Arsenic Toxicity Research Articles

Metabolomics reveals the metabolic disturbance caused by arsenic in the mouse model of inflammatory bowel disease

Arsenic exposure has long been a significant global health concern due to its association with various human diseases. The adverse health effects of arsenic can be influenced by multiple factors, resulting in considerable individual variability. Individuals with inflammatory bowel disease (IBD) are particularly vulnerable to the effects of toxin exposure, yet the specific impact of arsenic in the context of IBD remains unclear. In this study, we employed a non-targeted metabolomics approach to investigate how arsenic exposure affects metabolic homeostasis in an IBD model using Helicobacter trogontum-infected interleukin-10 deficient mice. Our results demonstrated that arsenic exposure disrupted the balance of various metabolites, including tryptophan, polyunsaturated fatty acids, purine and pyrimidine metabolites, and branched-chain amino acids, in mice with colitis but not in those without colitis. Notably, several crucial metabolites involved in anti-inflammatory responses, oxidative stress, and energy metabolism were significantly altered in mice with colitis. These results indicate that arsenic exposure in an IBD context can lead to extensive metabolic disturbances, potentially exacerbating disease severity and impacting overall health. This study underscores the necessity of evaluating arsenic toxicity in relation to IBD to better understand and mitigate associated health risks.

Neuroprotective Effects of Morin Against Cadmium- and Arsenic-Induced Cell Damage in PC12 Neurons.

Arsenic and cadmium, both toxic metals and widespread environmental pollutants, can trigger apoptosis and oxidative stress in various tissues and cells. Morin, a natural flavonoid with diverse biological properties, has been found to protect neurons from oxidative stress and apoptosis-induced damage. This research aimed to examine the protective properties of morin against neurotoxicity caused by arsenic and cadmium, utilizing PC12 cells as a model for nerve cells. The cells were pre-treated with different concentrations of morin and then exposed to arsenic and cadmium, after which cell viability and reactive oxygen species (ROS) production were assessed. Additionally, western blotting was performed to evaluate the protein levels of the Bax/Bcl-2 ratio and cleaved-caspase-3. Following exposure to arsenic and cadmium, there were significant increases in ROS, Bax/Bcl-2 ratio, and cleaved-caspase-3. However, the results of the study demonstrated the beneficial effects of morin at various concentrations, as it increased cell viability and decreased ROS production. Furthermore, morin at a concentration of 10 µM was found to reduce the elevated levels of cleaved-caspase-3 induced by arsenic and diminish the increased Bax/Bcl-2 ratio after exposure to arsenic and cadmium. The findings of this study suggest that morin can effectively protect cells from arsenic and cadmium-induced neurotoxicity through its antioxidant and anti-apoptotic effects. Thus, morin should be considered a promising agent for treating arsenic and cadmium toxicity.

Turmeric as a therapeutic agent against arsenic-induced metabolic dysregulation in rat models

Ethnopharmacological relevanceHealth hazards stemming from metalloid consumption, such as arsenic, pose a global concern. This study aimed to assess the protective effects of turmeric against arsenic-induced alterations in lipid profiles and energy metabolism in rats. MethodsThirty male rats were divided into three groups over a 90–180-day exposure period: Group 1 (Control) received standard rat chow; Group 2 received an arsenic diet; and Group 3 received arsenic plus turmeric supplemented diet. Blood and liver tissue samples were collected for lipid profiles, glucose levels, energy metabolism parameters, and PPAR-α mRNA expression using qRT-PCR. Statistical analysis was performed (p<0.05). ResultsResults indicated significant (p<0.05) increases in lipid profiles among arsenic-exposed rats after 180 days, elevating the risk of coronary artery diseases. Both arsenic and turmeric-exposed groups showed heightened total cholesterol (TC), triglycerides (TG), and low-density lipoprotein (LDL) levels at 90 and 180 days, with nuanced differences suggesting dyslipidemia and atherosclerosis. Blood glucose observations revealed hypoglycemia initially in arsenic-exposed rats, progressing to hyperglycemia by 180 days. Arsenic significantly (p<0.05) inhibited pyruvate kinase, hexokinase, and isocitrate dehydrogenase activities in the liver after 180 days, while turmeric exposure showed no significant (p<0.05) changes. Additionally, both arsenic and turmeric groups exhibited downregulation of PPAR-α expression at 180 days. In-silico analysis identified curcumin as a promising component for anti-atherosclerosis and arsenic-related conditions due to its strong binding affinities and multiple hydrogen bond formations. ConclusionIn conclusion, long-term turmeric consumption may mitigate arsenic-induced oxidative damage associated with early hyperglycemia, diabetes mellitus, cardiovascular diseases, and atherosclerosis. These findings underscore turmeric’s potential therapeutic role against arsenic toxicity, suggesting avenues for future research and public health interventions.

Synergistic effect between biochar and nitrate fertilizer facilitated arsenic immobilization in an anaerobic contaminated paddy soil

Nitrate nitrogen fertilizer was usually used to mitigate arsenic (As) release and mobilization in the anaerobic contaminated paddy soil. However, the effect of the interplay between nitrate fertilizer and biochar on As availability as well as the involved mechanism were poorly understood. Herein, the effects and mechanisms of biochar, nitrate fertilizer, and biochar-based nitrate fertilizer on the availability of As in the contaminated paddy soil were investigated via a microcosm incubation experiment. Results indicated that the application of biochar-based nitrate fertilizer significantly lessened the available As concentration in the contaminated paddy soil from 3.01 ± 0.03 (control group) to 2.24 ± 0.08 mg kg−1, which presented an immobilization efficiency of 26.6 % better than those of individual biochar (13.5 %) and nitrate fertilizer (17.6 %), exhibiting a synergistic effect. Moreover, the biochar-based nitrate fertilizer also facilitated the transformation of more toxic arsenite in the contaminated soil to less toxic arsenate. Further, biochar-based nitrate fertilizer increased soil redox potential (Eh), dissolved organic carbon, organic matter, and nitrate yet decreased soil pH and ammonium, which changed the microbial community in the soil, enhancing the relative abundance of Bacillus, Arthrobacter, and Paenibacillus. These functional microorganisms drove the coupled transformation between nitrate denitrification and Fe(II) or As(III) oxidation, favoring As immobilization in the anaerobic paddy soil. Additionally, the co-application of biochar offset the negative effect of single nitrate fertilizer on microbial community diversity. Overall, biochar-based nitrate fertilizer could be a promising candidate for the effective immobilization of As in the anaerobic paddy soil. The current research can provide a valuable reference to the remediation of As-contaminated paddy soil and the production of safe rice.

The roles of nanoparticle-enriched biochars in improving soil enzyme activities and nutrient uptake by basil plants under arsenic toxicity

Enriched biochar with improved properties and functionality can play a significant role in providing sustainable solutions for mitigating heavy metal contamination in soil. In this experiment, the effects of solid and enriched biochars (potassium-enriched biochar (BC-K), magnesium-enriched biochar (BC-Mg), both individually and combined) were examined on soil microbial and enzyme activities, as well as nutrient uptake by basil plants cultivated in a soil with three levels of arsenic (nontoxic, 50 mg As kg−1 soil, and 100 mg As kg−1 soil). Biochar-related treatments, increased soil organic matter (65–76%), while decreased availability of arsenic (6–55%) in the soil. The microbial biomass carbon (by about 123%) and soil basal respiration (by about 256%), and soil enzymatic activities (β-glucosidase, urease, alkaline phosphatase, and dehydrogenase) were enhanced by enriched biochars under arsenic toxicity. The solid and particularly enriched biochars decreased arsenic content and improved nitrogen and phosphorus contents of roots and shoots, root length, root activity, and root and shoot biomass in basil plants. Therefore, it is conceivable to suggest that enriched biochars are superior treatments for improving nutrient absorption rates and basil growth under arsenic toxicity through decreasing arsenic mobility and increasing soil microbial activities.

Active Role of Lactoferrin on Arsenic and Imidacloprid Toxicity in Broiler Chicks

Abstract This work aimed to evaluate the lactoferrin (LF) effect on arsenic (As) and imidacloprid (IMI) toxicity in broiler chicks. One-week old broiler chicks (n=105) were divided into seven groups (x15 each). The animals were orally supplemented with As, IMI, and/or LF for 4 weeks as follows: Control (G1) no supplements, G2 supplemented with As, G3 supplemented with IMI, G4 supplemented with As+IMI, G5 supplemented with As+LF, G6 supplemented with IMI+LF, G7 supplemented with As+IMI+LF. Body weight and weight gain were recorded on weekly interval. Blood, serum, liver, kidney, and muscle samples were collected at the end of the experimental period for biochemical and histopathological examination. Body weight performance, hematological, serum, and liver tissue biochemical analysis revealed adverse changes in G2, G3, and G4 compared to control, G5, G6, and G7. There was higher tissue residue of As and IMI in G4 and G5 compared to G5, G6, and G7. Liver histopathological changes in the groups supplemented with As and/or IMI were observed with necrosis, congestion, and inflammatory cell aggregates. The use of LF in broiler chicks improves weight gain performance and modulates the adverse effects of As and/or IMI toxicity.

Molecular and cell phenotype programs in oral epithelial cells directed by co-exposure to arsenic and smokeless tobacco.

Chronic arsenic exposure can lead to various health issues, including cancer. Concerns have been mounting about the enhancement of arsenic toxicity through co-exposure to various prevalent lifestyle habits. Smokeless tobacco products are commonly consumed in South Asian countries, where their use frequently co-occurs with exposure to arsenic from contaminated groundwater. To decipher the in vitro molecular and cellular responses to arsenic and/or smokeless tobacco, we performed temporal multi-omics analysis of the transcriptome and DNA methylome remodelling in exposed hTERT-immortalized human normal oral keratinocytes (NOK), as well as arsenic and/or smokeless tobacco genotoxicity and mutagenicity investigations in NOK cells and in human p53 knock-in murine embryonic fibroblasts (Hupki MEF). RNAseq results from acute exposures to arsenic alone and in combination with smokeless tobacco extract revealed upregulation of genes with roles in cell cycle changes, apoptosis and inflammation responses. This was in keeping with global DNA hypomethylation affecting genes involved in the same processes in response to chronic treatment in NOK cells. At the phenotypic level, we observed a dose-dependent decrease in NOK cell viability, induction of DNA damage, cell cycle changes and increased apoptosis, with the most pronounced effects observed under arsenic and SLT co-exposure conditions. Live-cell imaging experiments indicated that the DNA damage likely resulted from induction of apoptosis, an observation validated by a lack of exome-wide mutagenesis in response to chronic exposure to arsenic and/or smokeless tobacco. In sum, our integrative omics study provides novel insights into the acute and chronic responses to arsenic and smokeless tobacco (co-)exposure, with both types of responses converging on several key mechanisms associated with cancer hallmark processes. The generated rich catalogue of molecular programs in oral cells regulated by arsenic and smokeless tobacco (co-)exposure may provide bases for future development of biomarkers for use in molecular epidemiology studies of exposed populations at risk of developing oral cancer.

Arsenic and Chromium Induced Toxicity on Zebrafish Kidney: Mixture Effects on Oxidative Stress and Involvement of Nrf2-Keap1-ARE, DNA Repair, and Intrinsic Apoptotic Pathways.

In polluted water, cooccurrences of two carcinogens, arsenic (As) and chromium (Cr), are extensively reported. Individual effects of these heavy metals have been reported in kidney of fishes, but underlying molecular mechanisms are not well established. There is no report on combined exposure of As and Cr in kidney. Thus, the present study investigated and compared individual and combined effects of As and Cr on zebrafish (Danio rerio) kidney treating at their environmentally relevant concentrations for 15, 30, and 60 days. Increased ROS levels, lipid peroxidation, GSH level, and decreased catalase activity implied oxidative stress in treated zebrafish kidney. Damage in histoarchitecture in treated groups was also noticed. The current study involved gene expression study of Nrf2, an important transcription factor of cellular stress responses along with its negative regulator Keap1 and downstream antioxidant genes nqo1 and ho1. Results indicated activation of Nrf2-Keap1 pathway after combined exposure. Expression pattern of ogg1, apex1, polb, and creb1 revealed the inhibition of base excision repair pathway in treatments. mRNA expression of tumor suppressor genes p53 and brca2 was also altered. Expressional alteration in bax, bcl2, caspase9, and caspase 3 indicated apoptosis (intrinsic pathway) induction, which was maximum in combined group. Inhibition of DNA repair and induction of apoptosis indicated that the activated antioxidant system was not enough to overcome the damage caused by As and Cr. Overall, this study revealed additive effects of As and Cr in zebrafish kidney after chronic exposure focusing cellular antioxidant and DNA damage responses.

WRKY Transcription Factors in Response to Metal Stress in Plants: A Review.

Heavy metals in soil can inflict direct damage on plants growing within it, adversely affecting their growth height, root development, leaf area, and other physiological traits. To counteract the toxic impacts of heavy metals on plant growth and development, plants mitigate heavy metal stress through mechanisms such as metal chelation, vacuolar compartmentalization, regulation of transporters, and enhancement of antioxidant functions. WRKY transcription factors (TFs) play a crucial role in plant growth and development as well as in responses to both biotic and abiotic stresses; notably, heavy metal stress is classified as an abiotic stressor. An increasing number of studies have highlighted the significant role of WRKY proteins in regulating heavy metal stress across various levels. Upon the entry of heavy metal ions into plant root cells, the production of reactive oxygen species (ROS) is triggered, leading to the phosphorylation and activation of WRKY TFs through MAPK cascade signaling. Activated WRKY TFs then modulate various physiological processes by upregulating or downregulating the expression of downstream genes to confer heavy metal tolerance to plants. This review provides an overview of the research advancements regarding WRKY TFs in regulating heavy metal ion stress-including cadmium (Cd), arsenic (As), copper (Cu)-and aluminum (Al) toxicity.

Magical role of iron nanoparticles for enhancement of thermal efficiency and gene regulation of fish in response to multiple stresses

The present study addresses the challenges of uncontrolled temperature and pollution in aquatic environments, with a focus on fish ability to tolerate high temperature. The investigation aimed to determine the role of iron nanoparticles (Fe-NPs) in enhancing the thermal tolerance of Pangasianodon hypophthalmus exposed to high-temperature stress, arsenic (As), and ammonia (NH3) toxicity. Fe-NPs were synthesized using green approaches, specifically from fish gill. The dietary Fe-NPs were formulated and supplemented at 10, 15, and 20 mg kg⁻1 of feed. Notably, Fe-NPs at 15 mg kg⁻1 diet significantly reduced the critical thermal minimum (CTmin) (14.44 ± 0.21 °C) and the lethal thermal minimum (LTmin) (13.46 ± 0.15 °C), compared to the control and other treatment groups. Conversely, when Fe-NPs at 15 mg kg⁻1 were supplemented with or without exposure to stressors (As + NH3+T), the critical thermal maximum (CTmax) increased to 47.59 ± 0.16 °C, and the lethal thermal maximum (LTmax) increased to 48.60 ± 0.37 °C, both significantly higher than the control and other groups. A strong correlation was observed between LTmin and CTmin (R2 = 0.90) and between CTmax and LTmax (R2 = 0.98). Furthermore, dietary Fe-NPs at 15 mg kg⁻1 significantly upregulated the expression of stress-related genes, including HSP70, iNOS, Caspase-3a, CYP450, MT, cat, sod, gpx, TNFα, IL, TLR, and Ig. The enhanced thermal tolerance (LTmin and LTmax) can be attributed to these gene regulations, suggesting the mechanistic involvement of Fe-NPs in improving thermal resilience. Overall, the findings demonstrate that dietary supplementation with Fe-NPs, particularly at 15 mg kg⁻1, improves thermal tolerance and stress response in P. hypophthalmus by enhancing gene expression and overall thermal efficiency under stressor conditions.

Arsenic and young liver: a case report of hepatic steatosis due to arsenic toxicity.

Arsenic toxicity is rare in developed countries. It may be difficult to diagnose due to its heterogenous symptom presentation. We present a case of severe hepatic steatosis and cholestatic hepatitis associated with arsenic toxicity in an adult.

Screening of Arsenic toxicity in Oryza sativa L. (rice) and assessment of variation in growth, ROS, and antioxidant responses in tolerant and sensitive rice cultivars

ABSTRACT Arsenic (As) in rice plants has toxic effects on their quality and human health. In the present study, 100 rice cultivars have been screened in hydroponics to analyze As toxicity and select As-tolerant and sensitive rice cultivars. The findings showed that rice cultivars responded differently to As stress at varying levels of effect. As treatments significantly changed morphological traits, the arsenic tolerance index (ATI %), pigments, and H2O2 concentrations. The rice cultivars Luit and Swarna demonstrated remarkable results (tolerant and sensitive) in terms of growth, as well as in terms of ATI, chlorophyll content, H2O2 content, and enzymatic and non-enzymatic antioxidants. Arsenic-induced pigment degradation and antioxidant content reduction were greater in Swarna than in Luit. Moreover, the results of biochemical analysis correlated with the morphological parameters. The selected As-tolerant and sensitive cultivars may be used to explore the tolerance mechanism in greater depth, which will require further molecular investigations.

Unravelling the mechanism of arsenic resistance and bioremediation in Stenotrophomonas maltophilia: A molecular approach

The mechanism of arsenic resistance in bacteria is under studied and still lacks a clear understanding despite of wide research work. The advanced technologies can help in analysing the arsenic bioremediating bacteria at a molecular level. With this line of idea, highly efficient arsenic bioremediating S. maltophilia was subjected to extensive analysis to understand the mechanism of arsenic resistance and bioremediation. The cell surface analysis revealed that S. maltophilia induces only slight changes in cell surface in the presence of arsenic. Whereas, TEM analysis has indicated the bioaccumulation of arsenic in S. maltophilia. Also, arsenic was found to generate ROS in a concentration dependant manner, and in response, S. maltophilia activated SOD, catalase, thioredoxin reductase etc. to manage oxidative stress which is very much crucial in managing arsenic toxicity. S. maltophilia was found to possess genes such as arsC, aoxB, aoxC and aioA. These genes are involved in arsenic reduction and oxidation. Transcriptomics and proteomics analysis have shown that S. maltophilia detoxifies arsenic by upregulating ars operon, arsH, BetB etc. which are responsible for arsenic reduction, efflux methylation, oxidation etc. A detailed molecular mechanism of arsenic bioremediation in S. maltophilia was put forth.

Efficacy of two different forms of selenium towards reduction of arsenic toxicity and accumulation in Cicer arietinum L.

Arsenic migration from soil to crop plants and subsequently human consumption of contaminated foodstuffs is a serious threat for society. In the present study, two oxidation states of selenium [Se(0) and Se(VI)] were used to check their efficacy towards amelioration of arsenic toxicity in chickpeas (Cicer arietinum L.). Three different concentrations (1, 5, and 10 mg/L) of both oxidation states of selenium were applied separately and in combination against a fixed dose (10 mg/L) of arsenic [(As(V)] treatment on chickpea seedlings. Further, seed germination and seedling growth attributes, oxidative stress, and antioxidant defense under different treatments were analyzed. The changes in anatomical structures and arsenic accumulation in different parts of seedlings were also studied. Results revealed that increased generation of oxidative stress affected physiobiochemical parameters of seedlings and diminished plant growth and deformation in vascular bundles under arsenic stress. However, the combined application of Se with As showed overall improvement in seedling growth, reduced oxidative stress, and organized vascular bundles of chickpea seedlings as compared to arsenic stress alone. The arsenic uptake and accumulation in chickpea seedlings were also reduced upon supplementation of Se. The highest reduction of arsenic accumulation by 42 and 56 % in roots, while 47 and 58 % in shoots were recorded by the application of 10 mg/L of Se(0) and Se (VI) under As stress, respectively. Overall, Se(VI) showed much better performance towards the minimization of arsenic-induced phytotoxicity and arsenic accumulation as compared to Se(0). Therefore, this study explored the efficacy of different forms of selenium towards the mitigation of arsenic toxicity in plants.

Rhizophagus intraradices mediated mitigation of arsenic toxicity in wheat involves differential distribution of arsenic in subcellular fractions and modulated expression of Phts and ABCCs

Biomagnification of arsenic in food chain through wheat consumption poses a serious threat to human health. Therefore, it is necessary to elucidate mechanism of arsenic tolerance and detoxification in wheat. The study aimed to unravel the strategies adopted by arbuscular mycorrhizal fungi to alleviate arsenic toxicity in wheat. To accomplish this, independent and interactive effects of arsenic and Rhizophagus intraradices were assessed. Colonization by R. intraradices resulted in lower expression of high-affinity phosphate transporters (Phts) in comparison with non-mycorrhizal (NM) plants, thereby lowering arsenic concentrations in mycorrhizal (M) plants. Additionally, the subcellular fractionation analysis indicated differential distribution of arsenic. In NM plants, arsenic accumulated primarily in cell wall and organelle fractions. Conversely, in M plants arsenic was more concentrated in the cell wall and vacuolar fractions. This was related to higher levels of hydroxyl and aldehyde groups in cell wall fraction of root along with increased expression of C-type ATP-binding cassette transporters in root and leaves. These factors enabled effective sequestration of arsenic in the cell wall and vacuoles of M plants, thereby reducing its toxicity. Furthermore, the proportion of inorganic arsenic was lower in M plant, as it transformed it into less toxic organic forms.

Unveiling the link between arsenic toxicity and diabetes: an in silico exploration into the role of transcription factors.

The online version contains supplementary material available at 10.1007/s43188-024-00255-y.

Selenium Improves Arsenic-Induced Male Reproductive Dysfunction by Regulating H3K14ac Level.

Arsenic exposure has been known to be associated with male reproduction injury. Exploring the antidote of arsenic and ascertaining proper dose of antidote are important for detoxifying the male reproductive toxicity of arsenic. Selenium, which is essential for the male reproduction and spermatogenesis, can alleviate the toxicity of many environmental toxins, such as metals, and fluoride (F). Selenium relieves arsenic-induced reductions in spermatogenesis index and testicular function marker enzymes via promoting the antioxidative ability of rats. Our previous study has found that arsenic can induce male reproductive toxicity by affecting the level of H3K14ac in the testis, so we further investigate whether selenium can antagonize arsenic-induced male reproductive toxicity through the H3K14ac pathway and ascertain the appropriate dose of selenium. The results show that selenium intervention reduces the accumulation of arsenic in rat testis probably attributing to promote the excretion of arsenic from rat, then improves the testis injury induced by arsenic. Selenium intervention enhances sperm quality, testosterone level, and expression of steroidogenic genes by regulating H3K14ac level and expression of its associated enzymes (KAT2A, BAZ2A, and HDAC6), and thus alleviates the male reproductive toxicity of arsenic, and the proper dose of Se for mitigating arsenic male reproductive toxicity is 1mg/kg.

Trivalent arsenicals induce skin toxicity through thiol depletion

Arsenic, a widespread environmental contaminant, is highly toxic to human health. Arsenic exposure is associated with the occurrence of skin lesions and diseases. This study investigated the dermal toxicity of trivalent arsenicals (AsIII and MMAIII) and its underlying mechanism using human keratinocyte cell line and ex vivo porcine skin. AsIII and MMAIII induced concentration-dependent cell apoptosis and necrosis in HaCaT cells, which was confirmed in ex vivo porcine skin. AsIII and MMAIII increased reactive oxygen species generation and GSH depletion. Interestingly, radical scavenger antioxidants such as Vitamin C failed to mitigate arsenic-induced cytotoxicity, while thiol-containing compounds effectively alleviated it, suggesting a key role of thiol depletion in the trivalent arsenical-induced dermal toxicity. DMSA showed the strongest protective effects against AsIII and MMAIII-induced cytotoxicity in HaCaT cells. Of note, DMSA restored arsenical-induced tissue damage, and reduced the apoptosis in ex vivo porcine skin, highlighting its potential use to alleviate arsenic-induced skin lesions and diseases.

Arsenic exposure is associated with elevated sweat chloride concentration and airflow obstruction among adults in Bangladesh: a cross sectional study.

Arsenic is associated with lung disease and experimental models suggest that arsenic-induced degradation of the chloride channel CFTR (cystic fibrosis transmembrane conductance regulator) is a mechanism of arsenic toxicity. We examined associations between arsenic exposure, sweat chloride concentration (measure of CFTR function), and pulmonary function among 285 adults in Bangladesh. Participants with sweat chloride ≥ 60 mmol/L had higher arsenic exposures than those with sweat chloride < 60 mmol/L (water: median 77.5 µg/L versus 34.0 µg/L, p = 0.025; toenails: median 4.8 µg/g versus 3.7 µg/g, p = 0.024). In linear regression models, a one-unit µg/g increment in toenail arsenic was associated with a 0.59 mmol/L higher sweat chloride concentration, p < 0.001. We found that toenail arsenic concentration was associated with increased odds of airway obstruction (OR: 1.97, 95%: 1.06, 3.67, p = 0.03); however, sweat chloride concentration did not mediate this association. Our findings suggest that sweat chloride concentration may be a novel biomarker for arsenic exposure and also that arsenic likely acts on the lung through mechanisms other than CFTR dysfunction.

The combined toxicity of polystyrene microplastic and arsenate: From the view of biochemical process in wheat seedlings (Triticum aestivum L.)

Microplastics (MPs) are important carriers of various toxic metals and can alter their toxicity pattern in agricultural soil, leading to combined pollution, therefore posing new challenges to soil pollution management and environmental risk assessment. In this study, we observed the internalization of MPs in plants and conducted incubation experiments to evaluated the effects of arsenate (As(V)) alone and in combination with polystyrene (PS) MPs on wheat seedlings (Triticum aestivum L.). Under As(V) alone and combined with PS-MP exposure, dose-dependent toxicity in terms of root and stem elongation and biomass accumulation was observed. Compared with As(V) alone, the presence of PS-MPs reduced the accumulation of As in wheat roots by 11.43–58.91%, but PS-MPs intensified the transport of As to the aboveground parts of wheat, increasing As accumulation in wheat stems by 27.77–1011.54%. This causes more serious mechanical damage and oxidative stress to plant cells, increasing the accumulation of reactive oxygen species and lipid peroxidation in wheat roots and upregulating the activities of antioxidant enzymes such as superoxide dismutase (SOD) and peroxidase (POD). In addition, the co-exposure of As(V) and PS-MPs disrupts the photosynthetic system of wheat leaves and the secretion activities of roots. Therefore, the combination of As(V) and PS-MPs caused greater damage to wheat growth. Our findings contribute to a more comprehensive assessment of the combined toxicity of MPs and heavy metal to crops.