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Molecules (Basel, Switzerland) Dec 2021A sensitive electrochemical immunosensor was prepared for rapid detection of ASA based on arsanilic acid (ASA) monoclonal antibody with high affinity. In the preparation...
A sensitive electrochemical immunosensor was prepared for rapid detection of ASA based on arsanilic acid (ASA) monoclonal antibody with high affinity. In the preparation of nanomaterials, polyethyleneimine (PEI) improved the stability of the solution and acted as a reducing agent to generate reduced graphene oxide (rGO) with relatively strong conductivity, thereby promoting the transfer of electrons. The dual conductivity of rGO and silver nanoparticles (AgNPs) improved the sensitivity of the sensor. The synthesis of nanomaterials were confirmed by UV-Vis spectroscopy, X-ray diffraction, transmission electron microscopy and scanning electron microscopy. In the optimal experiment conditions, the sensor could achieve the detection range of 0.50-500 ng mL and the limit of detection (LOD) of 0.38 ng mL (S/N = 3). Moreover, the sensor exhibited excellent specificity and acceptable stability, suggesting that the proposed sensor possessed a good potential in ASA detection. Thus, the as-prepared biosensor may be a potential way for detecting other antibiotics in meat and animal-derived foods.
Topics: Arsanilic Acid; Biosensing Techniques; Electrochemical Techniques; Graphite; Immunoassay; Limit of Detection; Metal Nanoparticles; Nanocomposites; Polyethyleneimine; Reproducibility of Results; Silver
PubMed: 35011402
DOI: 10.3390/molecules27010172 -
Journal of Veterinary Science 2014This study was performed to assess the neurotoxic effects of methylmercury, arsanilic acid and danofloxacin by quantification of neural-specific proteins in vitro....
This study was performed to assess the neurotoxic effects of methylmercury, arsanilic acid and danofloxacin by quantification of neural-specific proteins in vitro. Quantitation of the protein markers during 14 days of differentiation indicated that the mouse ESCs were completely differentiated into neural cells by Day 8. The cells were treated with non-cytotoxic concentrations of three chemicals during differentiation. Low levels of exposure to methylmercury decreased the expression of GABAA-R and Nestin during the differentiating stage, and Nestin during the differentiated stage. In contrast, GFAP, Tuj1, and MAP2 expression was affected only by relatively high doses during both stages. Arsanilic acid affected the levels of GABAA-R and GFAP during the differentiated stage while the changes of Nestin and Tuj1 were greater during the differentiating stage. For the neural markers (except Nestin) expressed during both stages, danofloxacin affected protein levels at lower concentrations in the differentiated stage than the differentiating stage. Acetylcholinesterase activity was inhibited by relatively low concentrations of methylmercury and arsanilic acid during the differentiating stage while this activity was inhibited only by more than 40 μM of danofloxacin in the differentiated stage. Our results provide useful information about the different toxicities of chemicals and the impact on neural development.
Topics: Acetylcholinesterase; Animals; Arsanilic Acid; Cell Differentiation; Embryonic Stem Cells; Environmental Pollutants; Fluorescent Antibody Technique; Fluoroquinolones; Gene Expression Regulation; Methylmercury Compounds; Mice; Nerve Tissue Proteins; Neurons; Tetrazolium Salts; Thiazoles
PubMed: 24136205
DOI: 10.4142/jvs.2014.15.1.61 -
Poultry Science Dec 2006Three hundred seventy-five 63-d-old laying Japanese quail were randomly distributed into 3 experimental groups (125 birds per group) and fed the following diets for 40... (Randomized Controlled Trial)
Randomized Controlled Trial
Three hundred seventy-five 63-d-old laying Japanese quail were randomly distributed into 3 experimental groups (125 birds per group) and fed the following diets for 40 d, with 30 d on the experimental diets, followed by a 10-d withdrawal period: 1) control; 2) 50 mg of 4-arsanilic acid/kg of feed; and 3) 100 mg of 4-arsanilic acid/kg of feed. Each treatment consisted of 5 replicates of 25 birds. During the first 30 d of the experiment, all eggs were recorded, collected, individually weighed daily, and feed consumption was determined every 10 d. Five quail from each replicate in the experiment were euthanized by cervical dislocation at 0, 30, 35, and 40 d. Tissue samples from the liver, kidney, heart, gizzard, and the muscle on the breast and leg were collected for determination of As residue. The feces and eggs at 0, 30, 35, and 40 d of the experiment were selected for determination of As. Results showed that dietary inclusion of 50 and 100 mg/kg of 4-arsanilic acid significantly improved feed utilization and egg production, but the concentration of As in the tissues and feces in groups fed 4-arsanilic acid was higher than in control group. The results of the present study demonstrate that the use of organic As compounds as feed additives in diet is a matter for argument.
Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Arsanilic Acid; Arsenic; Bone and Bones; Coturnix; Diet; Dietary Supplements; Female; Gizzard, Avian; Kidney; Liver; Muscle, Skeletal; Myocardium; Oviposition; Ovum; Tissue Distribution
PubMed: 17135662
DOI: 10.1093/ps/85.12.2097 -
The Journal of Veterinary Medical... Feb 2011The study was designed to explore the toxic effects of arsanilic acid on piglet Sertoli cells. Sertoli cells were isolated from piglet testes using a two-step enzyme...
The study was designed to explore the toxic effects of arsanilic acid on piglet Sertoli cells. Sertoli cells were isolated from piglet testes using a two-step enzyme digestion followed by differential plating. Piglet Sertoli cells were cultured and classified into the following five groups: group A, the control without arsanilic acid treatment; group B, cultured with 5 µM arsanilic acid; group C, cultured with 50 µM arsanilic acid; group D, cultured with 0.5 mM arsanilic acid; and group E, cultured with 5 mM arsanilic acid. We found that Sertoli cell growth was inhibited by arsanilic acid at 0.5 mM compared with the control, group A. The oxidase activity of Sertoli cells was decreased by arsanilic acid at 0.5 mM as evidenced by the observations that arsanilic acid increased MDA content but decreased the SOD and GSH-Px activities of Sertoli cells. Moreover, 50 µM of arsanilic acid was observed to cause DNA damage in Sertoli cells. The results of our study suggest that exposure of Sertoli cells to arsanilic acid leads to induction of oxidative stress and inhibition of cell growth at a high concentration, while arsanilic acid causes DNA damage in Sertoli cells at a low concentration.
Topics: Animals; Arsanilic Acid; Cell Proliferation; Comet Assay; DNA; DNA Damage; Glutathione Peroxidase; Male; Malondialdehyde; Oxidoreductases; Sertoli Cells; Superoxide Dismutase; Swine
PubMed: 20944440
DOI: 10.1292/jvms.10-0236 -
Brain Sciences Nov 2019When vestibular function is lost, vestibular compensation works for the reacquisition of body balance. For the study of vestibular dysfunction and vestibular...
When vestibular function is lost, vestibular compensation works for the reacquisition of body balance. For the study of vestibular dysfunction and vestibular compensation, surgical or chemical labyrinthectomy has been performed in various animal species. In the present study, we performed chemical labyrinthectomy using arsanilic acid in mice and investigated the time course of vestibular compensation through behavioral observations and histological studies. The surgical procedures required only paracentesis and storage of 50 µL of -arsanilic acid sodium salt solution in the tympanic cavity for 5 min. From behavioral observations, vestibular functions were worst at 2 days and recovered by 7 days after surgery. Spontaneous nystagmus appeared at 1 day after surgery with arsanilic acid and disappeared by 2 days. Histological studies revealed specific damage to the vestibular endorgans. In the ipsilateral spinal vestibular nucleus, the medial vestibular nucleus, and the contralateral prepositus hypoglossal nucleus, a substantial number of c-Fos-immunoreactive cells appeared by 1 day after surgery with arsanilic acid, with a maximum increase in number by 2 days and complete disappearance by 7 days. Taken together, these findings indicate that chemical labyrinthectomy with arsanilic acid and the subsequent observation of vestibular compensation is a useful strategy for elucidation of the molecular mechanisms underlying vestibular pathophysiologies.
PubMed: 31752103
DOI: 10.3390/brainsci9110329 -
NeuroImage Feb 2021Unilateral damage to the inner ear results in an acute vestibular syndrome, which is compensated within days to weeks due to adaptive cerebral plasticity. This process,...
Unilateral damage to the inner ear results in an acute vestibular syndrome, which is compensated within days to weeks due to adaptive cerebral plasticity. This process, called central vestibular compensation (VC), involves a wide range of functional and structural mechanisms at the cellular and network level. The short-term dynamics of whole-brain functional network recruitment and recalibration during VC has not been depicted in vivo. The purpose of this study was to investigate the interplay of separate and distinct brain regions and in vivo networks in the course of VC by sequential [F]-FDG-PET-based statistical and graph theoretical analysis with the aim of revealing the metabolic connectome before and 1, 3, 7, and 15 days post unilateral labyrinthectomy (UL) in the rat. Temporal changes in metabolic brain connectivity were determined by Pearson's correlation (|r| > 0.5, p < 0.001) of regional cerebral glucose metabolism (rCGM) in 57 segmented brain regions. Metabolic connectivity analysis was compared to univariate voxel-wise statistical analysis of rCGM over time and to behavioral scores of static and dynamic sensorimotor recovery. Univariate statistical analysis revealed an ipsilesional relative rCGM decrease (compared to baseline) and a contralesional rCGM increase in vestibular and limbic networks and an increase in bilateral cerebellar and sensorimotor networks. Quantitative analysis of the metabolic connections showed a maximal increase from baseline to day 3 post UL (interhemispheric: 2-fold, ipsilesional: 3-fold, contralesional: 12-fold) and a gradual decline until day 15 post UL, which paralleled the dynamics of vestibular symptoms. In graph theoretical analysis, an increase in connectivity occurred especially within brain regions associated with brainstem-cerebellar and thalamocortical vestibular networks and cortical sensorimotor networks. At the symptom peak (day 3 post UL), brain networks were found to be organized in large ensembles of distinct and highly connected hubs of brain regions, which separated again with progressing VC. Thus, we found rapid changes in network organization at the subcortical and cortical level and in both hemispheres, which may indicate an initial functional substitution of vestibular loss and subsequent recalibration and reorganization of sensorimotor networks during VC.
Topics: Adaptation, Physiological; Animals; Arsanilic Acid; Brain; Connectome; Fluorodeoxyglucose F18; Glucose; Locomotion; Neural Pathways; Neuronal Plasticity; Nystagmus, Pathologic; Positron-Emission Tomography; Postural Balance; Radiopharmaceuticals; Rats; Vestibular Diseases; Vestibule, Labyrinth
PubMed: 33249212
DOI: 10.1016/j.neuroimage.2020.117588 -
Acta Crystallographica. Section E,... Feb 2012The title compound, C(6)H(8)NO(3)P, is isostructural with p-arsanilic acid. It exists as the zwitterion H(3)N(+)C(6)H(4)PO(3)H(-). In the crystal, mol-ecules are linked...
The title compound, C(6)H(8)NO(3)P, is isostructural with p-arsanilic acid. It exists as the zwitterion H(3)N(+)C(6)H(4)PO(3)H(-). In the crystal, mol-ecules are linked by O-H⋯O and N-H⋯O hydrogen-bond bridges, giving a three-dimensional network structure. The strongest hydrogen bonds are formed between adjacent PO(3)H groups with O⋯O distances of 2.577 (2) Å.
PubMed: 22346907
DOI: 10.1107/S1600536811055218 -
Canadian Medical Association Journal Sep 1953
Topics: Arsanilic Acid; Balantidiasis; Dysentery; Humans
PubMed: 13082481
DOI: No ID Found -
Environmental Science & Technology Aug 2016Microbes play a critical role in the global arsenic biogeocycle. Most studies have focused on redox cycling of inorganic arsenic in bacteria and archaea. The parallel...
Microbes play a critical role in the global arsenic biogeocycle. Most studies have focused on redox cycling of inorganic arsenic in bacteria and archaea. The parallel cycles of organoarsenical biotransformations are less well characterized. Here we describe organoarsenical biotransformations in the environmental microbe Shewanella putrefaciens. Under aerobic growth conditions, S. putrefaciens reduced the herbicide MSMA (methylarsenate or MAs(V)) to methylarsenite (MAs(III)). Even though it does not contain an arsI gene, which encodes the ArsI C-As lyase, S. putrefaciens demethylated MAs(III) to As(III). It cleaved the C-As bond in aromatic arsenicals such as the trivalent forms of the antimicrobial agents roxarsone (Rox(III)), nitarsone (Nit(III)) and phenylarsenite (PhAs(III)), which have been used as growth promoters for poultry and swine. S. putrefaciens thiolated methylated arsenicals, converting MAs(V) into the more toxic metabolite monomethyl monothioarsenate (MMMTAs(V)), and transformed dimethylarsenate (DMAs(V)) into dimethylmonothioarsenate (DMMTAs(V)). It also reduced the nitro groups of Nit(V), forming p-aminophenyl arsenate (p-arsanilic acid or p-AsA(V)), and Rox(III), forming 3-amino-4-hydroxybenzylarsonate (3A4HBzAs(V)). Elucidation of organoarsenical biotransformations by S. putrefaciens provides a holistic appreciation of how these environmental pollutants are degraded.
Topics: Animals; Arsenic; Arsenicals; Biotransformation; Cacodylic Acid; Roxarsone; Shewanella putrefaciens; Swine
PubMed: 27366920
DOI: 10.1021/acs.est.6b00235 -
The Journal of Experimental Medicine Apr 1924From the experiments which have been reported, it follows that animals sensitized with one azoprotein react not only to the antigen used for the sensitization, but also...
From the experiments which have been reported, it follows that animals sensitized with one azoprotein react not only to the antigen used for the sensitization, but also to other azoproteins made up from the same simple azo-compounds and another protein. Although the specificity of the reaction has not yet been tested with various azo-components, its actual existence can reasonably be assumed on the basis of the phenomena observed in precipitation reactions. The sensitization is brought about with less facility than sensitization against the usual antigens and the effects are not uniform. Still, after sufficient treatment, 40 per cent of the animals succumbed with typical anaphylactic symptoms, mostly within a short time while 16 per cent showed severe symptoms. The experiments show that it is possible to make animals hypersensitive against a simple chemical group like para-arsanilic acid, and from this point of view connection would seem to be established with the phenomena of drug allergy in human beings. There is an essential difference, however, in that the sensitized animals did not react on injections of simple compounds such as para-amino-phenyl-arsanilic acid and phenyl-4-arsonic-acid-azo-tyrosine uncombined with protein. It remains to be determined whether under changed conditions positive results in this direction can be obtained. For this purpose it seems advisable to make experiments with isolated organs, according to the method of Schultz and Dale. While the simple substances failed to elicit direct reactions, they protected (as was foreseen by Doerr) against a subsequent injection of the active antigen. Similar compounds not containing the arsanilic acid group were considerably less active. The phenomenon is comparable to the inhibition of precipitin reactions already described. Considering the protection as a condition of antianaphylaxis, one would suppose that the simple substances mentioned are fixed by the cells in which the anaphylactic reaction takes place. It may be concluded that: 1. Animals can be sensitized through injections of one azoprotein-protein combined with diazotized para-arsanilic acid-against another compound containing the same azo-component but a different protein. 2. Injections of related simple compounds, as for instance para-arsanilic acid and phenyl-4-arsonic-acid-azo-tyrosine did not cause shock in the sensitized animals under the conditions of the present experiments. 3. The simple compounds mentioned and other related substances as well protect against the anaphylactic action of azoprotein, by inducing a state of antianaphylaxis.
PubMed: 19868873
DOI: 10.1084/jem.39.5.631