Use Of Arsenic Compounds Research Articles

Arsenic induces hepatotoxicity in chickens via PANoptosis pathway

Environmental pollution caused by arsenic or its compounds is called arsenic pollution. Arsenic pollution mainly comes from people's mining and smelting of arsenic compounds. In addition, the widespread use of arsenic compounds, such as the use and production of arsenic-containing pesticides, is also a source of arsenic contamination. Arsenic contamination leads to an increased risk of arsenic exposure, and the multi-organ toxicity induced by arsenic exposure is a global health problem. As a non-mammalian vertebrate with high nutrient levels, chickens readily absorb and accumulate arsenic from their food. Relevant studies have shown that arsenic exposure induces hepatotoxicity in chickens, and there has been a steady stream of research into the specific mechanisms involved. PANoptosis, a newly discovered and unique mode of programmed cell death (PCD) characterized by both apoptosis, cellular pyroptosis, and necroptosis. There are no studies to indicate whether chicken liver toxicity due to arsenic is associated with PANoptosis. Therefore, we established chicken animal models and chicken primary hepatocyte models exposed to different arsenic concentrations to dissect the role and mechanism of PANoptosis in arsenic exposure-induced hepatotoxicity in chickens. Our histopathological results showed that arsenic treatment caused dose-dependent damage to chicken liver structure. Meanwhile, different doses of arsenic treatment groups caused significant up-regulation of the protein level of ZBP1, a key factor of PANoptosis. And then consequently triggered the abnormal gene and protein expression levels of apoptosis-associated factors (Caspase-8, Caspase-7, Caspase-3), cellular pyroptosis-associated factors (NLRP3, ASC, GSDMD) and necroptosis-associated factors (RIPK1, RIPK3, MLKL). In conclusion, our study revealed that PANoptosis is involved in arsenic-induced chicken hepatotoxicity. Our findings provide a new perspective on the pathogenesis of arsenic exposure-induced hepatotoxicity in chickens.

The history of arsenical pesticides and health risks related to the use of Agent Blue.

Arsenicals in agriculture. Beginning in the 1970s, the use of arsenic compounds for such purposes as wood preservatives, began to grow. By 1980, in the USA, 70% of arsenic had been consumed for the production of wood preservatives. This practice was later stopped, due to the US Environmental Protection Agency (EPA) ban of the arsenic-and chromium-based wood preservative chromated copper arsenate. In the past, arsenical herbicides containing cacodylic acid as an active ingredient have been used extensively in the USA, from golf courses to cotton fields, and drying-out the plants before harvesting. The original commercial form of Agent Blue was among 10 toxic insecticides, fungicides and herbicides partially deregulated by the US EPA in February 2004, and specific limits on toxic residues in meat, milk, poultry and eggs, were removed. Today, however, they are no longer used as weed-killers, with one exception - monosodium methanearsonate (MSMA), a broadleaf weed herbicide for use on cotton. Severe poisonings from cacodylic acid caused headache, dizziness, vomiting, profuse and watery diarrhea, followed by dehydration, gradual fall in blood pressure, stupor, convulsions, general paralysis and possible risk of death within 3-14 days.The relatively frequent use of arsenic and its compounds in both industry and agriculture points to a wide spectrum of opportunities for human exposure. This exposure can be via inhalation of airborne arsenic, contaminated drinking water, beverages, or from food and drugs. Today, acute organic arsenical poisonings are mostly accidental. Considerable concern has developed surrounding its delayed effects, for its genotoxic and carcinogenic potential, which has been demonstrated in epidemiological studies and subsequent animal experiments. <b>Conclusions.</b> There is substantial epidemiological evidence for an excessive risk, mostly for skin and lung cancer, among humans exposed to organic arsenicals in occupational and environmental settings. Furthermore, the genotoxic and carcinogenic effects have only been observed at relatively high exposure rates. Current epidemiological and experimental studies are attempting to elucidate the mechanism of this action, pointing to the question whether arsenic is actually a true genotoxic, or rather an epigenetic carcinogen. Due to the complexity of its effects, both options remain plausible. Its interactions with other toxic substances still represent another important field of interest.

Illicit utilization of arsenic compounds in pyrotechnics? An analysis of the suspended particle emission during Vienna’s New Year fireworks

In the course of an investigation of an electrostatic precipitation technique as a sampling method for airborne dust particles, elevated concentrations of As were found in the data collected during New Years Eve celebrations in Vienna. The original study confirmed the applicability of the new sampling device as a useful sampling method, showing elevated values for the elements Na, Mg, Al, Si, S, K, Cu, As, Br, Rb, Sr, Sb, Te and Ba, all associated with the use of pyrotechnics. The measured values for As could not be explained as a impurity in some other substances used. Thus, several unburned pyrotechnic products were investigated to find the source of As in the dust collected. The results showed only one product with higher than expected As contents (1.4 μg g−1), leading to the assumption of intentional—but illicit—use of arsenic compounds in pyrotechnics as a colouring agent for the production of blue light.

On How Could Light and Nanostructures Lead the Way to a Safer Anticancer Therapy

Destroying biological pathogens is easy. The point is how to destroy them while sparing the host. This is especially obvious when dealing with cancer. History shows that anticancer therapies have always been aggressive to patients. For instance, in the 19th century, arsenides and arsenic salts were commonly prescribed as anticancer drugs [1]. The use of arsenic derivatives for treating cancer was an art – hard to master, properly applied only by a few. Although arsenic was considered to be effective against cancer, it was difficult to deal with its narrow therapeutic window. In the early 20th century, improved therapies supplanted arsenic derivatives in anticancer treatment – actually, the use of arsenic compounds for therapeutic purposes is far from being left aside as it continues to be investigated and encouraged [1]. But important side effects persist. The problem is that anticancer drugs act without the precious help given by phylogenetic differences between the host and the biological pathogen. They should destroy abnormal eukaryotic cells, derived from host’s own cells. This is the main reason behind the harmful, sometimes lethal, side effects of conventional anticancer therapies. Over the last few decades, despite the efforts in developing and improving anticancer therapies, no major progress has been achieved.

Biological Responses to Arsenic Compounds

Arsenic is a metalloid that generates various biological effects on cells and tissues. Depending on the specific tissue exposed and the time and degree of exposure, diverse responses can be observed. In humans, prolonged and/or high dose exposure to arsenic can have a variety of outcomes, including the development of malignancies, severe gastrointestinal toxicities, diabetes, cardiac arrhythmias, and death. On the other hand, one arsenic derivative, arsenic trioxide (As(2)O(3)), has important antitumor properties. This agent is a potent inducer of antileukemic responses, and it is now approved by the Food and Drug Administration for the treatment of acute promyelocytic leukemia in humans. The promise and therapeutic potential of arsenic and its various derivatives have been exploited for hundreds of years. Remarkably, research focused on the potential use of arsenic compounds in the treatment of human diseases remains highly promising, and it is an area of active investigation. An emerging approach of interest and therapeutic potential involves efforts to target and block cellular pathways activated in a negative feedback manner during treatment of cells with As(2)O(3). Such an approach may ultimately provide the means to selectively enhance the suppressive effects of this agent on malignant cells and render normally resistant tumors sensitive to its antineoplastic properties.

Best practices for promoting farmers’ health: the case of arsenic history

The most important sources of environmental as well as occupational exposure of man to this metalloid are connected with the mining and smelting of nonferrous metals, the burning of coal for its higher content, the mass use of arsenicals as pesticides, and in both growth stimulators and wood preservatives. The use of arsenical insecticides in agriculture decreased dramatically following the introduction of dichlorodiphenyltrichloroethane (DDT), but the use of arsenical herbicides has increased. Beginning in the 1970s, the use of arsenic compounds, such as for wood preservatives, began to grow. By 1980, in the USA, 70% of arsenic had been consumed for production of wood preservatives. This practice was stopped 4 years ago, due to the US Environmental Protection Agency (EPA) ban of the arsenic- and chromium-based wood preservative chromated copper arsenate. This was, at least in the USA, an example of rational, stepwise risk management, which would mitigate exposure to arsenic for farmers and forestry and wood industry workers. The relatively frequent use of arsenic and its compounds, in both industry and agriculture, points to a wide spectrum of opportunities for human exposure; this exposure can be via inhalation of airborne arsenic, contaminated drinking water, beverages, or from food and drugs. Today, acute arsenic poisonings are mostly accidental. Considerable concern has developed surrounding its delayed effects, for its genotoxic and carcinogenic potential, which has been demonstrated in epidemiological studies and subsequent animal experiments. There is substantial epidemiological evidence for an excessive risk, mostly for skin and lung cancer, among workers exposed to arsenic. Furthermore, the genotoxic and carcinogenic effects have only been observed at relatively high exposure rates. Current epidemiological and experimental studies are trying to elucidate the mechanism for this action, pointing to the question of whether arsenic is actually the true genotoxic or rather an epigenetic carcinogen. Due to the complexity of its effects both options remain plausible. Its interactions with other toxic substances still represent another field of interest.

Arsenic — a Review. Part I: Occurrence, Toxicity, Speciation, Mobility

AbstractIn natural waters arsenic concentrations up to a few milligrams per litre were measured. The natural content of arsenic found in soils varies between 0.01 mg/kg and a few hundred milligrams per kilogram. Anthropogenic sources of arsenic in the environment are the smelting of ores, the burning of coal, and the use of arsenic compounds in many products and production processes in the past. A lot of arsenic compounds are toxic and cause acute and chronic poisoning. In aqueous environment the inorganic arsenic species arsenite (As(III)) and arsenate (As(V)) are the most abundant species. The mobility of these species is influenced by the pH value, the redox potential, and the presence of adsorbents such as oxides and hydroxides of Fe(III), Al(III), Mn(III/IV), humic substances, and clay minerals.

Arsenic compounds as anticancer agents.

In this paper the use of arsenic compounds as anticancer agents in clinical trials and in in vitro investigations is reviewed, including the experience at our institute. Treatment of newly diagnosed and relapsed patients with acute promyelocytic leukemia (APL) with arsenic trioxide (As2O3) has been found to result in complete remission (CR) rates of 85-93% when given by intravenous infusion for 2-3 h at a dose of 10 mg/day diluted in 5% glucose saline solution. Patients exhibit a response in 28-42 days. CR rates after administration of Composite Indigo Naturalis tablets containing arsenic sulfide and of pure tetraarsenic tetrasulfide reached 98% and 84.9%, respectively. At higher concentrations (1-2 microM), arsenic induced apoptosis, while at lower concentrations (0.1-0.5 microM), it triggered cell differentiation in vitro. As2O3-induced apoptosis has been observed in many cancer cell lines, including esophageal carcinoma, gastric cancer, neuroblastoma, lymphoid malignancies, and multiple myeloma. Its effectiveness was confirmed in the treatment of multiple myeloma. Arsenic compounds are effective agents in the treatment of APL and their activity against other types of cancer requires further investigation.

Arsenic trioxide as an inducer of apoptosis and loss of PML/RAR alpha protein in acute promyelocytic leukemia cells.

Retinoids, which are derivatives of vitamin A, induce differentiation of acute promyelocytic leukemia (APL) cells in vitro and in patients. However, APL cells develop resistance to retinoic acid treatment. Arsenic trioxide (As2O3) can induce clinical remission in patients with APL, including those who have relapsed after retinoic acid treatment, by inducing apoptosis (programmed cell death) of the leukemia cells. In this study, we investigated the molecular mechanisms by which As2O3 induces apoptosis in retinoic acid-sensitive NB4 APL cells, in retinoic acid-resistant derivatives of these cells, and in fresh leukemia cells from patients. Apoptosis was assessed by means of DNA fragmentation analyses, TUNEL assays (i.e., deoxyuridine triphosphate labeling of DNA nicks with terminal deoxynucleotidyl transferase), and flow cytometry. Expression of the PML/RAR alpha fusion protein in leukemia cells was assessed by means of western blotting, ligand binding, and immunohistochemistry. Northern blotting and ribonuclease protection assays were used to evaluate changes in gene expression in response to retinoic acid and As2O3 treatment. As2O3 induces apoptosis without differentiation in retinoic acid-sensitive and retinoic acid-resistant APL cells at concentrations that are achievable in patients. As2O3 induces loss of the PML/RAR alpha fusion protein in NB4 cells, in retinoic-acid resistant cells derived from them, in fresh APL cells from patients, and in non-APL cells transfected to express this protein. As2O3 and retinoic acid induce different patterns of gene regulation, and they inhibit the phenotypes induced by each other. Understanding the molecular basis of these differences in the effects of As2O3 and retinoic acid may guide the clinical use of arsenic compounds and provide insights into the management of leukemias that do not respond to retinoic acid.

ChemInform Abstract: Utilization of Inorganic and Organic Arsenic Compounds in New Technologies

This paper reviews the use of arsenic compounds in semiconductor manufacture and emphasizes the role of alkylated arsenic compounds.

Utilization of inorganic and organic arsenic compounds in new technologies

AbstractThis paper reviews the use of arsenic compounds in semiconductor manufacture and emphasizes the role of alkylated arsenic compounds.

Chemotherapy Studies of Histomoniasis

THE use of arsenical compounds as chemotherapeutic agents against histomoniasis was first reported by Tyzzer (1923), who found that tryparsamide, atoxyl and neoarsphenamine produced a more or less favorable effect. Delaplane and Stuart (1935), however, stated that neoarsphenamine, among other compounds, was of little or no value for preventing blackhead in turkeys. Hinshaw (1937) observed that atoxyl and neoarsphenamine had been tried with but little success. He stated that tryparsamide was the only promising compound of the two and confirmed Tyzzer’s statement that it was too expensive for general use. Similar conflicting reports concerning the use of mapharsen injections have been made by Blount (1938), Bolin and Vardiman (1941), McCulloch and Nicholson (1941), Jaquette and Marsden (1947) and by Glover (1948).Well controlled experiments by Sautter, Pomeroy and Roepke (1950) have shown that injections of tryparsamide were slightly beneficial but that the effect was nullified when medication was started 4 .

Advances in Entomology

Stomach Poisons ONE of the most important recent events affecting the use of arsenical compounds for controlling insects on fruits and vegetables is the change in the official tolerances for arsenic and lead. Effective August 10, 1940, the Federal Security Agency ( 9 ) has ruled that the tolerance for lead shall be increased to 0.05 grain Pb per pound of produce and that of arsenic to 0.025 grain As (as AS 2 O 3 ) per pound. The fluorine tolerance remains unchanged as of 1938 at 0.02 grain F per pound. These tolerances are subject to change if methods for evaluating the toxic effects of lead and arsenic on human beings are improved. Although this action may reduce somewhat the care necessary in applying sprays and dusts and in removing the residues, it will not halt the search for new insecticides less toxic to humans and more efficient than the compounds of lead, arsenic, and fluorine now in use. Several ...

The use of arsenical compounds in the control of deep-rooted perennial weeds

does not appear. First page follows. As chemical weed control becomes more generally practiced, the limitations as well as the possibilities of the various methods become more evident. The effectiveness of these methods depends upon certain factors which must be carefully considered if consistent results are to be obtained. Many of the factors may be controlled by the operator. It is, therefore, essential to the successful practice of any new method that a descriptive study of the more readily controlled factors be made; for only when we understand the underlying principles may we obtain the best results. This preliminary report describes the preparation and use of an arsenical solution recently employed with considerable success in controlling deep-rooted perennial weeds. It discusses the mechanism involved in the movement of the arsenical solution into the roots of plants, and submits data for comparing and evaluating the factors that tend to limit its action. It discusses also the conditions essential to successful practice and gives certain precautions for the handling of the reagents. One should understand at the outset that the arsenical herbicide described in the following pages will not completely eradicate perennial weeds. Such results cannot be expected of any chemical weed killer. This herbicide has, however, proved very satisfactory when prepared properly and applied under optimum conditions.