Introduction: The toxicity of arsenic is widely recognized globally, mainly harming human health by polluting water, soil, and food. However, its formulations can also be used for the clinical treatment of diseases such as leukemia and tumors. Arsenic has been used as a drug in China for over 2,400 years, with examples such as the arsenic-containing drug realgar mentioned in Shennong’s Herbal Classic. We have reviewed references on arsenic over the past thirty years and found that research has mainly focused on clinical, pharmacological, and toxicological aspects. Results and Discussion: The finding showed that in clinical practice, arsenic trioxide is mainly used in combination with all-trans retinoic acid (ATRA) at a dose of 10 mg/d for the treatment of acute promyelocytic leukemia (APL); realgar can be used to treat acute promyelocytic leukemia, myelodysplastic syndrome, and lymphoma. In terms of pharmacology, arsenic mainly exerts anti-tumor effects. The dosage range of the action is 0.01–80 μmol/L, and the concentration of arsenic in most studies does not exceed 20 μmol/L. The pharmacological effects of realgar include antiviral activity, inhibition of overactivated lactate dehydrogenase, and resistance to malaria parasites. In terms of toxicity, arsenic is toxic to multiple systems in a dose-dependent manner. For example, 5 μmol/L sodium arsenite can induce liver oxidative damage and promote the expression of pro-inflammatory factors, and 15 μmol/L sodium arsenite induces myocardial injury; when the concentration is higher, it is more likely to cause toxic damage.

Research progress on arsenic, arsenic-containing medicinal materials, and arsenic-containing preparations: clinical application, pharmacological effects, and toxicity

The global health implications of fine particulate matter (PM2.5) underscore the imperative need for research into its toxicity and chemical composition. In this study, zebrafish embryos exposed to the water-soluble components of PM2.5 from two cities (Harbin and Hangzhou) with differences in air quality, underwent microscopic examination to identify primary target organs. The Harbin PM2.5 induced dose-dependent organ malformation in zebrafish, indicating a higher level of toxicity than that of the Hangzhou sample. Harbin PM2.5 led to severe deformities such as pericardial edema and a high mortality rate, while the Hangzhou sample exhibited hepatotoxicity, causing delayed yolk sac absorption. The experimental determination of PM2.5 constituents was followed by the application of four algorithms for predictive toxicological assessment. The random forest algorithm correctly predicted each of the effect classes and showed the best performance, suggesting that zebrafish malformation rates were strongly correlated with water-soluble components of PM2.5. Feature selection identified the water-soluble ions F− and Cl− and metallic elements Al, K, Mn, and Be as potential key components affecting zebrafish development. This study provides new insights into the developmental toxicity of PM2.5 and offers a new approach for predicting and exploring the health effects of PM2.5. 

Prediction of developmental toxic effects of fine particulate matter (PM2.5) water-soluble components via machine learning through observation of PM2.5 from diverse urban areas

YTHDF2 phase separation promotes arsenic-induced keratinocyte transformation in a poly-m6A-dependent manner by inhibiting translational initiation of the key tumor suppressor PTEN

<title>Abstract</title> Background Hyunburikyung-tang exerts an anti-inflammatory effect by suppressing pro-inflammatory cytokines and prostaglandin E2 and is clinically used to improve dysmenorrhea in Korea. It contains various medicinal plants including peach seeds (<italic>Prunus persica</italic> Batsch) and safflower (<italic>Carthamus tinctorius</italic> Linn). Peach seeds contain amygdalin, which demonstrates teratogenic effects, and safflower is reported to cause reproductive toxicity and teratogenic effects in mice. These findings raise concerns regarding the teratogenic potential of these substances. A potential correlation exists between genotoxicity and teratogenicity. Genotoxic substances can damage DNA and cause mutations or chromosomal abnormalities, which may result in developmental malformations. Therefore, we aimed to assess whether Hyunburikyung-tang causes acute toxicity or genotoxicity. Methods Male and female rats were orally administered Hynburikyung-tang to assess acute toxicity. Body weight measurements, general symptom observations, and autopsy examinations were used to confirm toxic responses. Genotoxicity assessment was conducted with bacteria, cells, and mice, according to the Organization for Economic Cooperation and Development (OECD) test guidelines. Results Regarding acute toxicity assessment, no toxic reactions were observed when male and female rats received oral doses of Hyunburikyung-tang (626, 1,250, or 2,500 mg/kg). The genotoxicity tests, which included assessments of reverse mutations, chromosomal aberrations, and micronucleus formation, showed no genotoxic responses. Conclusions Our findings suggested that Hyunburikyung-tang does not induce acute toxicity or genotoxicity. Nevertheless, follow-up research should be conducted to confirm toxicity caused by repeated administration.

Genotoxicity and acute toxicity of Hyunburikyung-tang: assessing the safety of prescribing traditional Korean medicine for dysmenorrhea

The mechanisms that underlie arsenic tumorigenicity remain incompletely understood. Here, we show that arsenic regulates the abundance and the demethylase activity of ALKBH1, which, in turn, promotes arsenic-induced skin tumorigenesis. At the molecular level, knockdown of ALKBH1 in arsenic-exposed keratinocytes increases m6A enrichment in mRNA, and ALKBH1 demethylates m6A in vitro in an arsenic-dependent manner. Arsenic binds to the ALKBH1 protein at cysteine residues to regulate the m6A RNA demethylase activity of ALKBH1. m6A-immunoprecipitation (IP)-sequencing demonstrates that ALKBH1 regulates m6A demethylation on the NR2C2 transcript to inhibit NR2C2 protein translation in a YTHDF1-dependent manner. Functionally, knockdown of ALKBH1 increases NR2C2 expression, leading to decreased mTOR activation and global translation. Our work uncovers a previously unknown mechanism into arsenic tumorigenicity, adds understanding into the functional effect of arsenic binding to proteins, and implicates ALKBH1 as a potential druggable target and biomarker for arsenic tumorigenicity.

Arsenic regulates ALKBH1 abundance and substrate specificity to promote translation and tumorigenicity

Arsenic and antimony are metalloids with profound effects on biological systems and human health. Both elements are toxic to cells and organisms, and exposure is associated with several pathological conditions including cancer and neurodegenerative disorders. At the same time, arsenic- and antimony-containing compounds are used in the treatment of multiple diseases. Although these metalloids can both cause and cure disease, their modes of molecular action are incompletely understood. The past decades have seen major advances in our understanding of arsenic and antimony toxicity, emphasizing genotoxicity and proteotoxicity as key contributors to pathogenesis. In this review, we highlight mechanisms by which arsenic and antimony cause toxicity, focusing on their genotoxic and proteotoxic effects. The mechanisms used by cells to maintain proteostasis during metalloid exposure are also described. Furthermore, we address how metalloid-induced proteotoxicity may promote neurodegenerative disease and how genotoxicity and proteotoxicity may be interrelated and together contribute to proteinopathies. A deeper understanding of cellular toxicity and response mechanisms and their links to pathogenesis may promote the development of strategies for both disease prevention and treatment. 

Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony

This special issue of FEMS Yeast Research is dedicated to the memory of Professor Stefan Hohmann, one of the European pioneers of yeast molecular biology. Stefan was trained by one of the founders of yeast genetics and molecular biology, Professor Friedrich Zimmermann at the University of Darmstadt. Following his graduation, Stefan did a post doc at the Katholieke Universiteit Leuven with Professor Johan Thevelein, another world leader in the field of yeast genetics and molecular biology. Stefan continued his European journey in Gothenburg, where he influenced yeast and systems biology significantly. In Sweden, he received early on a prestigious grant from the Swedish Research Council as Research Professor, and shortly after he was appointed as Professor at the University of Gothenburg, where he played an instrumental role in gathering a number of young yeast researchers and establishing a very strong yeast research environment, impressive both by the breadth and the depth of competences. Thus today, more than 25 years after Stefan’s arrival to Gothenburg, thanks to the seeds of science and leadership that he planted, there is a large and thriving research environment on yeast genetics, molecular biology, systems biology, and metabolic engineering. Similarly, Stefan also made substantial contributions to the development of yeast research in South Africa, where he spent extensive periods of time as visiting professor at the universities in Bloemfontein and Stellenbosch. Stefan’s research was focused on signal transduction events, stress responses, and transport proteins, primarily related to osmotic stress in Saccharomyces cerevisiae. He made many pioneering discoveries on the high osmolarity glycerol (HOG) pathway in yeast, a branched mitogen activated protein kinase (MAPK) signal transduction system that is conserved across eukaryotes. The HOG pathway is engaged in sensing osmotic stress and activating production of glycerol, which is an osmo-protectant, and with the clear inand outputs of the pathway it has served as a model for eukaryotic MAPK pathways. Several of his research papers on the HOG pathway and its interactions stand out as influential contributions to science. Stefan also made key discoveries on transport systems involved in osmoadaptation, in particular on the role and regulation of yeast aquaporins and aquaglyceroporins. Stefan maintained a long-standing interest in yeast metabolism, and his research greatly contributed to our understanding of sugar, glycerol, and trehalose metabolism, in particular how these metabolites contribute to stress resistance. This interest led him to study other important signaling pathways and protein kinases including Snf1, which is the AMP-activated kinase of yeast. Although trained as a classical molecular biologist, Stefan was an early pioneer and supporter of systems biology. Stefan was one of the founders of the Yeast Systems Biology Network, which enabled coordination of new standards as well as leading to the foundation of several new research agendas that resulted in significant funding from both the EU and national governments in Europe. Professor Stefan Hohmann

Professor Stefan Hohmann (08.09.1956–02.07.2021)

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Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony

Professor Stefan Hohmann (08.09.1956–02.07.2021)