Potential value and mechanism of Rosa roxburghii tratt juice on pro-inflammatory responses in peripheral blood of patients with arsenic poisoning.

Increasing evidence supports the role of arsenic in dysregulated immune and inflammation responses, while, safe and effective treatments have not been fully examined. Rosa roxburghii Tratt (RRT), a traditional Chinese edible fruit with potential immunoregulatory activities, was considered as a dietary supplement to explore its protective effects and possible mechanism in arsenic-induced dysregulated inflammation responses. We enrolled 209 arsenicosis patients and 41 controls to obtain baseline data, including the degree of arsenic poisoning prior to the RRT juice (RRTJ) intervention. Then, based on criteria of inclusion and exclusion and the principle of voluntary participation, 106 arsenicosis patients who volunteered to receive treatment were divided into RRTJ (n = 53) and placebo (n = 53) groups randomly. After three months follow-up, 89 subjects (46 and 43 of the RRTJ and placebo groups, respectively) completed the study and were examined for the effects and possible mechanisms of RRTJ on the Th17 cells-related pro-inflammatory responses in peripheral blood mononuclear cells (PBMCs). The PBMCs had higher levels of Th17 and Th17-related inflammatory cytokines IL-17, IL-6, and RORγt. Furthermore, the gene expressions of STAT3 and SOCS3 in PBMCs increased and decreased, respectively. Conversely, RRTJ decreased the number of Th17 cells, secretion of IL-17, IL-6, RORγt, and relative mRNA levels of STAT3, and increased the transcript levels of SOCS3. This study provides limited evidence that possible immunomodulatory effects of RRTJ on the critical regulators, IL-6 and STAT3, of the Th17 cells in arsenicosis patients, which indicated that IL-6/STAT3 pathway might appear as a potential therapeutic target in arsenicosis.

Environmental exposure of arsenic and fluoride and their combined toxicity: A recent update.

Environmental exposure to arsenic (As) and fluoride (F) in the recent year has been increased because of excessive use of naturally contaminated ground water. Surface water is also regularly contaminated with these elements in various industrial areas. Arsenicosis and fluorosis upon individual exposure of As and F are reported in many studies. A syndrome of endemic As poisoning and fluorosis occurs during concurrent exposure of As and F. Previous reports showed synergistic, antagonistic and independent effects of these two compounds, although few recent reports also revealed antagonistic effects after co-exposure. Interaction during intestinal absorption and influence of F on As metabolism might be the cause of antagonism. The synergism/antagonism is thought to depend on the dose and duration of the co-exposure. However, the detailed mechanism is still not fully understood and needs further studies. Removal technologies of As and F from contaminated water is available but removal of such contaminants from food is yet to be developed. Antioxidants are useful to mitigate the toxic effects of As and F. This review focused on the effect of co-exposure, amelioration as well as removal techniques of As and F.

Treatment of lead and arsenic poisoning in anuric patients - a case report and narrative review of the literature.

BACKGROUND: Heavy metal poisoning can cause debilitating illness if left untreated, and its management in anuric patients poses challenges. Literature with which to guide clinical practice in this area is rather scattered. CASE PRESENTATION: We present a case of symptomatic lead and arsenic poisoning from use of Ayurvedic medicine in a 28-year-old man with end-stage kidney disease on chronic hemodialysis. We describe his treatment course with chelating agents and extracorporeal blood purification, and review the relevant literature to provide general guidance. CONCLUSION: Cumulative clinical experience assists in identifying preferred chelators and modalities of extracorporeal blood purification when managing such patients. However, a larger body of real-world or clinical trial evidence is necessary to inform evidence-based guidelines for the management of heavy metal poisoning in anuric patients.

Arsenic Exposure, Assessment, Toxicity, Diagnosis, and Management: Guidance for Occupational and Environmental Physicians.

: Arsenic is ubiquitous in the environment and human exposure can occur from multiple possible routes including diet. Occupational medicine physicians asked to evaluate workers with elevated urine arsenic levels may be unaware that many sources of arsenic exposure are not work related. In this paper, we address arsenic exposure sources and pathways, adverse health effects of arsenic exposure and those subpopulations at increased risk, and the evaluation and treatment of those exposed to elevated arsenic levels.

Application of ICP-MS and HPLC-ICP-MS for diagnosis and therapy of a severe intoxication with hexavalent chromium and inorganic arsenic.

ICP-MS and HPLC-ICP-MS were applied for diagnosis and therapeutic monitoring in a severe intoxication with a liquid containing hexavalent chromium (Cr(VI)) and inorganic arsenic (iAs). In this rare case a liver transplantation of was considered as the only chance of survival. We developed and applied methods for the determination of Cr(VI) in erythrocytes and total chromium (Cr) and arsenic (As) in blood, plasma, urine and liver tissue by ICP-MS. Exposure to iAs was diagnosed by determination of iAs species and their metabolites in urine by anion exchange HPLC-ICP-MS. Three days after ingestion of the liquid the total Cr concentrations were 2180 and 1070µg/L in whole blood and plasma, respectively, and 4540µg/L Cr(VI) in erythrocytes. The arsenic concentration in blood was 206µg/L. The urinary As species concentrations were <0.5, 109, 115, 154 and 126µg/L for arsenobetaine, As(III), As(V), methylarsonate (V) and dimethylarsinate (V), respectively. Total Cr and As concentrations in the explanted liver were 11.7 and 0.9mg/kg, respectively. Further analytical results of this case study are tabulated and provide valuable data for physicians and toxicologists.

The health effects of exposure to arsenic-contaminated drinking water: a review by global geographical distribution.

Chronic arsenic exposure through drinking water has been a vigorously studied and debated subject. However, the existing literature does not allow for a thorough examination of the potential regional discrepancies that may arise among arsenic-related health outcomes. The purpose of this article is to provide an updated review of the literature on arsenic exposure and commonly discussed health effects according to global geographical distribution. This geographically segmented approach helps uncover the discrepancies in the health effects of arsenic. For instance, women are more susceptible than men to a few types of cancer in Taiwan, but not in other countries. Although skin cancer and arsenic exposure correlations have been discovered in Chile, Argentina, the United States, and Taiwan, no evident association was found in mainland China. We then propose several globally applicable recommendations to prevent and treat the further spread of arsenic poisoning and suggestions of future study designs and decision-making.

White phosphorus burns and arsenic inhalation: a toxic combination.

White phosphorus is a common industrial and military compound, which can cause severe thermal and chemical burns beyond what would be predicted from body surface area alone. The authors present a rare case of a 45-year-old male patient who suffered white phosphorus burns combined with arsenic inhalation because of an industrial accident. The presented case is used to review the history and the toxicities of these chemicals as well as current methods of treatment. A literature review was performed to summarize the current knowledge of white phosphorus burns, as well as arsenic poisoning, and no similar case reports of the two combined were found. The patient ultimately recovered and was discharged, though with significant chronic complications. This case highlights the risk of burns and inhalation injury present in industrial manufacturing jobs, as well as the potential severity of these conditions. The systemic effects of chemicals absorbed across burned skin and via inhalation were the main contributors to our patient's severe illness, and required more intensive treatment than the burns themselves. Arsenic toxicity is rare and could easily have been missed without the appropriate patient history.

Arsenic-mediated activation of the Nrf2-Keap1 antioxidant pathway.

Arsenic is present in the environment and has become a worldwide health concern due to its toxicity and carcinogenicity. However, the specific mechanism(s) by which arsenic elicits its toxic effects has yet to be fully elucidated. The transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) has been recognized as the master regulator of a cellular defense mechanism against toxic insults. This review highlights studies demonstrating that arsenic activates the Nrf2-Keap1 antioxidant pathway by a distinct mechanism from that of natural compounds such as sulforaphane (SF) found in broccoli sprouts or tert-butylhyrdoquinone (tBHQ), a natural antioxidant commonly used as a food preservative. Evidence also suggests that arsenic prolongs Nrf2 activation and may mimic constitutive activation of Nrf2, which has been found in several human cancers due to disruption of the Nrf2-Keap1 axis. The current literature strongly suggests that activation of Nrf2 by arsenic potentially contributes to, rather than protects against, arsenic toxicity and carcinogenicity. The mechanism(s) by which known Nrf2 activators, such as the natural chemopreventive compounds SF and lipoic acid, protect against the deleterious effects caused by arsenic will also be discussed. These findings will provide insight to further understand how arsenic promotes a prolonged Nrf2 response, which will lead to the identification of novel molecular markers and development of rational therapies for the prevention or intervention of arsenic-induced diseases. The National Institute of Environmental Health Science (NIEHS) Outstanding New Environmental Scientist (ONES) award has provided the opportunity to review the progress both in the fields of arsenic toxicology and Nrf2 biology. Much of the funding has led to (1) the novel discovery that arsenic activates the Nrf2 pathway by a mechanism different to that of other Nrf2 activators, such as sulforaphane and tert-butylhydroquinone, (2) activation of Nrf2 by chemopreventive compounds protects against arsenic toxicity and carcinogenicity both in vitro and in vivo, (3) constitutive activation of Nrf2 by disrupting Keap1-mediated negative regulation contributes to cancer and chemoresistance, (4) p62-mediated sequestration of Keap1 activates the Nrf2 pathway, and (5) arsenic-mediated Nrf2 activation may be through a p62-dependent mechanism. All of these findings have been published and are discussed in this review. This award has laid the foundation for my laboratory to further investigate the molecular mechanism(s) that regulate the Nrf2 pathway and how it may play an integral role in arsenic toxicity. Moreover, understanding the biology behind arsenic toxicity and carcinogenicity will help in the discovery of potential strategies to prevent or control arsenic-mediated adverse effects.

Application of hybrid blood purification treatment for severe acute arsine poisoning.

OBJECTIVE: Severe acute arsine poisoning (SAAP) complicated by multiple organ dysfunction syndrome is a critical clinical illness. The limited efficacy of conventional drug therapy prompted us to investigate the application of hybrid blood purification treatment (HBPT) to improve the prognosis in critically ill patients. The present manuscript describes a series of cases treated with HBPT. METHODS: Eleven SAAP subjects were enrolled. The study did not include a control group, because of ethical issues. On the basis of conventional therapy, HBPT (plasma exchange [PE] + continuous venovenous hemofiltration [CVVH]) was used to treat SAAP. PE was performed once a day for 5 days, and CVVH was performed after each session of PE for 7 days or more; HBPT treatment duration amounted to an average of 10 days (range 7-18 days). Arsenic was detected in blood and discarded liquid. Clinical indicators, laboratory parameters, and prognostic indicators were assessed. RESULTS: HBPT was smoothly implemented without obvious adverse reaction. It can continuously remove arsenic and terminate hemolysis in a time-dependent manner. HBPT also significantly improved the poor clinical manifestations and laboratory indicators of SAAP, leading to a low mortality. Ten patients were discharged because of improved conditions, and only 1 patient died. CONCLUSIONS: The early application of HBPT can improve the prognosis of SAAP. The advantage of HBPT is that it can integrate the characteristics of different blood purification technologies to maximize treatment efficacy.

[Arsine: an unknown industrial chemical toxic]. / L'arsine : un toxique chimique industriel peu connu.

Arsines family includes many compounds with various toxicities. Arsenic trihydride or arsine is the most toxic form of arsenic. Powerful haemolytic gas, it has never been used as a chemical weapon because its toxicity is not immediate and it is non persistent. However, cases of industrial poisoning with arsine are still identified in spite of a strict regulation at work. It is also identified as a potential toxic of chemical terrorism. This agent, of which the mechanism of action is still not well defined, is badly recognized because of intoxications rarity. However, fast detection means are available. Health professionals and especially those who are involved in piratox plan need to learn to recognize arsine intoxication (hematuria, oliguria, haemolytic anemia) in order to provide early, specific treatment and avoid damages.

Inadvertent poisoning of seven teenagers with monosodium methanearsonate.

INTRODUCTION: Monosodium methanearsonate (MSMA) is an organo-arsenic containing herbicide. There is scant information available concerning the toxicity of this chemical in humans. CASE REPORT: Seven male teenagers, 15-18 years of age, inadvertently used a MSMA herbicide as cooking oil to fry fish. All had early gastrointestinal (GI) symptoms. Whole blood arsenic concentrations ranged from 348 to 613 µg/L and initial urine levels ranged from 81 400 to 226 300 µg-arsenic/g-creatinine. They were all treated with dimercaprol for 1 day and succimer for 19 days. They were followed for 15-months and had no evidence of any serious toxicity. CONCLUSION: MSMA produces early GI symptoms and very high levels of arsenic in blood and urine, but no evidence of long-term toxicity.

Heavy metal poisoning: management of intoxication and antidotes.

Of the known elements, nearly 80% are either metals or metalloids. The highly reactive nature of most metals result in their forming complexes with other compounds such oxygen, sulfide and chloride. Although this reactivity is the primary means by which they are toxic, many metals, in trace amounts, are vital to normal physiological processes; examples include iron in oxygen transport, manganese and selenium in antioxidant defense and zinc in metabolism. With these essential metals toxicity occurs when concentrations are either too low or too high. For some metals there are no physiological concentrations that are beneficial; as such these metals only have the potential to cause toxicity. This chapter focuses on four of these: arsenic, mercury, lead and thallium.

Arsenical peripheral neuropathy.

A 49-year-old white man returned urgently to the UK after spending 3 months in Goa. He had a several week history of vomiting, weight loss, a widespread desquamating skin rash, and symptoms and signs of a progressive painful sensorimotor neuropathy. He had a mild normocytic anaemia and lymphopenia. Nerve conduction studies revealed a severe predominantly axonal large fibre sensorimotor neuropathy, confirmed on subsequent sural nerve biopsy. Once he had left Goa most of his symptoms started to rapidly settle although the neuropathic symptoms remained severe. Arsenic poisoning was suspected. A spot urine arsenic concentration was 300 microg/l, confirming the diagnosis. He was treated with chelation therapy. Deliberate arsenic poisoning was highly likely.