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At least 19 recordsLinked to original sources
PubMed1977

Ultrastructural and biochemical effects of prolonged oral arsenic exposure on liver mitochondria of rats.

This investigation was undertaken to further delineate the subcellular manifestations of arsenic toxicity following chronic exposure using combined ultrastructural and biochemical techniques. Male rats were given access to deionized drinking water solutions containing 0, 20, 40, or 85 arsenic as arsenate (As(+5)) for 6 weeks. In situ swelling of liver mitochondria was the most prominent ultrastructural change observed. Mitochondrial respiration studies indicated decreased state 3 respiration and respiratory control ratios (RCR) for pyruvate/malate but not succinate mediated respiration. Specific activity of monoamine oxidase which is localized on the outer mitochondrial membrane showed increases of up to 150% of control and cytochrome-C oxidase which is localized on the inner mitochondrial membrane showed increases in specific activity of 150-200%. Activity of malate dehydrogenase which is localized in the mitochondrial matrix was unchanged at any dose level. These studies indicate that decreased mitochondrial respiration is only one aspect of arsenic toxicity to this organelle. Marked arsenic-mediated perturbation of important enzyme systems localized in mitochondria which participate in the control of respiration and other normal mitochondrial functions are also important manifestations of cellular dysfunction.

Administration, Oral↗
PubMed1975

[Chronic arsenic water pollution in the Republic of Argentina].

Arsenical pollution of water supplies is a chronic problem of great medical, social and sanitary importance in Argentina. The well-known cutaneous manifestations of chronic arsenical toxicity, palmar and plantar keratoses, melanoderma and multiple epitheliomas are described. The interest which this disease has evoked in the last few years is emphasized when new arsenical areas are discovered with clinical cases of chronic arsenical intoxication. Furthermore it is shown that the high content of arsenic in drinking water may be the determining factor in the incidence of visceral neoplasms. Contrary to classic beliefs, the chronic toxic effects from arsenic may be present in young children but the palmar and plantar keratoses may be absent. The histochemical localization of the arsenic in the skin and its relation to thyroid function and the production of leukoplakia and laryngeal cancer are noted. When one analyses all the recent reports it is evident that patients with chronic arsenical intoxication must now be thoroughly studied bearing in mind the multiple localization of this carcinogenic agent.

Argentina↗
PubMed2026

ARR1 and ARR12 negatively regulate arsenic stress tolerance by controlling flavonoid metabolism in Arabidopsis.

ARR1/12-mediated cytokinin signaling negatively regulates the accumulation of glycosylated flavonoids, thereby increasing plant susceptibility to As(III) stress. Cytokinins negatively regulate arsenic stress tolerance in plants through cytokinin-signaling type-B Arabidopsis response regulators (B-ARRs), specifically ARR1 and ARR12. However, the mechanism by which cytokinin signaling regulates plant metabolite dynamics, particularly antioxidant flavonoids, in response to arsenic toxicity remains largely unknown. Here, we hypothesized that ARR1/12-mediated cytokinin signaling modulates flavonoid metabolism to regulate arsenite [As(III)] tolerance. By comparing the global metabolic changes in roots of the arr1 12 double mutant (rD) and wild-type (WT) plants, we found that As(III) stress globally reduced metabolite abundance in WT roots. Importantly, the rD mutant accumulated significantly more flavonoids, most in glycosylated forms, than WT under As(III) exposure, which was supported by the specific upregulation of UDP-glycosyltransferase genes involved in flavonoid glycosylation. Accordingly, exogenous application of the glycosylated quercitrin-enhanced As(III) tolerance in WT roots, strengthening that the increase of glycosylated flavonoids in rD roots was beneficial for plant survival under As(III) exposure. Our data collectively strongly support that the increased glycosylation of flavonoids in the rD mutant improves their antioxidant functionality, thereby enhancing the As(III) stress tolerance. This study provides a new insight into the negative role of cytokinin signaling in repressing glycosylated flavonoid accumulation, causing increased susceptibility of plants to As(III) stress. Manipulation of cytokinin signaling or flavonoid glycosylation is, therefore, a promising approach for heavy metal stress mitigation in crops.

Arabidopsis↗
PubMed1979

Arsenic-induced bone marrow toxicity: ultrastructural and electron-probe analysis.

A patient with severe arsenic poisoning that resulted in marked peripheral blood and bone marrow abnormalities, including megaloblastic erythropoiesis experienced many of the previously reported hematologic complications of arsenic poisoning: leukopenia, granulocytopenia, absolute eosinophilia, and profound anemia. In this study we report an ultrastructural and electron-probe analysis of the bone marrow. Although megaloblastic anemia associated with arsenic poisoning has been described rarely, the presence of arsenic in the local bone marrow milieu has not been demonstrated previously. The ultrastructural features of arsenic-induced bone marrow toxicity are similar to those described in other dyserythropoietic states and include marked nuclear aberrations involving shape, chromatin distribution, and nuclear envelope. Using the technique of energy-dispersive x-ray analysis (electron probe) we demonstrated arsenic in bone marrow spicules; this supports the contention that arsenic can cause megaloblastic anemia. We suggest that this technique may be a useful tool in further studies that attempt to explore the mechanism of arsenic-induced hematologic toxicity. Finally, we suggest that arsenic has a direct toxic effect on DNA synthesis that results in marked disturbances of nuclear division. We recommend that the most appropriate screening procedure to evaluate possible arsenic poisoning is tissue arsenic measurements (hair and nails) rather than 24-hr urinary measurements.

Adult↗
PubMed2025

A deep-sea hydrothermal vent worm detoxifies arsenic and sulfur by intracellular biomineralization of orpiment (As2S3).

The alvinellid worm Paralvinella hessleri is the only animal that colonizes the hottest part of deep-sea hydrothermal vents in the west pacific. We found P. hessleri accumulates exceptionally high level of toxic element arsenic (>1% of wet weight) and tolerated elevated concentrations hydrogen sulphide. Using advanced microscopy, elementary analysis, and genomics and proteomics approaches, we identified a previously unrecognized arsenic-sulfide biomineralization process in P. hessleri. Our data suggest that arsenic accumulates within epithelial cell granules, where it likely reacts with sulphide diffused inward from the hydrothermal vent fluid, resulting in the intracellular formation of orpiment (As₂S₃) minerals. In this "fighting poison with poison" manner, the highly toxic arsenic and sulphide were simultaneously detoxified in the form of orpiment minerals within the intracellular granules of the single layer of epithelial cells. This process represents a remarkable adaptation to extreme chemical environments. Our study provides new insights into understanding animals' environment adaptation mechanisms and the diversity and plasticity of biomineralization.

Animals↗
PubMed2026

Toxicoproteomic analysis reveals arsenic-induced alterations in eye lens proteins of Labeo rohita.

Arsenic occurs extensively in the environment and is classified as a potent carcinogenic substance in humans. Prolonged intake of water contaminated with arsenic results in the development of arsenicosis. In the present study, a toxicoproteomic approach was employed to elucidate arsenic-induced alterations in lens proteins using a fish model. Juveniles of Labeo rohita were exposed to sodium meta-arsenite (NaAsO2) at concentrations of 5, 10, 15, and 20&#xa0;ppm for a period of 10&#xa0;days in triplicate experimental groups. Soluble lens proteins were analyzed using one- and two-dimensional gel electrophoresis, immunoblotting of &#x3b1;A-crystallin and MALDI-TOF mass spectrometry. Cataract development was observed at arsenic concentrations&#x2009;&#x2265;&#x2009;15&#xa0;ppm. Proteomic analyses revealed concentration-dependent alterations in lens protein abundance, including significant reductions in &#x3b2;B1, &#x3b2;B2, and &#x3b2;A2b-crystallin, small heat shock protein and skeletal &#x3b1;-actin (p&#x2009;<&#x2009;0.05). In addition, &#x3b1;A, &#x3b2;A2, and &#x3b2;A2a-crystallin exhibited reduced abundance trends, although these changes were not statistically significant. Two-dimensional immunoblotting revealed 15 distinct &#x3b1;A-crystallin isoforms in control lenses, several of which showed a progressive decrease with increasing arsenic exposure, culminating in complete degradation at 20&#xa0;ppm. These findings demonstrate that arsenic exposure is associated with substantial alterations in lens crystallins and other proteins involved in structural organization and protein homeostasis, coinciding with cataract development at higher exposure concentrations. The identified proteins may serve as potential toxicoproteomic biomarkers of lens damage in aquatic organisms and provide a foundation for future studies investigating the molecular mechanisms of arsenic-induced lens toxicity.

Animals↗
PubMedDate not supplied

Acute arsine posioning in two workers cleaning a clogged drain.

On February 6, 1978, two maintenance workers employed by a chemical company in Atlanta, Georgia, became ill after cleaning a clogged drain. Both were hospitalized with acute fulminant hemolytic anemia and renal failure. While the clinical picture suggested arsine or stibine poisoning, preliminary investigation of the plant revealed no obvious source of arsenic, antimony, or hydrogen gas. During the cleaning operation, the men drained a mixing tank that 5 yr before had been used to store arsenical herbicides. To unclog the drain, they added a standard drain cleaner containing sodium hydroxide and aluminum chips, a combination that reacted to release hydrogen gas. This gas combined with the arsenic residue to form toxic quantities of arsine gas (arsenic trihydride). Arsenic was found in the liquid and gas from the drain and in blood and urine of both patients, and of two other workers who worked in the vicinity of the drain. This investigation suggests that drain cleaners which react to release hydrogen should not be used in situations where arsenic or antimony may be present. Furthermore, maintenance men, who may be exposed to the chemicals used in a plant, should be educated, supervised, and screened so that their risk for occupational hazards may be reduced.

Acute Disease↗
PubMed1977

Metabolic interrelationships between arsenic and selenium.

In 1938, Moxon discovered that arsenic protected against selenium toxicity. Since that time it has been shown that this protective effect of arsenic against selenium poisoning can be demonstrated in many different animal species under a wide variety of conditions. Antagonistic effects between arsenic and selenium have also been noted in teratologic experiments. Early metabolic studies showed that arsenic inhibited the expiration of volatile selenium compounds by rats injected with acutely toxic doses of both elements. This was puzzling since pulmonary excretion had long been regarded as a means by which animals could rid themselves of excess selenium. However, later work demonstrated that arsenic increased the biliary excretion of selenium. Not only did arsenic stimulate the excretion of selenium in the bile, but selenium also stimulated the excretion of arsenic in the bile. This increased biliary excretion of selenium caused by arsenic provides a reasonable rationale for the ability of arsenic to counteract the toxicity of selenium, although the chemical mechanism by which arsenic does this is not certain. The most satisfactory explanation is that these two elements react in the liver to form a detoxication conjugate which is then excreted into the bile. This is consistent with the fact that both arsenic and selenium each increase the biliary excretion of the other. Several other metabolic interactions between arsenic and selenium have been demonstrated in vitro, but their physiological significance is not clear. Although arsenic decreased selenium toxicity under most conditions, there is a pronounced synergistic toxicity between arsenic and two methylated selenium metabolites, trimethylselenonium ion or dimethyl selenide. The ecological consequences of these synergisms are largely unexplored, although it is likely that selenium methylation occurs in the environment. All attempts to promote or prevent selenium deficiency diseases in animals by feeding arsenic have been unsuccessful. Over 30 years ago it was suggested that industrial hygienists use arsenic as a tonic to prevent or cure selenium poisoning in workers exposed to this hazard. Organic arsenical feed additives were tried as partial antidotes against selenium poisoning in livestock raised in seleniferous agricultural areas but were not found to be practical.

Animals↗
PubMed2024

Prenatal arsenic exposure alters EZH2-H3K27me3 occupancy at TNF-&#x3b1; promoter leading to insulin resistance and metabolic syndrome in a mouse model.

The global prevalence of Metabolic Syndrome (MetS) is continuously rising and exposure to environmental toxicants such as arsenic could be contributing to this rapid surge. In this study, we have assessed the effects of prenatal arsenic exposure on insulin resistance and MetS parameters in a mouse model, and an underlying mechanism was identified. We found that prenatal arsenic exposure promotes insulin resistance and adipocyte dysfunction which leads to the early onset of MetS in male offspring. Primary adipocytes isolated from 20-week-old arsenic-exposed offspring showed hypertrophy, elevated basal lipolysis, and impaired insulin response along with enhanced expression of Tumor necrosis factor-alpha (TNF-&#x3b1;). TNF-&#x3b1; levels were consistently high at gestational day 15.5 (GD15.5) as well as primary adipocytes of 6-week-old arsenic-exposed male offspring. Along with TNF-&#x3b1;, downstream p-JNK1/2 levels were also increased, which led to inhibitory phosphorylation of IRS1and reduced GLUT4 translocation upon insulin stimulation in adipocytes. Insulin response and downstream signaling were restored upon TNF-&#x3b1; inhibition, confirming its central role. The persistent overexpression of TNF-&#x3b1; in adipocytes of arsenic-exposed mice resulted from diminished EZH2 occupancy and reduced H3K27me3 (gene silencing histone marks) at the TNF-&#x3b1; promoter. This further led to chromatin relaxation, recruitment of c-Jun and CBP/p300, formation of an enhanceosome complex, and TNF-&#x3b1; expression. Our findings show how prenatal arsenic exposure can epigenetically modulate TNF-&#x3b1; expression to promote adipocyte dysfunction and insulin resistance which contributes to the early onset of MetS in offspring.

Animals↗
PubMed2026

Deficient arsenic methylation and global proteomic reprogramming in human keratinocytes during arsenic-induced skin carcinogenesis.

Chronic inorganic arsenic (iAs) exposure affects&#x2009;>&#x2009;220&#xa0;million people worldwide and skin cancer is a hallmark of long-term iAs exposure. Limited information exists regarding arsenic methylation by human keratinocytes and how methylation influences skin carcinogenesis. Inorganic arsenite (iAsIII) and its methylated metabolites disrupt diverse zinc finger proteins, leading to differential toxicity patterns. We examined arsenic methylation capacity in non-malignant human keratinocytes and interrogated proteomic remodeling across three stages of iAsIII induced malignant transformation using the well-established preclinical HaCaT model. Arsenic methylation was assessed by hydride generation cryotrapping inductively coupled-mass spectrometry and global proteomic changes were analyzed by tandem-mass tagging liquid chromatography-tandem mass spectrometry. Primary, hTERT-immortalized and HaCaT human keratinocytes exhibited negligible arsenic methylation, with iAsIII comprising at least 98.5% of total intracellular arsenic, attributable to minimal expression of arsenite methyltransferase. Proteomic profiling identified over 275 differentially expressed proteins at each stage of transformation, including multiple zinc finger proteins implicated in cell cycle control, RNA metabolism, and genome stability. Ingenuity&#xae; Pathway Analysis revealed progressive, coordinated disruption of cancer-associated pathways and regulatory networks over the transformation timeline, including zinc-coordinating upstream regulators that may explain widespread pathway dysregulation. Collectively, our findings suggest that iAsIII promotes skin carcinogenesis by disrupting C3H1- and C4-type zinc finger protein-centered regulatory networks that coordinate cancer-associated signaling and metabolic pathways in human keratinocytes, highlighting key candidates for future mechanistic studies.

Arsenic↗
PubMed2026

Health risk assessment of inorganic arsenic: an umbrella review.

Inorganic arsenic (iAs) is a toxic environmental pollutant linked to serious health risks, prompting global regulatory efforts. This study identifies major health conditions associated with iAs exposure using text network analysis, and assesses health risk assessments through an umbrella review and dose-response analysis. It synthesizes previous systematic reviews to offer a broader perspective on iAs-related health effects. An optimized text network analysis-based search strategy was applied across multiple databases to identify relevant systematic reviews. An umbrella review framework was employed to synthesize and reinterpret findings across systematic reviews. The methodological quality of included systematic reviews was assessed using the A MeaSurement Tool to Assess systematic Reviews 2 tool. Extracted data on study characteristics, exposure levels, and risk estimates were analyzed to evaluate the dose-response relationship between iAs exposure and health outcomes. From 922 systematic reviews, 36 were included and categorized into 10 health condition groups. For example, seven SRs found a significant dose-response relationship between iAs and bladder cancer, with one systematic review reporting relative risks of 2.70, 4.20, and 5.80 at 10, 50, and 150&#x202f;&#xb5;g/L, respectively. Individual study analysis further showed that each 10&#x202f;&#xb5;g/L increase in iAs raised bladder cancer risk by 3.11&#x202f;% (p=0.003). iAs exposure is associated with hypertension, diabetes, cardiovascular disease, and adverse fetal outcomes. Dose-dependent increases in bladder cancer, lung cancer, and hypertension risks were observed. These findings support more precise health risk assessments and regulatory strategies.

Humans↗
PubMed1977

Effects of concurrent administration of lead, cadmium, and arsenic in the rat.

Humans are exposed to a number of toxic elements in the environment; however, most experiments with laboratory animals investigate only one toxic element. To determine if concomitant exposure to lead (Pb), cadmium (Cd), and/or arsenic (As) modified the changes produced by any one metal in various parameters of toxicity, 168 male, Sprague-Dawley, young adult rats were fed nutritionally adequate diets to which had been added 0 or 200 ppm Pb as Pb acetate, or 50 ppm Cd as Cd chloride, or 50 ppm As as sodium arsenate or arsanilic acid in a factorial design for a period of 10 weeks. At these concentrations, Cd and As reduced weight gain even when differences in food intake were taken into account; administration of both Cd and As depressed weight gain more than did either metal alone. Pb did not adversely affect food consumption or weight gain. Increased numbers of red blood cells (RBCs) were observed following administration of Pb, Cd, or As; usually more cells were observed when two or three metals were administered, compared to individual metals. Despite increasing numbers of circulating RBCs, hemoglobin and hematocrit were reduced, especially with the Pb-Cd combination and the Cd-arsanilic acid combination. Specific effects of Pb on heme synthesis were observed, including increased urinary excretion of delta-aminolevulinic acid; this increase was reduced by the presence of dietary cadmium. Analyses of blood showed values for the laboratory rat within normal ranges for blood urea nitrogen, creatinine, cholesterol, calcium, albumin, total protein, and bilirubin. Uric acid was increased by Pb, with little modification by dietary Cd or As content. Serum glutamate-oxalate transaminase activity was reduced by As. Serum alkaline phosphatase was greatly reduced by either As or Cd but not Pb. Combinations of As and Cd did not further reduce the activity of this enzyme. Kidney weight and kidney weight/body weight ratios were increased by Pb alone, with no effects of Cd or As alone or as interactions. Liver weight/body weight ratios were reduced in animals fed 50 ppm dietary Cd. Kidney histology shows predominantly Pb effects, namely, intranuclear inclusion bodies and cloudy swelling. Ultrastructural evaluation of kidneys from Pb-treated animals disclosed nuclear inclusion bodies of the usual morphology and mitochondrial swelling. Concurrent administration of Cd greatly minimized Pb effects on the kidney under conditions of this experiment. Liver histology suggests an increased rate of cell turnover with either As compound, but few specific changes.

Administration, Oral↗
PubMed1978

Biological interaction of selenium with other trace elements in chicks.

Studies were conducted to determine whether or not elements whose valence shell of electrons was similar to that of selenium would reverse the toxicity of selenium to chicks. The elements studied were arsenic, tellurium, tin, and lead. Each of these elements, when added to the diet of chicks, reversed the toxicity of 25 ppm selenium as measured by weight gain. In spite of the protection afforded by these elements, there was no decrease in liver concentration of selenium except with levels of arsenic higher than that needed for reversal of toxicity.

Animals↗
PubMedDate not supplied

[Effect of wolfram, molybdenum, copper and arsenic on intrauterine fetal development].

Experients showed tungsten, molibdenum, copper and arsenic employed in doses producing no general toxic effect on the organism with their prolonged introduction to act adversely on the embryogenesis. Tungsten copper and arsenic were found to increase the embryonal lethality and tungsten and molebdenum to inhibit the processes of bones ossification in fetuses. The authors presume that the embryotoxic effect of the study elements is due to their direct action on the developing organism. Tungsten molibdenum and copper amass in the organism of test fetuses without being arrested in the placenta. A possible embryotoxic effect should be taken account of in chosing biogenic doses of trace elements.

Administration, Oral↗
PubMed1978

Therapy of leishmaniasis: superior efficacies of liposome-encapsulated drugs.

Liposomes containing antimonial compounds trapped in the aqueous phase were tested in the treatment of experimental leishmaniasis. The rationale of this approach was based on the hypothesis that the liposomes and the parasite are taken up by the same cell, the reticuloendothelial cell, and we present electron microscopic evidence that supports this hypothesis. Suppression of leishmaniasis was quantified by determining the total number of parasites per liver from impression smears. When two antimonials, meglumine antimoniate and sodium stibogluconate, were encapsulated within liposomes, each was more than 700 times more active compared to either of the free (unencapsulated) drugs. After infection, if untreated, all of the hamsters eventually would die from the disease. Liposome-encapsulated meglumine antimoniate was about 330-640 times more effective in causing a drop in the death rate than was the free antimonial. The efficacy of treatment was influenced by the lipid composition and charge of the liposomes. For example, positively charged liposomes containing egg phosphatidylcholine were much less effective than negatively charged ones. In contrast, positively and negatively charged sphingomyelin liposomes were equally effective. Liposomes containing phosphatidylserine (which were negatively charged, but also had a much higher charge density) were among the less-effective preparations. Among those tested, the most consistently efficacious liposomes contained highly saturated long-chain phospholipids (eg., dipalmitoyl phosphatidylcholine), cholesterol, and a negative charge. We conclude that liposomes may be useful as carriers of drugs to treat infectious diseases involving the reticuloendothelial system. The toxicities of antimony are very similar to those of arsenic. Encapsulation of antimonial drugs and reduction of the dose required for effective therapy should minimize such systemic toxicities as acute cardiomyopathy and toxic nephritis.

Animals↗
PubMed1979

Toxic effects of metals from the environment on hair growth and structure.

Diffuse alopecia related to ingestion of toxic metals from the environment has been observed in 36 patients. Copper, arsenic, mercury and cadmium were involved and the intensity of disturbance of the hair cycle, heralded by presence of dystrophic hairs, was proportional to the amount of toxic material detected in blood and urine. Toxicity can be observed in vitro by measuring labeled cells on squash preparations after incorporation of tritiated uridine and thymidine in plucked hairs. The labeling indexes, as well as the ratio between cells entering the S phase and the viable cells were always lower in toxic alopecia than in normal hair. Toxic metals do not seem to affect the morphology of the hair shaft.

Arsenic Poisoning↗