Identification of a MarR subfamily that regulates arsenic resistance genes

In this study, comprehensive analyses were performed to determine the function of an atypical MarR homolog in Achromobacter sp. As-55. Genomic analyses of Achromobacter sp. As-55 showed that this marR is located adjacent to an arsV gene. ArsV is a flavin-dependent monooxygenase that confers resistance to the antibiotic methylarsenite (MAs(III)), the organoarsenic compound roxarsone(III) (Rox(III)), and the inorganic antimonite (Sb(III)). Similar marR genes are widely distributed in arsenic-resistant bacteria. Phylogenetic analyses showed that these MarRs are found in operons predicted to be involved in resistance to inorganic and organic arsenic species, so the subfamily was named MarR ars . MarR ars orthologs have three conserved cysteine residues, which are Cys36, Cys37 and Cys157 in Achromobacter sp. As-55, mutation of which compromises the response to MAs(III)/Sb(III). GFP-fluorescent biosensor assays show that AdMarR ars (MarR protein of Achromobacter deleyi As-55) responds to trivalent As(III) and Sb(III) but not to pentavalent As(V) or Sb(V). The results of RT-qPCR assays show that arsV is expressed constitutively in a marR deletion mutant, indicating that marR represses transcription of arsV . Moreover, electrophoretic mobility shift assays (EMSA) demonstrate that AdMarR ars binds to the promoters of both marR and arsV in the absence of ligands and that DNA binding is relieved upon binding of As(III) and Sb(III). Our results demonstrate that AdMarR ars is a novel As(III)/Sb(III)-responsive transcriptional repressor that controls expression of arsV, which confers resistance to MAs(III), Rox(III) and Sb(III). AdMarR ars and its orthologs form a subfamily of MarR proteins that regulate genes conferring resistance to arsenic-containing antibiotics. IMPORTANCE In this study, a MarR family member, AdMarR ars was shown to regulate the arsV gene, which confers resistance to arsenic-containing antibiotics. It is a founding member of a distinct subfamily that we refer to as MarR ars , regulating genes conferring resistance to arsenic and antimony antibiotic compounds. AdMarR ars was shown to be a repressor containing conserved cysteine residues that are required to bind As(III) and Sb(III), leading to a conformational change and subsequent derepression. Here we show that members of the MarR family are involved in regulating arsenic-containing compounds.

Elemental Composition of Algae-Based Supplements by Energy Dispersive X-ray Fluorescence

The aim of this study is to evaluate the elemental composition of fifteen algae-based supplements commonly sold in the Portuguese market, by energy dispersive X-ray fluorescence. Despite the fact that the majority of Kelp samples were a good source of iodine, the levels observed might well contribute to an excess in the human body, which can cause dysfunction of the thyroid gland. Furthermore, the presence of lead in Sea spaghetti, Arame, Hijiki and Wakame caused a considerable risk to public health vis a vis possible ingestion of a high daily dose. Regarding arsenic, great variability was observed in all the samples with concentrations equal to or above 60 μg/g in the case of Arame, KelpJ and Hijiki. Although algae mainly accumulate organic arsenic, some also contain high levels of its inorganic form, as is commonly pointed out for Hijiki. Thus, regular ingestion of these supplements must also take into account the mentioned facts. There is no doubt that these supplements are also good sources of other nutrients, but the lack of accurate regulations and control should alert consumers to avoid indiscriminate use of these types of products.

Specifically designed amine functional group doped sludge biochar for inorganic and organic arsenic removal

Usages of hospital sludge as a biochar adsorbent for wastewater treatment plants were investigated. Microwave carbonization was used to carbonize the sludge and then chemically activated with ZnCl2 to increase surface area and porosity. A newly designed amine functional group’s doped Sludge Biochar Carbon (SBC) presents effective inorganic arsenic (As (III)) and organic arsenic (Dimethylarsinic Acid, DMA) adsorption in water. The pore volume, pore size distribution and specific surface area were determined by performing nitrogen adsorption-desorption measurements. The Fourier Transform Infrared of the SBC was recorded to study the functional groups at room temperature. The composition of SBC was further determined by X-ray Photoelectron Spectroscopy. In order to understand the effect of amine functional complexes on arsenic adsorption, the adsorption mechanism of As (III) and DMA on SBC surfaces modified with amine functional complexes was studied using Density Functional Theory (DFT). DFT results showed that both physical and chemical adsorption of As (III) and DMA on SBC surfaces occurred. The participation of amine functional complexes greatly promoted the surface activity of SBC surface and its adsorption capacity on arsenic. The physical adsorption energies of As (III) and DMA on SBC surface with amine functional complexes were − 38.8 and − 32.4 kJ mol− 1, respectively. The chemical adsorption energies of As (III) and DMA on SBC surface with amine functional complexes were − 92.9 and − 98.5 kJ mol− 1, respectively.

On the effect of salvarsan on blood clotting. Trost (Arch. f. Derm. u. Syph., 1922, Bd. 139)

In order to find out the effect of organic arsenic compounds in the form of salvarsan and its derivatives on blood clotting the author set a series of in vitro and in vivo experiments by the methods of Brkеrʹa and Schultz'a. These experiments convinced the author that organic arsenic compounds such as salvarsan already in minimal amounts cause in vitro clotting retardation.

Identification of a MarR subfamily that regulates arsenic resistance genes

In this study, comprehensive analyses were performed to determine the function of an atypical MarR homolog. Genomic analyses showed that this marR is located in an arsenic gene island in Achromobacter sp. As-55 adjacent to an arsV gene. ArsV is a flavin-dependent monooxygenase that confers resistance to the antibiotic methylarsenite (MAs(III)), the organoarsenic compound roxarsone(III) (Rox(III)), and the inorganic antimonite (Sb(III)). Similar marR genes are widely distributed in arsenic-resistant bacteria. Phylogenetic analyses showed that these MarRs are found in operons predicted to be involved in resistance to inorganic and organic arsenic species, so the subfamily was named MarRars. MarRars orthologs have three conserved cysteine residues, which are Cys36, Cys37 and Cys157 in Achromobacter sp. As-55, mutation of which compromises the response to MAs(III)/Sb(III). GFP-fluorescent biosensor assays show that AdMarRars (MarR protein of Achromobacter deleyi As-55) responds to trivalent As(III) and Sb(III) but not to pentavalent As(V) or Sb(V). The results of RT-qPCR assays show that arsV is expressed constitutively in a marR deletion mutant, indicating that marR represses transcription of arsV. Moreover, electrophoretic mobility shift assays (EMSA) demonstrate that AdMarRars binds to the promoters of both marR and arsV in the absence of ligands and that DNA binding is relieved upon binding of As(III) and Sb(III). Our results demonstrate that AdMarRars is a novel As(III)/Sb(III)-responsive transcriptional repressor that controls expression of arsV, which confers resistance to MAs(III), Roxarsone(III) and Sb(III). AdMarRars and its orthologs form a subfamily of MarR proteins that regulate genes conferring resistance to arsenic-containing antibiotics.

210 cases of relapsing fever baked by neosal-varsan

The issue of treating relapsing fever with organic arsenic compounds is 15-17 years old.

VALIDATION OF AN ANALYTICAL METHOD FOR THE DETERMINATION OF INORGANIC AND ORGANIC ARSENIC IN FISH SAUCE BY HYDRIDE GENERATION ATOMIC ABSORPTION SPECTROSCOPY

The validation of an analytical method was carried out for the determination of arsenic components in fish sauce by HG-AAS. The total arsenic content (tAs) was analyzed after digesting the sample by dry and wet combined digestion method in a Teflon flask at 450 °C and then reducing As (V) to As (III) with a mixture of reducing agents KI/ascorbic acid. For inorganic arsenic content (iAs), the sample was hydrolyzed with HCl solution for 14 hours, converted As (V) to As (III), then reacted with hydrazine 1.5%. Extracted in CHCl3 and re-extracted in HNO3. The organic arsenic content (oAs) was calculated by the difference tAs and iAs. Determined the linear concentration range 2 - 30 μg/L and the standard curve was y = 0.0128x + 0.0007 with R² = 0.9996 at the concentration range 2 - 20 μg/L. LODs, LOQs for total and inorganic arsenic contents were found and all they were 0.015 mg/L and 0.05 mg/L, respectively. For total arsenic, the recovery efficiencies on the organic arsenic standard and inorganic arsenic standard all ranged from 81 to 109%;...

Synthetic Iowaite Can Effectively Remove Inorganic Arsenic from Marine Extract

For the removal of arsenic from marine products, iowaite was prepared and investigated to determine the optimal adsorption process of arsenic. Different chemical forms of arsenic (As(III), As(V)) with varying concentrations (0.15, 1.5, 5, 10, 15, and 20 mg/L) under various conditions including pH (3, 5, 7, 9, 11) and contact time (1, 2, 5, 10, 15, 30, 60, 120, 180 min) were exposed to iowaite. Adsorption isotherms and metal ions kinetic modeling onto the adsorbent were determined based on Langmuir, Freundlich, first- and second-order kinetic models. The adsorption onto iowaite varied depending on the conditions. The adsorption rates of standard solution, As(III) and As(V) exceeded 95% under proper conditions, while high complexity was noted with marine samples. As(III) and As(V) from Mactra veneriformis extraction all decreased when exposed to iowaite. The inclusion morphology and interconversion of organic arsenic limit adsorption. Iowaite can be efficiently used for inorganic arsenic removal from wastewater and different marine food products, which maybe other adsorbent or further performance of iowaite needs to be investigated for organic arsenic.

Coenzyme Q10 protected against arsenite and enhanced the capacity of 2,3-dimercaptosuccinic acid to ameliorate arsenite-induced toxicity in mice

Background Arsenic poisoning affects millions of people. The inorganic forms of arsenic are more toxic. Treatment for arsenic poisoning relies on chelation of extracellularly circulating arsenic molecules by 2,3-dimecaptosuccinic acid (DMSA). As a pharmacological intervention, DMSA is unable to chelate arsenic molecules from intracellular spaces. The consequence is continued toxicity and cell damage in the presence of DMSA. A two-pronged approach that removes extracellular arsenic, while protecting from the intracellular arsenic would provide a better pharmacotherapeutic outcome. In this study, Coenzyme Q10 (CoQ10), which has been shown to protect from intracellular organic arsenic, was administered separately or with DMSA; following oral exposure to sodium meta-arsenite (NaAsO2) – a very toxic trivalent form of inorganic arsenic. The aim was to determine if CoQ10 alone or when co-administered with DMSA would nullify arsenite-induced toxicity in mice. Methods Group one represented the control; the second group was treated with NaAsO2 (15 mg/kg) daily for 30 days, the third, fourth and fifth groups of mice were given NaAsO2 and treated with 200 mg/kg CoQ10 (30 days) and 50 mg/kg DMSA (5 days) either alone or in combination. Results Administration of CoQ10 and DMSA resulted in protection from arsenic-induced suppression of RBCs, haematocrit and hemoglobin levels. CoQ10 and DMSA protected from arsenic-induced alteration of WBCs, basophils, neutrophils, monocytes, eosinophils and platelets. Arsenite-induced dyslipidemia was nullified by administration of CoQ10 alone or in combination with DMSA. Arsenite induced a drastic depletion of the liver and brain GSH; that was significantly blocked by CoQ10 and DMSA alone or in combination. Exposure to arsenite resulted in significant elevation of liver and kidney damage markers. The histological analysis of respective organs confirmed arsenic-induced organ damage, which was ameliorated by CoQ10 alone or when co-administered with DMSA. When administered alone, DMSA did not prevent arsenic-driven tissue damage. Conclusions Findings from this study demonstrate that CoQ10 and DMSA separately or in a combination, significantly protect against arsenic-driven toxicity in mice. It is evident that with further pre-clinical and clinical studies, an adjunct therapy that incorporates CoQ10 alongside DMSA may find applications in nullifying arsenic-driven toxicity.