High Doses Of Arsenic Research Articles

The arsenic eaters of Styria, the toxicophagi

Introduction From at least the fifteenth to late nineteenth centuries, peasants in the Austrian province of Styria ate up to several hundred milligrams of arsenic trioxide or sulfide daily or weekly for periods up to a number of years. Taking these doses of arsenic was believed to increase muscular power and enhance the beauty and sexual attractiveness of peasant girls. There do not appear to be contemporaneous records of the known consequences of chronic arsenic exposure. The historical records of arsenic eating there are reviewed and appear to be valid. The benefits are subjective judgements by arsenic eaters. The lack of objective reports of the anticipated external and internal clinical and pathological effects of arsenic poisoning depends on a smaller number of clinical accounts and autopsy reports and the general medical literature of those times, so it is weaker, but it is consistent. Can the claimed benefits of arsenic eating and the apparent absence of harmful toxic effects be true? Why the arsenic eaters did not show the well-known consequences of prolonged exposure to high doses of arsenic is not known. Possible explanations include increases in detoxifying metabolism in the consumers due to induced genomic changes and selection in people and in the gut microbiome, as shown in other populations. Whether these effects would suffice to protect people against their high doses of arsenic has not been explored. Conclusion Although the nature and mechanisms of arsenic toxicity have been extensively described, much still remains to be discovered.

Arsenic-induced neurotoxicity in patients with acute promyelocytic leukaemia.

Arsenic trioxide is an essential component of therapy for acute promyelocytic leukaemia (APL) and is currently dosed on actual body weight with no upper limit. Arsenic-induced neurotoxicity is a well-recognised complication; however, there is uncertainty about its relationship to arsenic dose and obesity. We conducted a large multicentre retrospective study of 487 patients with APL treated with arsenic-based therapy across 23 sites in Australia from 2008 to 2023. The primary outcome was incidence of neurotoxicity, and secondary outcomes included relationship of neurotoxicity to obesity and cumulative arsenic dose. Any-grade neurotoxicity occurred in 113 (23%) patients, predominantly peripheral neuropathy (91%). Most events were grade 1-2 severity (85%), with grade 3 events in 12% and grade 4-5 in 3%. The incidence of neurotoxicity increased with BMI (non-obese: 16%, obesity class I: 25%, obesity class II-III: 41%; p < 0.001). On univariable analysis, obesity class I (OR 1.81, p = 0.036), obesity class II-III (OR 3.93, p < 0.001), weight >100 kg (OR 2.72, p < 0.001), daily arsenic trioxide dose >15 mg (OR 5.05, p < 0.001) and cumulative induction dose >500 mg (OR 3.95, p < 0.001) were all significantly associated with neurotoxicity. Obesity class II-III and induction dose >500 mg remained significant on multivariable analysis. Our study highlights the strong association between BMI, arsenic trioxide dose and neurotoxicity. Pre-emptive dose reductions should be considered for obese patients receiving high doses of arsenic.

Occupational arsenic exposure and genitourinary cancer: systematic review and meta-analysis.

Existing evidence suggests that ingestion of high doses of arsenic through drinking water is associated with an increased risk of genitourinary cancers, while systematic evidence on workers exposed to arsenic is lacking. The aim of this study is to systematically review the evidence on the association between occupational exposure to arsenic and genitourinary cancer risk and mortality. A systematic literature search was carried out on Pubmed, Web of Science and Embase by including cohort and case-control studies. Study-specific relative risks (RRs) and the corresponding 95% confidence intervals (CIs) were pooled using Mandel-Paule random-effects model. Contour-enhanced funnel plot and Egger's test were used to assess the occurrence of publication bias. A total of 17 studies were included in the meta-analysis, 7 on cancer incidence (n = 161,244 individuals) and 10 on cancer mortality (n = 91,868). Most of them were cohort (71%) and industry-based studies (59%). The meta-analysis failed to detect an increased risk of genitourinary cancers among workers exposed to arsenic, except for a suggestive but not significant positive association for bladder cancer incidence (RR: 1.26, 95% CI: 0.89, 1.80), although this estimate was based on only three studies. No compelling evidence of publication bias was found (P = 0.885). Our findings did not show an association between occupational exposure to arsenic and genitourinary cancers, although further high-quality studies with detailed exposure assessment at the individual level are needed to clarify this relationship.

Arsenic activates STAT3 signaling during the transformation of the human bronchial epithelial cells

Arsenic (As3+), a metalloid abundant in environment, is classified as a group I carcinogen associated with several common human cancers, including cancers in lung, skin, bladder, liver, and prostate (Wei et al., 2019). The mechanisms of As3+-induced carcinogenesis had been extensively studied, and different mechanisms might be involved in different types of cancer (Wei et al., 2019). Recent studies showed that exposure to a high dose of arsenic is able to induce lung cancer. Meanwhile, prolonged exposure to a low concentration of arsenic can increase the risk of lung cancer also (Liao et al., 2009; Fernández et al., 2012). Emerging evidence indicated that prolonged exposure to arsenic promotes malignant transformation and some of the transformed cells have cancer-stem-like properties (Ngalame et al., 2014). In the present report, we revealed that exposure to As3+ for short time period inhibited tyrosine-705 phosphorylation of signal transducer and activator of transcription 3 (pSTAT3Y705) and induced Src homology region 2 domain-containing phosphatase-1 (SHP-1) in bronchial epithelial cell line, BEAS-2B. In addition, we found that long term exposure of the cells to As3+ activates phosphorylation of STAT3 at serine 727 (pSTAT3S727) as well as pSTAT3Y705. Moreover, As3+ is able to induce the expression of miRNA-21 (miR-21) and decrease the expression of PDCD4. Taken together, our data suggest that activation of STAT3 and induction of miR-21 are important contributing factors to the reduced expression of PDCD4, which may play significant role in As3+-induced transformation of BEAS-2B cells.

Amerigo Filia (1873-1925) and the first School of Pediatrics in the island of Sardinia

Amerigo Filia was born on July 18, 1873, in Sassari, Sardinia, Italy. After attaining his Medicine degree at the University of Turin in 1900, he went to Rome to study Pediatrics at the School of Pediatrics directed by Professor Luigi Concetti. His academic career began in Sassari when he was appointed as teacher of Pediatrics in 1911, becoming Full Professor in 1917, Dean of the School of Medicine and Surgery in 1918 and, finally, Rector of the University in 1919. He distinguished himself as the founder of the Pediatric Clinic and the School of Pediatrics in Sassari, both being the first ones in Sardinia, and as the promoter of the restoration of the front of the main building of the University of Sassari (“Palazzo dell’Universita”), as well as of new buildings to host Scientific Institutes and Clinics. Moreover, in 1923, he succeeded in preventing the suppression of Sassari University as a consequence of the “Gentile” reform. As documented by his scientific publications, Filia’s research activity included both experimental and clinical studies focusing on the renal excretion of high dose of arsenic, the effects of Lactobacilli in infantile enteritis, as well as on renal tuberculosis and pulmonary echinococcosis in children. Amerigo Filia died suddenly on December 21, 1925, in Rome, where he was participating in a university competition as a committee member.

Genome Sequence of Brevundimonas sp., an Arsenic Resistant Soil Bacterium

Brevundimonas sp. is a bacteria able to grow in metal(loid) contaminated soil from Puchuncaví Valley, central Chile. This study has isolated a bacterial strain capable of growth under high doses of arsenic (As) (6000 mg L−1), and a draft genome sequence was generated. Additionally, real-time PCR was performed to examine the effect of As on some genes related to As resistance. Results demonstrated a total of 3275 predicted annotated genes with several genes related to the ars operon, metal(loid) resistance-related genes, metal efflux pumps, and detoxifying enzymes. Real-time PCR showed that the arsB involved in the efflux of As was down-regulated, whereas arsR, arsH, and ACR3 did not show differences with the addition of As. Our study provides novel evidence of diverse As regulating systems in tolerant bacteria that will lead to a better understanding of how microorganisms overcome toxic elements and colonize As contaminated soils and to the possible use of their specific properties in bioremediation.

Изучение токсичности мышьяксодержащих соединений, выделенных из бурой водоросли Saccharina japonica, на лабораторных животных

The ability of various marine organisms, especially algae and invertebrates, to accumulate arsenic in high concentrations can pose a threat to public health when consumed. It is known from the literature that inorganic arsenic compounds (arsenites and arsenates) are the most toxic, in comparison with methylated forms of the element, and especially with complex organic compounds (arsenobetain, arsenocholine, tetramethylarsonium, arsenoriboses), which are considered non-toxic for live organisms. Monitoring of safety indicators of aquatic biological resources in the main commercial basins of the Russian Federation has shown that the most common excess of total arsenic content is characteristic for algae. According to TR CU 021/2011, the total arsenic content in algae should be 5 mg / kg and the established norm without separation of organic and inorganic arsenic compounds creates a barrier to the rational use of seafood. In this regard, the justification of the norms for the content of inorganic arsenic in algae and the assessment of their toxicity is a very urgent problem. Study of the samples of commercial brown algae Saccharina (=Laminaria) japonica and its derivates with ICP-MS, HPLC–MS-ISP methods, the maximum permissible level of arsenic was found to be exceeded, but the most toxic inorganic forms made up from 6 to14 % of the total amount of arsenic in the raw material. Acute toxicity on laboratory animals (rats) was studied and the absence of toxic effects was shown when an oral suspension containing high doses of arsenic was administered. Repeated administration of the same substances to laboratory mice of the CD 1 line has shown no toxic effects even after multiple doses of arsenic isolated from algae.

Fumaric acids as a novel antagonist of TLR-4 pathway mitigates arsenic-exposed inflammation in human monocyte-derived dendritic cells

Exposure to environmentally relevant doses of arsenic has several harmful effects on the human immune system. In traditional Eastern medicines, nettle has been used as an anti-inflammatory agent to treat rheumatism and osteoarthritis. Fumaric acid (FA) as a major effective compound in nettle was chosen based on very accurate virtual screening to find antagonist for TLR4/MD structure. In this study, the in vitro therapeutic effects of FA on arsenic-exposed monocytes-derived dendritic cells (MDDCs) were evaluated. All the canonical functions of dendritic cells in bridging innate and adaptive immune system including phagocytosis and antigen-presenting capacity, and also cytokines secretion, were evaluated after exposure to arsenic/FA. FA profoundly over-expressed antigen-presenting capacity of MDDCs after exposure to arsenic through the upregulation of MHCιι. However, phagocytosis capacity of arsenic-exposed MDDCs is not compensated for, by treatment with FA. Arsenic up-regulates pro-inflammatory cytokines independents of TLR4 pathway. FA surprisingly mitigates the up-regulation of IL-1β and TNF-α but not TLR4 and NF-kB. Moreover, FA increases the viability of MDDCs even at a high dose of arsenic. Totally, FA reduced inflammatory factors induced by arsenic. This finding confirmed that nettle and other medicinal plants containing similar structures with FA could be further analyzed as valuable candidates for the reduction of drastic effects of arsenic in human immune systems.

A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway.

Arsenic is a toxic metal, which ultimately leads to cell apoptosis. ERK is considered a key transcriptional regulator of arsenic-induced apoptosis. Due to a few controversial issues about arsenic-mediated extracellular signal-regulated MAP kinases (ERK) signaling, a meta-analysis was performed. Subgroup analyses demonstrated that high doses (≥2 µmol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (<2 µmol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups. Long term exposure (>24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (≤24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2. Furthermore, normal cells exposed to arsenic exhibited higher production levels of Ras and p-ERK. Conversely, exposure of cancer cells to arsenic showed a lower level of production of Ras and p-ERK as well as higher level of p-ERK1 and p-ERK2 as compared to control group. Short-term exposure of normal cells to high doses of arsenic may promote ERK signaling pathway. In contrast, long-term exposure of cancer cells to low doses of arsenic may inhibit ERK signaling pathway. This study may be helpful in providing a theoretical basis for the diverging result of arsenic adverse effects on one hand and therapeutic mechanisms on the other concerning arsenic-induced apoptosis.

Arsenic exposure and prevalence of the varicella zoster virus in the United States: NHANES (2003-2004 and 2009-2010).

BackgroundArsenic is an immunotoxicant. Clinical reports observe the reactivation of varicella zoster virus (VZV) in people who have recovered from arsenic poisoning and in patients with acute promyelocytic leukemia that have been treated with arsenic trioxide.ObjectiveWe evaluated the association between arsenic and the seroprevalence of VZV IgG antibody in a representative sample of the U.S. population.MethodsWe analyzed data from 3,348 participants of the National Health and Nutrition Examination Survey (NHANES) 2003–2004 and 2009–2010 pooled survey cycles. Participants were eligible if they were 6–49 years of age with information on both VZV IgG and urinary arsenic concentrations. We used two measures of total urinary arsenic (TUA): TUA1 was defined as the sum of arsenite, arsenate, monomethylarsonic acid, and dimethylarsinic acid, and TUA2 was defined as total urinary arsenic minus arsenobetaine and arsenocholine.ResultsThe overall weighted seronegative prevalence of VZV was 2.2% for the pooled NHANES sample. The geometric means of TUA1 and TUA2 were 6.57 μg/L and 5.64 μg/L, respectively. After adjusting for age, sex, race, income, creatinine, and survey cycle, odds ratios for a negative VZV IgG result in association with 1-unit increases in natural log-transformed (ln)-TUA1 and ln-TUA2 were 1.87 (95% CI: 1.03, 3.44) and 1.40 (95% CI: 1.0, 1.97), respectively.ConclusionsIn this cross-sectional analysis, urinary arsenic was inversely associated with VZV IgG seroprevalence in the U.S. population. This finding is in accordance with clinical observations of zoster virus reactivation from high doses of arsenic. Additional studies are needed to confirm the association and evaluate causal mechanisms.CitationCardenas A, Smit E, Houseman EA, Kerkvliet NI, Bethel JW, Kile ML. 2015. Arsenic exposure and prevalence of the varicella zoster virus in the United States: NHANES (2003–2004 and 2009–2010). Environ Health Perspect 123:590–596; http://dx.doi.org/10.1289/ehp.1408731

IDENTIFICATION OF ARSENIC LEVELS1N SRI LANKAN GROUNDWATERS AND DEVGLO•PMENT OF LOW-COST ARSENIC REMOVAL METHO'DOLOGY

Arsenic. which is highly toxic to humans even at low concentrations is a dominant tracepollutant found in drinking water. Sri Lannkan standard (SLS 614,1983) for drinking water is 50ppb whereas WHO and proposed USEPA standard are 10 ppb. Arsenic originates both fromnatural and anthropogenic sources. Acute short-term exposure to high doses of arsenic can causeadverse health effects. Most commonly reported symptoms of chronic arsenic exposure areconjunctivitis, melanosis, hyperkeratosis and some other skin lesions. In severe cases, gangrenein the limbs has also been observedIn our region, Bangladesh is facing a severe pollution of drinking water due to arsenic. Thisarsenic derives from the geological strata underlying Bangladesh. The effect became dominantdue to large drops in groundwater levels. Due to Farakka darn, on the river Gangas in India,groundwater level is being lowered markedly during the dry season in the Northwestern andWestern regions of Bangladesh, exposing the dry sediment layer to oxidation. As a result, pyriteshave been dissolved in groundwater releasing arsenic into drinking water supplies.In Sri Lanka also groundwater consumption and construction of darns across rivers areincreasing. Within the last twenty years many large darns were constructed. Therefore highdrawdown of water table in downstream areas of these darns may lead to problems similar toBangladesh since the geological aspects are similar (pyrites are found in calcipyres and graphite-bearing veins in Sri Lanka (Cooray, 1984». Hence the problem may exist in Sri Lanka, thoughit is not reported yet. One reason for absence of such data is the lack of facilities to measurearsenic. Therefore in this research the basic data on arsenic levels and its spatial variation inaquifers in Sri Lanka are being obtained. To reliably analyze the arsenic level in water, a methodbased on the Hydride Generation -Atomic Adsorption Spectrometry (HG-AAS) is beingdeveloped at the Faculty of Engineering, University of Peradeniya.Most of the available arsenic treatment technologies perform well at high cost. It is important todevelop a low-cost treatment method for low-income countries. Presently SORAS method,introduced by a Switzerland-Bangladesh joint research group (Wegelin et al., 2000), is used athousehold level to treat drinking water. In this study a new low cost treatment method forarsenite, As (III) removal by sorption on laterite, has been researched. Laterite found abundantlyin South-western Sri Lanka contains iron. Mainly As (III) will be studied due to its high toxicity,mobility and solubility than arsenate, As (Y).Also as a part of this study, the adsorption behaviour of arsenite on goethite was studied. Whenreviewing past studies it was found that many studies have been carried out on arsenate removalusing goethite. There have been fewer experiments on arsenite removal. Almost 90% arseniteremoval could be achieved using goethite and the high removal was observed within the naturalpH range. This will lead to an efficient arsenite removal process from the natural water since nopH adjustment is needed.

Utility of arsenic-treated bird skins for DNA extraction

BackgroundNatural history museums receive a rapidly growing number of requests for tissue samples from preserved specimens for DNA-based studies. Traditionally, dried vertebrate specimens were treated with arsenic because of its toxicity and insect-repellent effect. Arsenic has negative effects on in vivo DNA repair enzymes and consequently may inhibit PCR performance. In bird collections, foot pad samples are often requested since the feet were not regularly treated with arsenic and because they are assumed to provide substantial amounts of DNA. However, the actual influence of arsenic on DNA analyses has never been tested.FindingsPCR success of both foot pad and body skin samples was significantly lower in arsenic-treated samples. In general, foot pads performed better than body skin samples. Moreover, PCR success depends on collection date in which younger samples yielded better results. While the addition of arsenic solution to the PCR mixture had a clear negative effect on PCR performance after the threshold of 5.4 μg/μl, such high doses of arsenic are highly unlikely to occur in dried zoological specimens.ConclusionsWhile lower PCR success in older samples might be due to age effects and/or DNA damage through arsenic treatment, our results show no inhibiting effect on DNA polymerase. We assume that DNA degradation proceeds more rapidly in thin tissue layers with low cell numbers that are susceptible to external abiotic influences. In contrast, in thicker parts of a specimen, such as foot pads, the outermost horny skin may act as an additional barrier. Since foot pads often performed better than body skin samples, the intention to preserve morphologically important structures of a specimen still conflicts with the aim to obtain optimal PCR success. Thus, body skin samples from recently collected specimens should be considered as alternative sources of DNA.

Modulation of DNA polymerase beta-dependent base excision repair in cultured human cells after low dose exposure to arsenite

Base excision repair (BER) is crucial for development and for the repair of endogenous DNA damage. However, unlike nucleotide excision repair, the regulation of BER is not well understood. Arsenic, a well-established human carcinogen, is known to produce oxidative DNA damage, which is repaired primarily by BER, whilst high doses of arsenic can also inhibit DNA repair. However, the mechanism of repair inhibition by arsenic and the steps inhibited are not well defined. To address this question we have investigated the regulation of DNA polymerase β (Pol β) and AP endonuclease (APE1), in response to low, physiologically relevant doses of arsenic. GM847 lung fibroblasts and HaCaT keratinocytes were exposed to sodium arsenite, As(III), and mRNA, protein levels and BER activity were assessed. Both Pol β and APE1 mRNA exhibited significant dose-dependant down regulation at doses of As(III) above 1 μM. However, at lower doses Pol β mRNA and protein levels, and consequently, BER activity were significantly increased. In contrast, APE1 protein levels were only marginally increased by low doses of As(III) and there was no correlation between APE1 and overall BER activity. Enzyme supplementation of nuclear extracts confirmed that Pol β was rate limiting. These changes in BER correlated with overall protection against sunlight UV-induced toxicity at low doses of As(III) and produced synergistic toxicity at high doses. The results provide evidence that changes in BER due to low doses of arsenic could contribute to a non-linear, threshold dose response for arsenic carcinogenesis.

Arsenic: In Search of an Antidote to a Global Poison

Arsenic. No other element has such a complex and variegated past. As early as 500 B.C. the ancients knew about arsenic, whose name comes from the Greek word for potent. Through the centuries, this “king of poisons” was a common means of homicide. And yet, arsenic’s image has not always been so morbid. People in the Middle Ages wore arsenic amulets around their necks to ward off the bubonic plague, and women in Victorian times applied arsenic compounds to their faces to whiten their complexions. Hippocrates, the father of western medicine, recorded arsenic’s usefulness as a topical remedy for skin ulcers.

Proteinated Elemental Selenium Potentiates Anti-Tumor Effect of Ionizing Radiation and Chemotherapeutic Agents but Is Only Minimally Affected by Drug Resistance Mechanisms.

Elemental selenium generated by the photobleaching of selone photosensitizers combined with serum albumin and lipoproteins to generate conjugates that were highly cytotoxic to leukemia and selected solid tumor cells but well tolerated by normal CD34-positive hematopoietic cells. Selenium-protein conjugates were internalized by an endocytotic mechanism and localized in lysosomes. Internalized conjugates caused an extremely rapid and extensive (up to 80% in 1 hour) depletion of intracellular glutathione (GSH), the oxidation of 2′,7′-dichlorofluorescin, a loss of plasma membrane asymmetry, a breakdown of mitochondrial potential, and the activation of several caspases. Additive or synergistic anti-tumor effects were obtained when Se-protein conjugates were used in combination with ionizing radiation, melphalan, amifostine, 4-hydroperoxycyclophosphamide, edelfosine, buthionine sulfoximine, or moderate doses of arsenic (III) oxide. For example, pretreatment with a nontoxic dose of amifostine enhanced the depletion of L1210 leukemia cells from 7 log to 12 log (depletions in excess of 6 log estimated from linear extrapolations of survival curves) while the yield of normal CD34-positive cells remained at 100%. Antagonistic interactions were obtained with simultaneously applied cisplatin or very high doses of arsenic (III) oxide. The antagonistic interaction with cisplatin probably reflected a competition of cisplatin and selenium for the same binding site at or near cysteine-34 of albumin. Melphalan-resistant L1210/L-PAM1 leukemia cells (elevated intracellular GSH) were more sensitive to Se-protein conjugates than wild-type cells because of an unexpected increase in conjugate uptake by mutant cells. Cisplatin-resistant H69/CDDP cells (elevated GSH, metallothioneine, glutathione-S-transferase-pi) were slightly more sensitive than wild-type cells. Cisplatin-resistant PC14/CDDP cells (reduced drug uptake) and adriamycin-resistant HL-60/ADR cells (MRP-mediated efflux) were slightly less sensitive than the corresponding wild-type cells. In the latter cases, the reduced sensitivity of mutant tumor cells correlated with reduced conjugate uptake and/or higher intracellular GSH levels. Taken together, the above results suggest that compounds modeled after our Se-protein conjugates may prove useful for the systemic therapy of leukemia and selected solid tumors. Supported by CA77387, MACC Fund, Children's Hospital Foundation, and Wisconsin Breast Cancer Showhouse for a Cure.

Arsenic essentiality: A role affecting methionine metabolism

AbstractAlthough there is no known biological function of arsenic, considerable evidence suggests that arsenic has a physiological role related to methionine metabolism. In early studies using amino acid‐based diets, it was found that arsenic deprivation had little effect on growth in rats fed adequate methionine. However, in rats fed suboptimal methionine, arsenic deprivation resulted in a significant reduction in body weight. Other studies showed that feeding methyl depletors caused severe signs of arsenic deprivation. Because it was found that alteration in methionine status or methyl metabolism affected signs of arsenic deprivation, and that many of these signs were related to methionine or methyl metabolism, it was hypothesized that arsenic has a physiological role affecting methionine metabolism. In animal studies testing this hypothesis, it was shown that arsenic deprivation reduces the hepatic concentration of S‐adenosylmethionine. Additionally, arsenic status affects DNA methylation in animal and cell culture models; very low or high doses of arsenic, compared with control amounts, result in an apparent hypomethylation of DNA. Because global DNA hypomethylation is associated with an increased incidence of cancer, we tested whether dietary arsenic (deficient, adequate, or excess; 0, 0.5 or 50 μg arsenic/g diet, respectively) would affect the formation of aberrant crypts in rats treated with the carcinogen dimethylhydrazine. Aberrant crypts are preneoplastic lesions that have been associated with colon carcinomas. More aberrant crypts were observed in rats fed the high amount of dietary arsenic compared to those fed adequate arsenic. The number of aberrant crypts in the arsenic‐deprived group also tended to be higher than those found in rats fed adequate arsenic. Thus, many findings indicate that arsenic plays a role in methionine/methyl metabolism; however, the site of action of arsenic remains unknown. Possibly, arsenic is instrumental in maintaining the metabolic pool of S‐adenosylmethionine. These results show that compared to controlled amounts, having too little or too much arsenic in the diet is harmful. That is, there is an amount of dietary arsenic that is not only not harmful, but beneficial. J. Trace Elem. Exp. Med. 16:345–355, 2003. Published 2003 Wiley‐Liss, Inc.

Sensitivity of wild cotton rats (Sigmodon hispidus) to the immunotoxic effects of low-level arsenic exposure.

Arsenic is a ubiquitous contaminant of many toxic waste sites around the country and experimental animal trials have indicated that arsenic may be immunotoxic to laboratory rodents. Because wild rodents such as the herbivorous cotton rat (Sigmodon hispidus) reside on many of these toxic waste sites, we explored the sensitivity of their immune systems to oral exposures of environmentally relevant concentrations of inorganic arsenic. We exposed adult male cotton rats (n = 36) to either 0 (controls), 5 (low dose), or 10 (high dose) ppm sodium arsenite in drinking water for 6 weeks. Daily food intake decreased in a dose-dependent manner, ranging from an average of 10.03 +/- 0.45 in the high-dose group to 11.27 +/- 0.42 (SE) g/animal/day in the control group. Mass of testes in the low-dose group increased significantly compared to controls, but there was no difference between the high-dose and control groups. Masses of liver, kidney, adrenals, popliteal lymph nodes, spleen, epididymides, and seminal vesicles and selected hematological parameters were unaffected by arsenic exposure. In vivo cell-mediated immunity, as measured by a phytohemagglutinin-hypersensitivity response to an intradermal challenge, was suppressed 30% in the low-dose group compared to controls; however, responses of those receiving a high dose of arsenic were similar to controls. Arsenic treatment did not have a measurable impact on lymphoproliferative responses of cultured splenocytes to the mitogens Concanavalin A and Pokeweed mitogen, or to the lymphokine interleukin-2. We also observed no impact of low-level arsenic exposure on macrophage phagocytic activity and tumoricidal activity of lymphokine-activated killer cells in vitro. It is possible that malnutrition caused by decreased food intake may eventually lead to atrophy of lymphoid organs and render animals more susceptible to environmental pathogens. However, direct effects of low-level arsenic exposure on immune function of cotton rats was minimal (a moderate depression in the in vivo cell-mediated immunity assay) and may not be clinically relevant with regard to susceptibility to disease in the wild.

High energy As ion implantation to GaAs

Over the last few years there have been many studies of GaAs layers grown in the temperature range from 180°C to 300°C called LT-GaAs. These studies were motivated by the potential applications of that material in microwave and fast optoelectronic devices. Annealed LT-GaAs layers have interesting electrical properties including high resistivity and short photocarrier lifetime connected with the nonstoichiometry of that material. However, it is still not clear whether arsenic antisite point defects or arsenic precipitates formed during annealing cause these interesting properties of LT GaAs.A second method of creating highly nonstoichiometric GaAs beside low temperature MBE growth is implantation with a high dose of arsenic. This method first applied two years ago showed that 200 keV arsenic ion implantation also leads to semi-insulating properties and that successive post-implantation annealing results in arsenic precipitate formation, similar to that observed in LT GaAs. Recently, more elaborate studies concerning photocarrier lifetime, resistivity, mobility and some structural characteristics were performed on GaAs implanted with high energy arsenic ions.

A simple model for dry oxidation of silicon ion implanted with high doses of arsenic

A simple model for dry oxidation of silicon ion implanted with high doses of arsenic

Anomalous oxidation rate of silicon implanted with very high doses of arsenic

An anomalous increase in oxidation rate was observed during low-temperature thermal oxidation of very high dose (5×1016, 7×1016/cm2) As+ ion implanted silicon. Oxidation of Si at 850 °C was faster than that at 950 °C. This effect was attributed to the snowplowing of arsenic (which was more pronounced at lower temperatures) creating a glassy Si-O-As layer near the Si-SiO2 interface.