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This book provides an overview to researchers, graduate, and undergraduate students, as well as academicians who are interested in arsenic. It covers human health risks and established cases of human ailments and sheds light on prospective control measures, both biological and physico-chemical. Arsenic (As) is a widely distributed element in the environment having no known useful physiological function in plants or animals. Historically, this metalloid has been known to be used widely as a poison. Effects of arsenic have come to light in the past few decades due to its increasing contamination in several parts of world, with the worst situation being in Bangladesh and West Bengal, India. The worrying issue is the ingestion of arsenic through water and food and associated health risks due to its carcinogenic and neurotoxic nature. The impact of the problem is widespread, and it has led to extensive research on finding both the causes and solutions. These attempts have allowed us to understand the various probable causes of arsenic contamination in the environment, and at the same time, have provided a number of possible solutions. It is reported that more than 200 mineral species contain As. Generally, As binds with iron and sulfur to form arsenopyrite. According to one estimate from the World Health Organization (WHO), contextual levels of As in soil ranges from 1 to 40 mg kg-1. Arsenic toxicity is related to its oxidation state which is present in the medium. As is a protoplastic toxin, due to its consequence on sulphydryl group it interferes in cell enzymes, cell respiration and in mitosis. Exposure of As may occur to humans via several industries, such as refining or smelting of metal ores, microelectronics, wood preservation, battery manufacturing, and also to those who work in power plants that burn arsenic-rich coal.

The toxicity of arsenic has challenged life for billions of years, but the timing of when complex organisms first evolved strategies to cope with this threat remains elusive. Here, we study 2.1-billion-year-old (Ga) Francevillian macrofossils, some of Earth’s earliest complex life forms, to establish their biogenicity and to ascertain how they managed arsenic toxicity. The studied specimens thrived in low-arsenic marine waters, yet displayed strikingly high levels of arsenic, which was actively sequestered in specialized compartments in their bodies to mitigate toxicity. Upon their death, arsenic was released and incorporated into pyrite nuclei. The patterns observed in the fossils are distinct from abiotic concretions but similar to some seen in later eumetazoans, reinforcing their biological affinity. Our findings highlight that early complex life faced significant arsenic stress, even in low-concentration marine environments, which prompted the development of essential survival mechanisms. Arsenic incorporation into pyrite nuclei reveals that the 2.1-billion-year-old Francevillian biota actively detoxified arsenic by sequestration in specialized body compartments.

The World Health Organization estimates that > 140 million people worldwide are exposed to arsenic (As)-contaminated drinking water. As undergoes biologic methylation, which facilitates renal As elimination. In folate-deficient individuals, this process is augmented by folic acid (FA) supplementation, thereby lowering blood As (bAs). Creatinine concentrations in urine are a robust predictor of As methylation patterns. Although the reasons for this are unclear, creatine synthesis is a major consumer of methyl donors, and this synthesis is down-regulated by dietary/supplemental creatine. Our aim was to determine whether 400 or 800 μg FA and/or creatine supplementation lowers bAs in an As-exposed Bangladeshi population. We conducted a clinical trial in which 622 participants were randomized to receive 400 μg FA, 800 μg FA, 3 g creatine, 3 g creatine+400 μg FA, or placebo daily. All participants received an As-removal filter on enrollment, and were followed for 24 weeks. After the 12th week, half of the two FA groups were switched to placebo to evaluate post-treatment bAs patterns. Linear models with repeated measures indicated that the decline in ln(bAs) from baseline in the 800-μg FA group exceeded that of the placebo group (weeks 1-12: β= -0.09, 95% CI: -0.18, -0.01; weeks 13-24: FA continued: β= -0.12, 95% CI: -0.24, -0.00; FA switched to placebo: β= -0.14, 95% CI: -0.26, -0.02). There was no rebound in bAs related to cessation of FA supplementation. Declines in bAs observed in the remaining treatment arms were not significantly different from those of the placebo group. In this mixed folate-deficient/replete study population, 12- and 24-week treatment with 800 μg (but not 400 μg) FA lowered bAs to a greater extent than placebo; this was sustained 12 weeks after FA cessation. In future studies, we will evaluate whether FA and/or creatine altered As methylation profiles.

Background: Diabetes affects an estimated 346 million persons globally, and total deaths from diabetes are projected to increase > 50% in the next decade. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. In 2011, the National Toxicology Program (NTP) organized a workshop to assess the literature for evidence of associations between certain chemicals, including inorganic arsenic, and diabetes and/or obesity to help develop a focused research agenda. This review is derived from discussions at that workshop. Objectives: Our objectives were to assess the consistency, strength/weaknesses, and biological plausibility of findings in the scientific literature regarding arsenic and diabetes and to identify data gaps and areas for future evaluation or research. The extent of the existing literature was insufficient to consider obesity as an outcome. Data Sources, Extraction, and Synthesis: Studies related to arsenic and diabetes or obesity were identified through PubMed and supplemented with relevant studies identified by reviewing the reference lists in the primary literature or review articles. Conclusions: Existing human data provide limited to sufficient support for an association between arsenic and diabetes in populations with relatively high exposure levels (≥ 150 μg arsenic/L in drinking water). The evidence is insufficient to conclude that arsenic is associated with diabetes in lower exposure (< 150 μg arsenic/L drinking water), although recent studies with better measures of outcome and exposure support an association. The animal literature as a whole was inconclusive; however, studies using better measures of diabetes-relevant end points support a link between arsenic and diabetes.

Arsenic (As) pollution is a serious concern worldwide. Recent studies under environmentally relevant conditions revealed that, in the aquatic plant Ceratophyllum demersum, pigments are the first observable target of toxicity, prior to any effect on photosynthetic parameters or to oxidative stress. Lethal toxicity was initiated by a change of As species and their distribution pattern in various tissues. Here, the localization of As was investigated at the subcellular level through X-ray fluorescence using a submicron beam and a Maia detector. Further, it was possible to obtain useful tissue structural information from the ratio of the tomogram of photon flux behind the sample to the tomogram of Compton scattering. The micro-X-ray fluorescence tomograms showed that As predominantly accumulated in the nucleus of the epidermal cells in young mature leaves exposed to sublethal 1 μM As. This suggests that As may exert toxic effects in the nucleus, for example, by interfering with nucleic acid synthesis by replacing phosphorous with As. At higher cellular concentrations, As was mainly stored in the vacuole, particularly in mature leaves. An analysis of precursors of chlorophyll and degradation metabolites revealed that the observed decrease in chlorophyll concentration was associated with hindered biosynthesis, and was not due to degradation. Coproporphyrinogen III could not be detected after exposure to only 0.5 μM As. Levels of subsequent precursors, for example, protoporphyrin IX, Mg-protoporphyrin, Mg-protoporphyrin methyl ester, and divinyl protochlorophyllide, were significantly decreased at this concentration as well, indicating that the pathway was blocked upstream of tetrapyrrole synthesis.

Main conclusion Omics approaches provide comprehensive insights into plant arsenic stress responses, setting the stage for engineering arsenic-tolerant crops. Understanding arsenic (As) toxicity in plants is crucial for environmental and agricultural sustainability, considering the implications of As in impacting soil productivity and environmental health. Although some articles already examined the detailed molecular mechanisms behind As toxicity and tolerance, a comprehensive review of recent omics advancements in studying plant responses to As exposure is needed. The present review highlights the valuable contribution of omics approaches (genomics, transcriptomics, proteomics, and metabolomics) to characterize the intricate response to As overall, which could empower As-tolerant plant development. Genomic techniques, such as QTL mapping, GWAS, RAPD, and SSH, hold the potential to provide valuable insights into the genetic diversity and expression patterns associated with the plant response to As stress, highlighting also the power of new advanced technology such as CRISPR–Cas9. Transcriptomics approaches (e.g., microarrays and RNA sequencing) revealed gene expression patterns in plants under As stress, emphasizing the role of sulfur metabolism in As tolerance. Proteomics, using 2-DE combined with MALDI-ToF MS or ESI–MS/MS, offers insights into the stress-inducible proteins and their involvement in As toxicity mitigation, while iTRAQ-based proteomics enabled an understanding of cultivar-specific responses under high As concentration. Metabolomics, with LC–MS, GC–MS, (U)HPLC, and NMR, elucidated small molecule alterations and complex metabolic activities occurring under As plant exposure. Compendium of data and evidence-related tools offers a foundation for advancing As-tolerant plant development and promoting environmental and agricultural resilience.

The toxic and non-essential metalloid arsenic (As) is ubiquitous in the environment with its absorption from the soil into the plants’ roots posing detrimental effects on the crop plants and hence the food availability and food security are also threatened. The present study was intended to reduce the As-induced toxicity in rice seedlings ( Oryza sativa L.) by phosphate (PO 4 3− ). For this, three concentrations of potassium phosphate (KH 2 PO 4 ), 50, 100 and 150 μM were supplemented along with 50 μM As exposure to hydroponically grown 7-day-old rice seedlings. Supplementation of PO 4 3− significantly recovered arsenic-induced diminutions in growth parameters and photosynthetic pigment contents which were due to the significant increase in superoxide radical (SOR, O 2 • ¯) and hydrogen peroxide (H 2 O 2 ). Supplementation of 50 μM PO 4 3− could significantly increase the activity of APX (ascorbate peroxidase) and GR (glutathione reductase) while 100 μM PO 4 3− could increase the activity of DHAR (dehydroascorbate reductase) and monodehydroascorbate reductase (MDHAR). As the amount of PO 4 3− was increased, the ratio of AsA/DHA (reduced to oxidized ascorbate) and GSH/GSSG (reduced to oxidized glutathione) was increased significantly due to increase in the reduced form of the non-enzymes i.e. AsA and GSH. The activity of SOD (superoxide dismutase) and GPX (guaiacol peroxidase) decreased significantly after a substantive increase in their activities due to As stress while the CAT (catalase) activity further enhanced after the supplementation of 50 and 100 μM PO 4 3− . Thus, the As-induced oxidative stress in the rice seedlings was managed by concerted modulations in the activities of SOD, GPX, CAT and AsA-GSH cycle enzymes and metabolites. Graphical abstract

Climate change impact has disturbed the rainfall pattern worsening the problems of water availability in the aquatic ecosystem of India and other parts of the world. Arsenic pollution, mainly through excessive use of groundwater and other anthropogenic activities, is aggravating in many parts of the world, particularly in South Asia. We evaluated the efficacy of selenium nanoparticles (Se-NPs) and riboflavin (RF) to ameliorate the adverse impacts of elevated temperature and arsenic pollution on growth, anti-oxidative status and immuno-modulation in Pangasianodon hypophthalmus . Se-NPs were synthesized using fish gill employing green synthesis method. Four diets i.e., Se-NPs (0 mg kg −1 ) + RF (0 mg kg −1 ); Se-NPs (0.5 mg kg −1 ) + RF (5 mg kg −1 ); Se-NPs (0.5 mg kg −1 ) + RF (10 mg kg −1 ); and Se-NPs (0.5 mg kg −1 ) + RF (15 mg kg −1 ) were given in triplicate in a completely randomized block design. The fish were treated in arsenic (1/10th of LC 50 , 2.68 mg L −1 ) and high temperature (34 °C). Supplementation of the Se-NPs and RF in the diets significantly (p < 0.01) enhanced growth performance (weight gain, feed efficiency ratio, protein efficiency ratio, and specific growth rate), anti-oxidative status and immunity of the fish. Nitroblue tetrazolium (NBT), total immunoglobulin, myeloperoxidase and globulin enhanced (p < 0.01) with supplementation (Se-NPs + RF) whereas, albumin and albumin globulin (A:G) ratio (p < 0.01) reduced. Stress biomarkers such as lipid peroxidation in the liver, gill and kidney, blood glucose, heat shock protein 70 in gill and liver as well as serum cortisol reduced (p < 0.01) with supplementation of Se-NPs and RF, whereas, acetylcholine esterase and vitamin C level in both brain and muscle significantly enhanced (p < 0.01) in compared to control and stressors group (As + T) fed with control diet. The fish were treated with pathogenic bacteria after 90 days of experimental trial to observe cumulative mortality and relative survival for a week. The arsenic concentration in experimental water and bioaccumulation in fish tissues was also determined, which indicated that supplementation of Se-NPs and RF significantly reduced (p < 0.01) bioaccumulation. The study concluded that a combination of Se-NPs and RF has the potential to mitigate the stresses of high temperature and As pollution in P. hypophthalmus .

Arsenic exposure has been linked to poor pulmonary function, and inefficient arsenic metabolizers may be at increased risk. Dietary rice has recently been identified as a possible substantial route of exposure to arsenic, and it remains unknown whether it can provide a sufficient level of exposure to affect pulmonary function in inefficient metabolizers. Within 12,609 participants of HCHS/SOL, asthma diagnoses and spirometry-based measures of pulmonary function were assessed, and rice consumption was inferred from grain intake via a food frequency questionnaire. After stratifying by smoking history, the relationship between arsenic metabolism efficiency [percentages of inorganic arsenic (%iAs), monomethylarsenate (%MMA), and dimethylarsinate (%DMA) species in urine] and the measures of pulmonary function were estimated in a two-sample Mendelian randomization approach (genotype information from an Illumina HumanOmni2.5-8v1-1 array), focusing on participants with high inferred rice consumption. Among never-smoking high inferred consumers of rice (n = 1395), inefficient metabolism was associated with past asthma diagnosis and forced vital capacity below the lower limit of normal (LLN) (OR 1.40, p = 0.0212 and OR 1.42, p = 0.0072, respectively, for each percentage-point increase in %iAs; OR 1.26, p = 0.0240 and OR 1.24, p = 0.0193 for %MMA; OR 0.87, p = 0.0209 and OR 0.87, p = 0.0123 for the marker of efficient metabolism, %DMA). Among ever-smoking high inferred consumers of rice (n = 1127), inefficient metabolism was associated with peak expiratory flow below LLN (OR 1.54, p = 0.0108/percentage-point increase in %iAs, OR 1.37, p = 0.0097 for %MMA, and OR 0.83, p = 0.0093 for %DMA). Less efficient arsenic metabolism was associated with indicators of pulmonary dysfunction among those with high inferred rice consumption, suggesting that reductions in dietary arsenic could improve respiratory health.

Background: Arsenic (As) occurs as monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) in humans, and the methylation pattern demonstrates large interindividual differences. The fraction of urinary MMA is a marker for susceptibility to As-related diseases. Objectives: We evaluated the impact of polymorphisms in five methyltransferase genes on As metabolism in two populations, one in South America and one in Southeast Asia. The methyltransferase genes were arsenic(+ III oxidation state) methyltransferase (AS3MT), DNA-methyltransferase 1a and 3b (DNMTla and DNMT3b, respectively), phosphatidylethanolamine N-methyltransferase and betaine-homocysteine methyltransferase (BHMT). AS3MT expression was analyzed in peripheral blood. Methods: Subjects were women exposed to As in drinking water in the Argentinean Andes [n = 172; median total urinary As (U-As), 200 fig/L] and in rural Bangladesh [n = 361; U-As, 100 ug/L; all in early pregnancy). Urinary As metabolites were measured by high-pressure liquid chromatography/inductively coupled plasma mass spectrometry. Polymorphisms (n = 22) were genotyped with Sequenom, and AS3MT expression was measured by quantitative real-time polymerase chain reaction using TaqMan expression assays. Results: Six AS3MT polymorphisms were significantly associated with As metabolite patterns in both populations (p > < 0.01). The most frequent AS3MT haplotype in Bangladesh was associated with a higher percentage of MMA (% MMA), and the most frequent haplotype in Argentina was associated with a lower % MMA and a higher percentage of DMA. Four polymorphisms in the DNMT genes were associated with metabolite patterns in Bangladesh. Noncoding AS3MT polymorphisms affected gene expression of AS3MT in peripheral blood, demonstrating that one functional impact of AS3MT polymorphisms may be altered levels of gene expression. Conclusions: Polymorphisms in AS3MT significantly predicted As metabolism across these two very different populations, suggesting that AS3MT may have an impact on As metabolite patterns in populations worldwide.