western-blotting were used to detect the levels of related genes and proteins, such as Foxa2, XIAP, Smac, Bax, Bcl2, Caspase9, and Caspase3. Subsequently, GSH was administered at the same time as high arsenic exposure, and changes in the above parameters were observed. After a comprehensive analysis of the above results, we demonstrate that GSH treatment alleviates arsenic-induced oxidative stress and inhibits the mitochondrial pathway of apoptosis, which can be regulated through the Foxa2 and XIAP axis. The present study would be helpful in elucidating the molecular mechanism of arsenic-induced liver injury and identifying a new potential therapeutic target. And we also provided new theoretical support for glutathione in the treatment of liver damage caused by arsenic.

Arsenic (As) is enriched in wild edible fungi, which is one of the main important sources of As in humans' diet. In this study, two wild edible fungi were employed for investigation: (1) Pleurotus citrinopileatusone, which contains a high content of inorganic As (iAs) and (2) Agaricus blazei Murill, which contains a high content of organic As. This study investigated the changes in As content and its speciation after different daily cooking methods. We found that the content of As in Pleurotus citrinipileatus and Agaricus blazei Murill reduced by soaking plus stir-frying by 55.4% and 72.9%, respectively. The As content in Pleurotus citrinipileatus and Agaricus blazei Murill decreased by 79.4% and 93.4%, respectively, after soaking plus boiling. The content of As speciation in dried wild edible fungi reduced significantly after different treatments. Among them, iAs decreased by 31.9~88.3%, and organic As decreased by 33.3~95.3%. This study also investigated the bioaccessibility of As in edible fungi after different cooking processes via an in-vitro physiologically based extraction test (PBET). The results showed that the bioaccessibility of As was relatively high if the edible fungi were uncooked, boiled, or stir-fried. The gastric (G) bioaccessibility of As ranged from 51.7% to 93.0% and the gastrointestinal (GI) bioaccessibility of As ranged from 63.5% to 98.1%. Meanwhile, the bioaccessibility of inorganic As was found to be as high as 94.6% to 151%, which indicates that further evaluation of the potential health risks of wild edible fungi is necessary.

Inorganic arsenic is highly toxic and carcinogenic to humans. Exposed individuals vary in their ability to metabolize arsenic, and variability in arsenic metabolism efficiency (AME) is associated with risks of arsenic-related toxicities. Inherited genetic variation in the 10q24.32 region, near the arsenic methyltransferase (AS3MT) gene, is associated with urine-based measures of AME in multiple arsenic-exposed populations. To identify potential causal variants in this region, we applied fine mapping approaches to targeted sequencing data generated for exposed individuals from Bangladeshi, American Indian, and European American populations (n = 2,357, 557, and 648 respectively). We identified three independent association signals for Bangladeshis, two for American Indians, and one for European Americans. The size of the confidence sets for each signal varied from 4 to 85 variants. There was one signal shared across all three populations, represented by the same SNP in American Indians and European Americans (rs191177668) and in strong linkage disequilibrium (LD) with a lead SNP in Bangladesh (rs145537350). Beyond this shared signal, differences in LD patterns, minor allele frequency (MAF) (e.g., rs12573221 ~13% in Bangladesh ~0.2% among American Indians), and/or heterogeneity in effect sizes across populations likely contributed to the apparent population specificity of the additional identified signals. One of our potential causal variants influences AS3MT expression and nearby DNA methylation in numerous GTEx tissue types (with rs4919690 as a likely causal variant). Several SNPs in our confidence sets overlap transcription factor binding sites and cis-regulatory elements (from ENCODE). Taken together, our analyses reveal multiple potential causal variants in the 10q24.32 region influencing AME, including a variant shared across populations, and elucidate potential biological mechanisms underlying the impact of genetic variation on AME.

For 23 years, Charles V "The Wise" of France suffered from a mysterious fistula on his left arm that continuously drained pus. For all this time, he believed that as soon as the fistula ceased to weep, he would have a mere 15 days before death followed. His death in 1380, at the young age of 42, seemingly proved this assumption correct. This paper explores the possible explanations from arsenic poisoning at the hands of his longtime nemesis Charles II, as many of his contemporaries believed, to an undiagnosed case of hidradenitis suppurativa, to an underlying tuberculosis infection, to the possibility that his condition was entirely self-inflicted. While it is impossible to determine a definitive cause, it is highly unlikely that Charles II "The Bad" of Navarre had anything to do with his rival's strange condition.

Objective: Establishing an analysis method for the detection of six arsenic compounds trivalent arsenic, pentavalent arsenic, methyl arsenic, dimethyl arsenic, arsenical choline and arsenical betaine in urine by high-performance liquid chromatography-inductively coupled plasma-mass spectrometry (HPLC-ICP-MS) and providing a theoretical basis for health assessment of arsenic poisoning patients. Methods: HPLC-ICP-MS was used to detect six arsenic compounds with the hamilton PRP-X100 column and aqueous ammonium phosphate in a gradient elution as mobile phase. Results: There was a good linear relationship in the selected range of six arsenic compounds evidenced by a linear correlation coefficient greater than 0.999. The detection limit of 6 arsenic compounds was 0.46~0.57 μg/L, and the minimum quantitative concentration were 1.52~1.91 μg/L. The recovery rates of six arsenic compounds were 96.5%~106.4%, The within-run and between-run relative standard deviation was 2.9%~6.2% and 3.8%~8.7%. Conclusion: The established method with high accuracy and precision is suitable for detecting arsenic levels in urine of occupational arsenic exposure population.

Historically, heavy metal measurement and interpretation has been a highly specialised area performed only in a handful of centres within the UK. However, recent years have seen a move to more local testing due to the repatriation of referred work into pathology networks and the increased availability of inductively coupled plasma mass spectrometry technology. While management of significant poisoning is still overseen by tertiary care poisoning specialists, management of milder cases may be undertaken locally.Non-specialist clinical scientists and clinicians need to know when heavy metal testing is appropriate, which samples are required (and any specific requirements around collection) and how to interpret and act on the results.This Best Practice article provides guidance on the investigation and monitoring of the toxic elements most frequently encountered in general medical practice; lead, mercury and arsenic. It is intended as a reference guide for the non-specialist and as a comprehensive summary for clinical toxicologists and clinical scientists.

The golden eagle (Aquila chrysaetos) and the white-tailed eagle (Haliaeetus albicilla), being apex predators and facultative scavengers, can bioaccumulate different environmental contaminants, including toxic elements that may adversely affect their health. We analyzed the levels of cadmium (Cd), lead (Pb), and other metals and metalloids, including arsenic (As), barium (Ba), beryllium (Be), cobalt (Co), chromium (Cr), copper (Cu), iron (Fe), magnesium (Mg), manganese (Mn), molybdenum (Mo), selenium (Se), thorium (Th), thallium (Tl), uranium (U), vanadium (V), and zinc (Zn) in liver samples taken from three golden eagles and 36 white-tailed eagles that were found dead across Poland to verify their exposure. We also used a systematic review to summarize the available literature data on Cd, Pb, and other studied elements in the liver of both eagle species. Analyses of trace elements in the liver samples of the Polish eagles revealed interspecific differences in Cd, Cu, and Mn and differences in Co, Mn, Tl, and Zn among study regions. All elements tested except Pb were below the suggested thresholds linked with adverse health effects in birds. The hepatic Pb found in almost half of all the tested individuals suggests environmental exposure to this toxic element. One of the tested white-tailed eagles had hepatic Pb above the threshold of sublethal poisoning. Although our results seem optimistic, as previous Polish studies showed a higher prevalence of birds with hepatic Pb exceeding the toxicity threshold, they indicate that exposure to this toxic metal could still pose an additional threat to the health of Polish eagles.

Over 50 countries are affected by arsenic contamination. The problem is becoming worse as the number of affected people increases and new sites are reported globally.

Inorganic arsenic is a well-known environmental toxicant and carcinogen, and there is overwhelming evidence for an association between this metalloid poisoning and hepatic diseases. However, the biological mechanism involved is not well characterized. In the present study, we probed how inorganic arsenic modulates the hepatic polarization of macrophages, as well as roles of PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy participates in regulating the metalloid-mediated macrophage polarization. Our results indicate that acute arsenic exposure induced macrophage polarization with up-regulated gene expression of inducible nitric oxide synthase (Inos) and arginase-1 (Arg1), monocyte chemotactic protein-1 (Mcp-1) and macrophage inflammatory protein-2 (Mip-2), tumor necrosis factor (Tnf)-α, interleukin (Il)-1β and Il-6, as well as anti-inflammatory factors Il-4 and Il-10. In parallel, we demonstrated the disrupted hepatic redox balance typically characterized by the up-regulation of hydrogen peroxide (H2O2) and glutathione (GSH), and activation of PINK1/Parkin-mediated mitophagy in the livers of acute arsenic-exposed mice. In addition, our results demonstrate that it might be the PINK1/Parkin-mediated mitophagy that renders hepatic macrophage refractory to arsenic-induced up-regulation of the genes Inos, Mcp-1, Mip-2, Tnf-α, Il-1β, Il-6 and Il-4. In this regard, this is the first time the protective effects of PINK1/Parkin-mediated mitophagy in inorganic arsenic-induced hepatic macrophage polarization in vivo have been reported. These findings add novel insights into the arsenical immunotoxicity and provide a basis for the preve.ntive and therapeutic potential of PINK1/Parkin-mediated mitophagy in arsenic poisoning.

Arsenic (As) poisoning has proven to be a major threat worldwide because of its toxic effects on the human body. As toxicity through drinking water is a global health concern. The toxicity of As is known to affect the liver, kidney, lungs, muscles, cardiovascular system, and nervous system and can even induce diabetes. Further As can cause skin lesions leading to notable diseases in the skin like Bowen's disease. Chronic exposure to As has caused many tragedies in Eastern, and several Southeast Asian and Latin American countries. Long-term exposure to As makes it an immediate threat that should be dealt with as a priority, and one of the ways to handle it may be with the use of antioxidants. In this review, we have discussed the natural and anthropogenic sources of As, its metabolism, pathophysiology, and mechanism of toxicity. Besides, we have also discussed some of the synthetic chelators and the ameliorative role of antioxidants and natural compounds in reducing As toxicity.

Thallium poisoning is usually accidental. We present a case of a 51-year-old woman who was evaluated in June 2018 for myalgia, vertigo, asthenia, and abdominal pain. Physical examination revealed temporal-spatial disorientation, jaundice, and asterixis. The laboratory reported the following: bilirubin, 10.3 mg/dL; aspartate transaminase, 78 U/L; alanine transaminase, 194 U/L; albumin, 2.3 g/dL; prothrombin time, 40%; and platelet count, 60,000/mm3. Serology performed for hepatitis A, B, and C; Epstein-Barr virus; cytomegalovirus; and human immunodeficiency virus was negative, and a collagenogram was negative. Physical reevaluation revealed alopecia on the scalp, armpits, and eyebrows; macules on the face; plantar hyperkeratosis; and ulcers on the lower limbs. Tests for lead, arsenic, copper, and mercury were carried out, which were normal; however, elevated urinary thallium (540 µg/g; range, 0.4-10 µg/g) was observed. The patient was treated with ᴅ-penicillamine 1,000 mg/day and recovered her urinary thallium levels were within normal range at annual follow-up. Thallium poisoning is extremely rare and can be fatal in small doses. An adequate clinical approach can facilitate early diagnosis.

Arsenic (As) poisoning has caused an environmental catastrophe in Bangladesh as millions of people are exposed to As-contaminated drinking water. Chronic As-exposure causes depression, memory impairment, and liver injury in experimental animals. This study was carried out to assess the protective effect of mulberry leaves juice (Mul) against As-induced neurobehavioral and hepatic dysfunctions in Swiss albino mice. As-exposed mice spent significantly reduced time in open arms and increased time spent in closed arms in the elevated plus maze (EPM) test, whereas they took significantly longer time to find the hidden platform in the Morris water maze (MWM) test and spent significantly less time in the desired quadrant when compared to the control mice. A significant reduction in serum BChE activity, an indicator of As-induced neurotoxicity-associated behavioral changes, was noted in As-exposed mice compared to control mice. Supplementation of Mul to As-exposed mice significantly increased serum BChE activity, increased the time spent in open arms and reduced time latency to find the hidden platform, and stayed more time in the target quadrant in EPM and MWM tests, respectively, compared to As-exposed-only mice. Also, a significantly reduced activity of BChE, AChE, SOD, and GSH in brain, and elevated ALP, AST, and ALT activities in serum were noted in As-exposed mice when compared to control mice. Mul supplementation significantly restored the activity of these enzymes and also recovered As-induced alterations in hepatic tissue in As-exposed mice. In conclusion, this study suggested that mulberry leaves juice attenuates As-induced neurobehavioral and hepatic dysfunction in mice.

Arsenic is a common metal-like element. Drinking arsenic-containing water and occupational exposure to arsenic are the main ways exposure to arsenic for population. Long-term exposure to arsenic can cause various organs dysfunction and cancer. After entering the body, inorganic arsenic is mainly methylated into monomethyl arsenic and dimethyl arsenic in the liver. Only a small part of inorganic arsenic is metabolized in the kidneys and lungs, and finally the metabolites of arsenic are excreted in the urine. understanding the biological characteristics of arsenic absorption, metabolism, and distribution in the body and formulating biological indicators related to occupational exposure to arsenic and can provide a scientific basis for the prevention and treatment of arsenic-related diseases. This article will review the biological monitoring indicators of occupational exposure to arsenic and the metabolic process of arsenic in the body.

Background and Purpose: Arsenic exposure can lead to skin lesions and multiple organ damage, which are not easily reversible and for which there is no effective therapeutics. Identification of reliable epigenetic markers is essential for early recognition of arsenic poisoning risk. Anomalous DNA methylation of immune homeostasis regulator FOXP3 is a critical mechanism for triggering arsenic poisoning. This study aims to explore the value of FOXP3 methylation in the identification of arsenic poisoning risk.Methods: 88 arsenic poisoning subjects and 41 references were recruited. Urinary arsenic contents and FOXP3 methylation in PBLCs was measured by ICP-MS and pyrosequencing, respectively.Results: The results showed that the elevated FOXP3 methylation in PBLCs were associated with the increased levels of urinary arsenic and were positively associated with the increased risk of arsenic poisoning and its progression. The result of mediation analysis revealed that 24.3% of the effect of arsenic exposure on the risk of arsenic poisoning was mediated by increased FOXP3 methylation. Additionally, we constructed a nomogram model with FOXP3 methylation as an epigenetic predictor to assess the probability of individual arsenic poisoning. The model showed a robust ability in the discrimination of arsenic poisoning risk, with an area under receiver operating characteristics curve of 0.897(0.845-0.949) and more than 70% accuracy. The calibration curves and the Harrell concordance index showed that the consistency rate between the probability predicted by the nomogram model and the actual probability is 89.7%.Conclusions: Taken together, we found the great potential of FOXP3 methylation for the identification of arsenic poisoning risk and provided a new approach to the application of epigenetic markers in accurately quantifying the risk of adverse outcomes.

Rodenticides or “rat poisons” are mixed compounds used to eradicate rodents. They are one of the most toxic agents commonly found in households. Historically, heavy metals such as arsenic were the first agents used to control rodent populations, but the most common rodenticide used in the twenty-first century is anticoagulants.[1] When a clinician suspects rodenticide poisoning, every effort should be made to identify the substance, including package information (i.e., brand name, chemical name, signal word, presence of skull or crossbones on the label) and description (odor, appearance, color). This step may involve staff returning to the point of potential exposure where the patient was last seen and searching for evidence of the rodenticide. In cases of serious ingestion, poison control and/or a medical toxicologist should be contacted.

The quality of irrigation water sources can significantly affect the concentrations of heavy metals (HMs) in cultivated vegetables. This study aimed to investigate the effect of various water resources, including treated wastewater effluent (TWE), river water (RW), and well water with chemical fertilizer (WW+F), on the accumulation of heavy metals (HMs) in the three most widely consumed edible vegetables (Coriander, Radish, and Basil) in Iran. A total of 90 samples of edible vegetables, 13 samples of irrigation water, and 10 soil samples were collected to determine HMs concentrations. Iron (Fe), Zinc (Zn), Copper (Cu), Manganese (Mn), Lead (Pb), Cadmium (Cd), Chromium (Cr), Nickel (Ni,) and Arsenic (As) were analyzed by inductively coupled plasma optical emission spectrometry (ICP-OES). Eventually, the Total Target Hazard Quotient (TTHQ) for the toxic metals of As, Pb, and Cd was determined. The results revealed that the TTHQ of toxic metals in vegetables was less than the allowable limits (TTHQ = 1). Also, TWE was the best irrigation water type since the HMs content of vegetables was low. By comparing the results with national and international standards, it can be concluded that the Gharasou RW for irrigation of edible vegetables was inappropriate.

Arsenic (As) is a toxic metalloid that affects many organs through drinking water. This study aims to examine the efficacy of ozone therapy on chronic arsenic toxicity. Twenty-four male Wistar albino rats were housed in individual cages and grouped as control, As, O3, and As + O3. As was applied by adding 5 mg/kg/day in drinking water for 60 days. Ozone therapy was applied at 0.5 mg/kg/day (i.p.) O3 in the last 5 days of the experimental period. Tissues were harvested and analyzed for histopathological injury and apoptotic markers. There was no significant difference between the As + O3 and O3 groups (p = 0.186 and p = 0.599) for light microscopic criteria: inflammatory cell infiltration and hydropic degeneration in liver tissue.In TUNEL assessments, similar outcomes were obtained in the control and As + O3 groups. A statistically significant increase was observed in p53 and Caspase 3 (Casp-3) expression levels in the As group compared to the O3 and As + O3 groups. There was no significant difference between the As + O3 and O3 groups on peritubular hemorrhage and desquamation parameters in kidneys (p = 0.147 and p = 0.094). The KIM-1 expression level was significantly increased in the As group compared to the As + O3 group (p = 0.01), and the Casp-3 expression level was not significantly changed in the O3 group compared to the As + O3 group (p = 0.59). In conclusion, it is determined that ozone therapy has ameliorative effects on the microscopic injury of liver and kidney tissues. In addition to microscopic improvement, KIM-1 gene expression levels were ameliorated in the kidneys. The apoptotic cell counts and the Casp-3 and p53 gene expression levels were decreased by O3 administration. Thus, ozone therapy can be a treatment choice for As toxicity.

Arsenic is a ubiquitous metalloid element in the environment. Arsenic is classified as a group A carcinogen and has caused serious impacts on human health. For example, chronic poisoning caused by arsenic in groundwater is a global health problem. The forms of arsenic in environmental water are diverse, which can easily be transformed into each other during the sampling process and transportation, resulting in errors in laboratory analysis results. Therefore, developing on-site analytical methods for arsenic and acquiring accurate data are the basis for the study of the morphological transformation and bio-absorption process of arsenic and accurately evaluating its toxicity. In the past few decades, laboratory-based analytical methods for arsenic have developed rapidly, but there are still huge challenges in the on-site analysis of arsenic. This review summarized the relevant reviews on analytical methods of arsenic in environmental water in the past decade (2011-2022); discussed the advances in on-site analytical methods such as colorimetric methods, luminescence-based methods, and electrochemical methods of arsenic; anticipated the future development of on-site analytical methods for arsenic in environmental waters; and provided references for the development and applications of new methods.

Due to structural racism and income inequality, exposure to environmental chemicals is tightly linked to socioeconomic factors. In addition, exposure to psychosocial stressors, such as racial discrimination, as well as having limited resources, can increase susceptibility to environmentally induced disease. Yet, studies are often conducted separately in fields of social science and environmental science, reducing the potential for holistic risk estimates. To tackle this gap, we developed the Chemical and Social Stressors Integration Technique (CASS-IT) to integrate environmental chemical and social stressor datasets. The CASS-IT provides a framework to identify distinct geographic areas based on combinations of environmental chemical exposure, social vulnerability, and access to resources. It incorporates two data dimension reduction tools: k-means clustering and latent profile analysis. Here, the CASS-IT was applied to North Carolina (NC) as a case study. Environmental chemical data included toxic metals - arsenic, manganese, and lead - in private drinking well water. Social stressor data were captured by the CDC's social vulnerability index's four domains: socioeconomic status, household composition and disability, minority status and language, and housing type and transportation. Data on resources were derived from Federal Emergency Management Agency (FEMA's) Resilience and Analysis Planning Tool, which generated measures of health resources, social resources, and information resources. The results highlighted 31 NC counties where exposure to both toxic metals and social stressors are elevated, and health resources are minimal; these are counties in which environmental justice is of utmost concern. A census-tract level analysis was also conducted to demonstrate the utility of CASS-IT at different geographical scales. The tract-level analysis highlighted specific tracts within counties of concern that are particularly high priority. In future research, the CASS-IT can be used to analyze United States-wide environmental datasets providing guidance for targeted public health interventions and reducing environmental disparities.

Exposure to coal-burning arsenic leads to an increased risk of cancer, multi-systems damage and chronic diseases, with DNA methylation one potential mechanism of arsenic toxicity. There are few studies on genome-wide methylation in the coal-burning arsenic poisoning population. Illumina 850 K methylation beadchip is the most suitable technology for DNA methylation of epigenome-wide association analysis. This study used 850 K to detect changes in Genome-wide DNA methylation in whole blood samples of 12 patients with coal-burning arsenic poisoning (Arsenic poisoning group) and four healthy control participants (Healthy control group). There is clearly abnormal genome-wide DNA methylation in coal-burning arsenic poisoning, with 647 significantly different methylation positions, 524 different methylation regions and 335 significantly different methylation genes in arsenic poisoning patients compared with healthy controls. Further functional analysis of Gene ontology (GO) and Kyoto encyclopedia of genes (KEGG) found 592 GO items and 131 KEGG pathways between patients of coal-burning arsenic poisoning and healthy control. Then, analysis of gene degree and combined-score identified NAPRT1, NT5C3B, NEDD4L, SLC22A3 and RAB11B as target genes. Further validation by qRT-PCR indicates that mRNA expression of five genes changes significantly in the arsenic poisoning group (n = 72) compared to the healthy control group (n = 72). These results showed the genome-wide methylation pattern and highlighted five critical genes within the coal-burning arsenic poisoning population that involve Nicotinate and nicotinamide metabolism, Choline metabolism in cancer, and Ubiquitin mediated proteolysis. Next, the methylation profile of coal burning arsenic poisoning will be further excavation and the mechanism of coal burning arsenic poisoning will be further explored from five genes related pathways and functions.

The presence of arsenic in natural gas and liquid hydrocarbons is of great concern for oil companies. In addition to health risks due to its toxicity as well as environmental issues, arsenic is responsible for irreversible poisoning of catalysts and clogging of pipes via the accumulation of As-containing precipitates. To address these problems and to better design treatment units, robust methods for the analysis of arsenic and its compounds in oil streams are required. In addition, the use of feedstocks as a novel source of energy is becoming increasingly important. Most biomasses used as feedstocks are contaminated with arsenic. To avoid problems related to the presence of this element, it is therefore also necessary to have reliable methods for the analysis of arsenic and its compounds in these new fluids. This review outlines the sampling techniques, sample preparation methods, and arsenic analysis techniques developed during recent decades and commonly used in the oil industry and in the new feedstock energy domain.

Chronic arsenic poisoning is a global health problem that affects millions of people, and studies have found that long-term ingestion of arsenic-containing compounds can lead to lung damage, but the exact mechanism is unknown. In this study, Sprague-Dawley (SD) rats were used as the research object, and the proteomic analysis method based on sequential window acquisition of all theoretical fragment ions (SWATH) was used to detect the changes in the expression levels of related proteins in the lung tissue of arsenic-exposed rats, and to explore the mechanism of arsenic compound-induced lung injury. The results showed that arsenic exposure resulted in the abnormal expression of collagen type III and proteins involved in metabolic, immune, and cellular processes, leading to the dysfunction of important pathways associated with these proteins, resulting in lung injury. It suggested that the underlying mechanism of arsenic-induced lung injury may be related to oxidative stress, immune injury, cell junction, and collagen type III. This result provides a new research idea for revealing the mechanism of lung injury caused by arsenic exposure.

Facing the increasing demand of atmosphere pollutant control, selective catalytic reduction (SCR) technology has been widely applied in various industries for NOx abatement. However, in the condition of complicated flue gas components, the heavy metal issue is a great challenge to the catalyst deactivation and atmospheric pollution control. In this review, with the comprehensive consideration of SCR catalysts in heavy metal-rich flue gas scenarios, the distribution character of heavy metals in SCR system is firstly summarized, then the detailed interaction mechanism between heavy metals and the vanadium‑titanium-based catalyst is discussed. Focusing on the mercury oxidation as well as against arsenic/lead poisoning, certain modification strategies are also concluded to develop novel SCR catalysts with multiple functions. Furthermore, the state-of-the-art technologies regarding the regeneration, the valuable metal recovery, and the harmless treatment of the spent SCR catalyst are also reported. This paper provides theoretical guidance for the manufacture of novel SCR catalysts under multiple scenarios, as well as the synergistic control of NOx and heavy metals.

We report a novel and as yet undescribed clinical scenario in a young girl with liver failure, in whom, the liver histopathology was suggestive of alcoholic hepatitis in the background of hepatoportal sclerosis and incomplete septal cirrhosis. An extensive clinical and investigational evaluation revealed chronic consumption of multiple Ayurvedic herbal medications for seizure disease. Six months after stopping herbal medicines, the repeat liver biopsy demonstrated resolution of alcohol-related changes but persistence of classical features of non-cirrhotic portal hypertension. Analysis of the retrieved agents, including state of the art chemical and toxicology analysis, using gas chromatography and mass spectroscopy methods demonstrated multiple organic and inorganic toxins associated with acute alcohol and arsenic poisoning related hepatoportal sclerosis/incomplete septal cirrhosis in the young girl.

Cobalt (Co) metal is a gray, ductile, magnetic element with an atomic number of 27 and an atomic weight of 58.9 Da. In the environment, cobalt is a component of naturally occurring minerals and is found in combination with other elements such as copper, nickel, manganese, arsenic, sulfur, and oxygen. Due to its ferromagnetic properties, high melting point (1495.05 C), and high boiling point (2927 C), cobalt is widely used in industry to produce hard metals and superalloys. For example, the alloy Alnico is a blend of iron, aluminum, nickel, and cobalt used for its permanent magnetic properties. A common source of chronic cobalt exposure is in the production of tungsten carbide, which is used for its hardness, heat resistance, and strength.  Historically, cobalt chloride (CoCl2) has been used in medicine as a treatment for anemia due to its ability to promote erythropoiesis. However, due to its adverse effects of thyroid dysfunction and the development of goiters, the use of cobalt in treating anemia has fallen out of favor. A biochemically important cobalt compound is cyanocobalamin (vitamin B12) which contains a Co3+-ion. Vitamin B12 is an essential nutrient naturally found in foods of animal origin, such as dairy, eggs, fish, poultry, and meat. Deficiencies in vitamin B12 may lead to pernicious anemia as well as peripheral neuropathy. The precursor hydroxocobalamin is used as an antidote for cyanide poisoning and may have a role in treating vasoplegic shock. Potential cobalt exposure can occur via oral, respiratory, and dermal routes.