Relevant bibliographies by topics / DL-penicillamine / Journal articles

To see the other types of publications on this topic, follow the link: DL-penicillamine.

Journal articles on the topic 'DL-penicillamine'

Author: Grafiati

Published: 5 June 2025

Last updated: 15 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'DL-penicillamine.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

Bhushan, Ravi, and Rajender Kumar. "Enantioresolution of dl-penicillamine." Biomedical Chromatography 24, no. 1 (2010): 66–82. http://dx.doi.org/10.1002/bmc.1355.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Kodama, Hiroko, Yasumi Anan, Yoichi Izumi, Yasuhiro Sato, and Yasumitsu Ogra. "Copper and zinc concentrations in the breast milk of mothers undergoing treatment for Wilson’s disease: a prospective study." BMJ Paediatrics Open 5, no. 1 (2021): e000948. http://dx.doi.org/10.1136/bmjpo-2020-000948.

Full text

Abstract:

ObjectiveTo evaluate the concentrations of copper and zinc in the breast milk of mothers undergoing treatment for Wilson’s disease (WD) and clarify whether they can safely breast feed their infants.DesignThis was an observational and prospective study in an individual-based case series.SettingBreast milk samples were collected from participants across Japan from 2007 to 2018 at the Department of Pediatrics, Teikyo University in Tokyo. This was a primary-care level study. Clinical data were collected from the participants’ physicians.PatientsEighteen Japanese mothers with WD who were treated with trientine, penicillamine or zinc, and 25 healthy mothers as controls, were enrolled.Main outcome measuresWhey exacted from the milk was used to evaluate the distribution of copper by high-performance liquid chromatography-inductively coupled plasma mass spectrometry. Copper and zinc concentrations in the breast milk samples were analysed by atomic absorption spectrometry.ResultsCopper distribution was normal in the breast milk of mothers with WD treated with trientine, penicillamine or zinc. No peak was detected for trientine-bound or penicillamine-bound copper. The mean copper concentrations in the mature breast milk of patients treated with trientine, penicillamine and zinc were 29.6, 26 and 38 µg/dL, respectively, and were within the normal range compared with the value in healthy controls (33 µg/dL). Likewise, mean zinc concentrations were normal in the mature breast milk of patients treated with trientine and penicillamine (153 and 134 µg/dL, respectively vs 160 µg/dL in healthy controls). Zinc concentrations in the breast milk of mothers treated with zinc were significantly higher than those in control milk. All infants were born normally, breast fed by mothers undergoing treatment and exhibited normal development.ConclusionsOur results suggest that mothers with WD can safely breast feed their infants, even if they are receiving treatment for WD.

APA, Harvard, Vancouver, ISO, and other styles

Badsar, Alireza, Zeynab Gholami, Morteza Rahbar Taramsari, Zahra Atrkar Roshan, Hamid Mohammadi Kojidi, and Monireh Aghajany Nasab. "The Biochemical Outcome of two Treatment Protocols in Patients With Opium-associated Lead Poisoning: A Cross-sectional Study in North of Iran." International Journal of Medical Toxicology and Forensic Medicine 11, no. 1 (2021): 32329.1–32329.8. http://dx.doi.org/10.32598/ijmtfm.v11i1.32329.

Full text

Abstract:

Background: Lead is a potent toxin that targets heme synthesis and some antioxidant enzymes that induce oxidative stress. Lead exposure remains one of the significant health concerns all over the world. Chelating agents have been used as antidotes for acute and chronic lead poisoning. The present study was conducted to evaluate the biochemical outcome of two different chelating therapies. Methods: This descriptive cross-sectional study was performed in the Razi University Hospital, Rasht, Guilan. Fifty-six patients with a history of opium use were enrolled in the study who were treated symptomatically. Blood lead Llevels (BLL), Hemoglobin (Hb), Red Blood Cell (RBC), White Blood Cell (WBC), urea, creatinine, Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), and Alkaline Phosphatase (ALP) were evaluated before and after treatment. The BLL more than 100μg/dl with clinical symptoms was considered as severe lead poisoning (n=34) who received 4 days of DMPS (2,3-dimercaptopropane-1-sulfonate) injection. Other cases with BLL of 20-100μg/dl were considered as those with mild poisoning (n=22) that were treated with oral D-Penicillamine for 14 days. Results: The mean age of patients was 49.73±14.11 years. Data analysis indicated no significant differences between the groups at baseline regarding the demographic variables. A significant reduction was observed in BLL before and after the intervention using the D-Penicillamine from 75.88±26.22 to 44.3±17.51 μg/dl (P=0.0001). The BLL reduced from 105.5±34.04 to 24.51±24.08 μg/dl after treatment with DMSP (P=0.0001). The levels of ALT, AST, and WBC significantly decreased post-treatment following using D-penicillamine and DMPS (P<0.05). The D-Penicillamine-treated group showed an increase in Hb and RBC (P<0.05). Conclusion: According to the results, penicillamine improves low to moderate lead toxicity. Although DMSP decreases BLL significantly and reverses liver enzymes, further investigations on Hb and RBC, are needed.

APA, Harvard, Vancouver, ISO, and other styles

Røgeberg, E., J. Aaseth, and W. Lund. "CHEMICAL AFFINITY OF METHYLMERCURY TO D-PENICILLAMINE, GLUTATHIONE AND N-ACETYL-DL-PENICILLAMINE." Acta Pharmacologica et Toxicologica 59 (March 13, 2009): 555–57. http://dx.doi.org/10.1111/j.1600-0773.1986.tb02824.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Heaster, Hope, and Patrick E. Hoggard. "d- and dl-penicillamine complexes of chromium(III)." Polyhedron 13, no. 3 (1994): 333–37. http://dx.doi.org/10.1016/s0277-5387(00)81641-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Lifshitz, Matitiahu, and Jacov Levy. "Efficacy of d-Penicillamine in Reducing Lead Concentrations in Children: A Prospective, Uncontrolled Study." Journal of Pharmacy Technology 16, no. 3 (2000): 98–101. http://dx.doi.org/10.1177/875512250001600306.

Full text

Abstract:

Objective: To evaluate the efficacy of oral d-penicillamine therapy in children with high blood lead concentrations. Design: A prospective, uncontrolled study. Methods and Patients: Seven children (2–16 y old; mean 8.7) with elevated blood lead concentrations but no symptoms of lead poisoning were treated with oral d-penicillamine. Lead-contaminated homemade flour as found to be the source of poisoning. Mean ± SD blood lead concentrations prior to therapy were 60.3 ± 12.9 μg/dL (range 47.8–83). Mean blood zinc protoporphyrin (ZPP) was 337.86 ± 58.55 μmol/mol hemoglobin (Hb) (range 247–394). Results: Ninety days of treatment with d-penicillamine lowered the mean blood lead concentration by 31.7% to a mean of 40.7 ± 8.6 μg/dL (range 30–53) and lowered mean ZPP blood concentrations by 40% to a mean of 201.14 ± 14 μmol/mol Hb (range 150–278). Three patients with blood lead concentrations >45 μg/mL at the end of this therapy were subsequently treated with succimer, an alternative oral chelator; the blood lead concentrations were further reduced to <45 μg/mL. Conclusions: d-Penicillamine therapy significantly reduced blood lead concentrations but did not achieve acceptable lead and ZPP concentrations for young children. Therefore, we conclude that 90 days of d-penicillamine treatment is of limited effectiveness in young children who have high blood lead concentrations and also show symptoms of lead poisoning.

APA, Harvard, Vancouver, ISO, and other styles

Pandey, D. S., and U. C. Agarwala. "N-Acetyl-Dl-Penicillamine Thionitrite - A Potential Nitrosylating Agent." Synthesis and Reactivity in Inorganic and Metal-Organic Chemistry 21, no. 3 (1991): 361–74. http://dx.doi.org/10.1080/15533179108018345.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Subhasis, Mallick, Mandal Arup, K. Bera Biplab, et al. "Kinetic and mechanistic studies on the interaction of DL-penicillamine with di-µ-hydroxobis(bipyridyl)dipalladium(II) ion in aqueous solution." Journal of Indian Chemical Society Vol. 88, Jun 2011 (2011): 859–63. https://doi.org/10.5281/zenodo.5770231.

Full text

Abstract:

Department of Chemistry, The University of Burdwan, Burdwan-713 104, West Bengal, India <em>E-mail</em> : alakghosh2002@yahoo.co.in Department of Chemistry, National Institute of Technology, Durgapur-713 209, West Bengal, India <em>Manuscript received 09 April 2010, revised 05 October 2010, accepted 28 October 2010</em> The kinetics of interaction between DL-penicillamlne and the title complex is a two-step process in which the first step is ligand dependent, but the second step is ligand independent and is assigned to ring closure. The rate and activation parameters, conductivity studies, IR data were used to deduce a plausible mechanism.

APA, Harvard, Vancouver, ISO, and other styles

PANDEY, D. S., and U. C. AGARWALA. "ChemInform Abstract: N-Acetyl-DL-penicillamine Thionitrite. A Potential Nitrosylating Agent." ChemInform 23, no. 11 (2010): no. http://dx.doi.org/10.1002/chin.199211090.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Adrie, Christophe, Christoph Richter, Maria Bachelet, et al. "Contrasting effects of NO and peroxynitrites on HSP70 expression and apoptosis in human monocytes." American Journal of Physiology-Cell Physiology 279, no. 2 (2000): C452—C460. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c452.

Full text

Abstract:

The free radicals nitric oxide (·NO) and superoxide (O2 −·) react to form peroxynitrite (ONOO−), a highly toxic oxidant species. In this study we investigated the respective effects of NO and ONOO− in monocytes from healthy human donors. Purified monocytes were incubated for 6 or 16 h with a pure NO donor ( S-nitroso- N-acetyl-dl-penicillamine, 0–2 mM), an ·NO/ONOO− donor (3-morpholinosydnonimine chlorhydrate, 0–2 mM) with and without superoxide dismutase (200 IU/ml), or pure ONOO−. We provide evidence that 3-morpholinosydnonimine chlorhydrate alone represents a strong stress to human monocytes leading to a dose-dependent increase in heat shock protein-70 (HSP70) expression, mitochondrial membrane depolarization, and cell death by apoptosis and necrosis. These phenomena were abolished by superoxide dismutase, suggesting that ONOO−, but not ·NO, was responsible for the observed effects. This observation was further strengthened by the absence of a stress response in cells exposed to S-nitroso- N-acetyl-dl-penicillamine. Conversely, exposure of cells to ONOO− alone also induced mitochondrial membrane depolarization and cell death by apoptosis and necrosis. Thus ONOO− formation may well explain the toxic effect generally attributed to ·NO.

APA, Harvard, Vancouver, ISO, and other styles

Perez-Benito, Joaquin F., Driss Lamrhari, and Conchita Arias. "Oxidation of DL-penicillamine by chromium(VI). Kinetics of formation of the thioester intermediate." Canadian Journal of Chemistry 72, no. 7 (1994): 1637–44. http://dx.doi.org/10.1139/v94-206.

Full text

Abstract:

The kinetics of formation of the thioester involved as an intermediate in the reaction between chromium(VI) and DL-penicillamine in aqueous media (pH = 1–8) containing different buffers (acetate, citrate, and phosphate) has been studied by monitoring the disappearance of chromium(VI) at 370 nm and application of the initial-rates method. The initial rate is directly proportional to the initial concentrations of both oxidant and reductant, and the rate vs. pH plots show bell-shaped profiles. The reaction is catalyzed by the buffer present in the medium, the catalytic power of each buffer increasing in the order acetate < citrate < phosphate. This is explained in terms of a mechanism involving the formation of a complex between the acidic form of the buffer and HCrO4− previous to the formation of the thioester. Potassium chloride and sodium sulfate do not seem to have important specific effects on the reaction rate, their effect being that of an acceleration of the reaction as the ionic strength increases. On the contrary, the sulfates of magnesium, manganese(II), and zinc (the latter only in the presence of acetate buffer) have specific effects, indicating the probable formation of several complexes. The spectrophotometric detection of the thioester at 430 nm has allowed to confirm some of the conclusions extracted from the measurement of initial rates, and suggests that this intermediate might approach a steady-state behavior in the three buffers at pH > 6.25, and also that a bimolecular reaction with DL-penicillamine might be involved in its destruction.

APA, Harvard, Vancouver, ISO, and other styles

Komarova, A. D., A. S. Potapov, K. V. Savostyanov, et al. "Challenges in the diagnosis of Wilson’s disease in young children." Voprosy detskoj dietologii 22, no. 2 (2024): 13–21. https://doi.org/10.20953/1727-5784-2024-2-13-21.

Full text

Abstract:

Objective. To evaluate the clinical course of Wilson’s disease (WD) and the effectiveness of a scoring algorithm for diagnosis in children with early onset of the disease. Patients and methods. Data from 85 case histories of children with WD observed at the National Medical Research Center for Children’s Health between 2012 and 2023 were retrospectively analyzed. Results. Clinical and laboratory manifestations of WD at the age of 5 years and under were observed in 36 children. The mean ransaminase level was 128 U/L for alanine aminotransferase and 82 U/L for aspartate aminotransferase. Ceruloplasmin concentrations of <20 mg/dL were found in 32 (89%) patients, of which 47% had <10 mg/dL. Daily urinary copper excretion was determined in 33 of 36 children, and only 9 of them had levels of >100 mcg/day. In the group of children with normal urinary copper levels, the D-penicillamine challenge test was positive in 5 of 12 patients, with all 8 having copper concentrations of 50–100 mcg/dL. Liver copper levels were >250 mcg/g in 4 of 5 children. The most common pathogenic variant in the ATP7B gene was p. (His1069Gln), detected in 55% of children on 25 (34.7%) alleles. Using the Leipzig algorithm, the diagnosis of WD was made in 13 children without genetic testing, with the identification of Kayser-Fleischer rings, liver copper determination, and D-penicillamine challenge test being the decisive criteria. Conclusion. The onset of WD at a young age is characterized by the absence of specific clinical and laboratory manifestations. Since some tests have low sensitivity in children and genetic testing is not available in certain cases, it is necessary to use a comprehensive approach to diagnosis. Key words: Wilson’s disease, genetics, children, diagnosis, molecular genetic diagnosis, ATP7B

APA, Harvard, Vancouver, ISO, and other styles

Salas, E., M. A. Moro, S. Askew, et al. "Comparative pharmacology of analogues of S-nitroso-N-acetyl-dl-penicillamine on human platelets." British Journal of Pharmacology 112, no. 4 (1994): 1071–76. http://dx.doi.org/10.1111/j.1476-5381.1994.tb13192.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Mocanu, Cristina-Manuela. "Occupational lead intoxication from terracotta tiles manufacturing: a case study." Romanian Journal of Occupational Medicine 73, no. 1 (2022): 12–17. http://dx.doi.org/10.2478/rjom-2022-0002.

Full text

Abstract:

Abstract We report the case of a 63-year-old terracotta tiles manufacturer who presented with acute abdomen and normocytic anaemia. The patient presented with elevated levels of urinary delta-aminolaevulinic acid without any increase in the levels of urine porphobilinogen or urine coproporphyrin. Detection of elevated lead blood levels (1939 µg/dL one month before hospital admission in the occupational medicine clinic and 44.70 µg/dL at hospital admission, values come from two different laboratories) confirmed the diagnosis of chronic lead poisoning due to occupational exposure. Chelation therapy with D-penicillamine resulted in the improvement of clinical symptoms and lead blood levels. Clinicians should be aware that lead poisoning caused by occupational exposure can still occur sporadically in terracotta tiles manufacturing workers, lead poisoning being a neglected diagnosis in abdominal pain.

APA, Harvard, Vancouver, ISO, and other styles

Dixon, Donovan A., Tara P. Dasgupta, and Novelette P. Sadler. "Mechanism of the oxidation of DL-penicillamine and glutathione by chromium(VI) in aqueous solution." Journal of the Chemical Society, Dalton Transactions, no. 13 (1995): 2267. http://dx.doi.org/10.1039/dt9950002267.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Kwiatkowski, P. A., J. Puc, W. Rowinski, and P. Fiedor. "Effects of DL-Penicillamine on Cytotoxic Reaction between Baboon Performed Xenoantibodies and Pig Endothelial Cells." International Journal of Artificial Organs 20, no. 7 (1997): 375–78. http://dx.doi.org/10.1177/039139889702000704.

Full text

Abstract:

The purpose of this study was to evaluate effects of DL-Penicillamine (DLP), a compound interrupting S-S bonds (IgM pentamers) on binding and cytotoxicity of adult baboon performed xenoantibodies to pig endothelial cells. Pooled baboon serum was treated with different concentrations of DLP during various periods of time. Complement-mediated cytotoxicity assay was used to determine the reactivity of baboon xenoantibodies to pig aortic endothelial cells (PAEC). To assess IgM and IgG binding to PAEC, ELISA method was applied. Serum treated with DLP revealed significant reduction of cytotoxicity in a dose dependent manner. Cytotoxicity was also reduced during time prolongation of DLP exposure to PAEC. Results indicate that baboon performed IgM and IgG xenoantibodies bind to pig endothelial cells, but only IgM is able to cause degradation of the complement. DLP significantly reduces cytotoxicity and eliminates binding of IgMs to PAEC in spite of continued binding of IgG xenoantibodies to the surface of endothelium.

APA, Harvard, Vancouver, ISO, and other styles

Buglyó, Péter, Eszter Márta Nagy, and Imre Sóvágó. "Vanadium(III) binding strengths of small biomolecules." Pure and Applied Chemistry 77, no. 9 (2005): 1583–94. http://dx.doi.org/10.1351/pac200577091583.

Full text

Abstract:

The hydrolysis of vanadium(III) and the complex formation reactions between V(III) and weakly coordinating [glycine (GLY), DL-aspartic acid (ASP), D-penicillamine (PEN), DL-histidine (HIS)] or strongly coordinating [N,O] donor [picolinic (PIC) or 6-methylpicolinic acid (MePIC)] and [O,O] donor [maltol (MALT), 1,2-dimethyl-3-hydroxy-4-(1H)-pyridinone (DHP), tiron (TIR)] ligands were studied at 25.0 °C and an ionic strength of 0.20 M (KCl) in aqueous solution using combined pH-potentiometric and UV-vis spectroscopic techniques. Although some interaction between the amino acids and V(III) was found, we could not obtain reliable models for these systems owing to the intensive hydrolysis of the metal ion and the formation of polynuclear hydroxo complexes. With pyridine carboxylates or [O,O] donor ligands 1:1, 1:2 (in the latter case, also 1:3 species) were found to be present as major complexes in solution. The similarities and differences in binding V(III) by these ligands are discussed.

APA, Harvard, Vancouver, ISO, and other styles

Chowdhury, Shahed Haider, Khondoker Ehsanul Arefin, and Mohsina Akter Lucky. "Wilson’s Disease- A Child with An Atypical Presentation." Scholars Journal of Medical Case Reports 12, no. 03 (2024): 271–73. http://dx.doi.org/10.36347/sjmcr.2024.v12i03.009.

Full text

Abstract:

Wilson’s disease is a hereditary disorder of copper metabolism which leads to copper overload in different tissues of the body. Clinical presentation of Wilson disease can vary widely; therefore, diagnosis is not always straightforward. Here we report a 13-year-old girl presented with diffuse persistent stabbing pain in the abdomen, jaundice & dark urine. She had no history of unconsciousness, convulsion, deterioration of school performance, or alteration of sleep pattern. On examination, she was ill-looking, pale, and icteric. The liver was enlarged. Higher psychic Function was intact, with no neurological deficit. A slit-lamp examination by an ophthalmologist promptly revealed the presence of a “Kayser Fleischer Ring” in both eyes. On investigation, hemoglobin was 5.73g/dl, Total bilirubin-37.82mg/dl, ALT-50 IU, AST-95 IU, PT/INR-3.20, serum ceruloplasmin 21mg/dl. Twenty-four hours of urinary copper excretion after penicillamine challenge was 8784 μg/24 hours. We diagnosed the case as Wilson’s disease. This case report aims to share our experience regarding the clinical presentation and diagnosis of Wilson’s disease in a child where Kayser–Fleischer rings in eyes appeared before neurological manifestation occurs and normal serum ceruloplasmin which often creates a diagnostic dilemma.

APA, Harvard, Vancouver, ISO, and other styles

Altun, Ahmet, Mustafa Ergül, Ali Kemal Filiz, Mesut Parlak, Merve Ergül, and Tijen Kaya Temiz. "The Effects of Daily Repeated Magnetic Field on S-Nitroso-N-acetyl-DL penicillamine Induced Hyperalgesia." Cumhuriyet Medical Journal 36, no. 3 (2014): 310. http://dx.doi.org/10.7197/cmj.v36i3.1008002547.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Monroy, A., C. Ríos, and S. Montes. "Additive effect of dl-penicillamine plus Prussian blue for the antidotal treatment of thallotoxicosis in rats." Toxicology Letters 196 (July 2010): S303. http://dx.doi.org/10.1016/j.toxlet.2010.03.958.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Montes, Sergio, Gabriela Pérez-Barrón, Moisés Rubio-Osornio, et al. "Additive effect of dl-penicillamine plus Prussian blue for the antidotal treatment of thallotoxicosis in rats." Environmental Toxicology and Pharmacology 32, no. 3 (2011): 349–55. http://dx.doi.org/10.1016/j.etap.2011.07.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Gigante, A., C. Chillemi, D. Quaglino, M. Miselli, and I. Pasquali-Ronchetti. "DL-penicillamine induced alteration of elastic fibers of periosteum-perichondrium and associated growth inhibition: an experimental study." Journal of Orthopaedic Research 19, no. 3 (2001): 398–404. http://dx.doi.org/10.1016/s0736-0266(00)90033-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Aaseth, Jan. "Mobilization of Methyl Mercury in Vivo and in Vitro using N-acetyl-DL-penicillamine and other Complexing Agents." Acta Pharmacologica et Toxicologica 39, no. 3 (2009): 289–301. http://dx.doi.org/10.1111/j.1600-0773.1976.tb03180.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Frost, Megan C., and Mark E. Meyerhoff. "Controlled Photoinitiated Release of Nitric Oxide from Polymer Films ContainingS-Nitroso-N-acetyl-dl-penicillamine Derivatized Fumed Silica Filler." Journal of the American Chemical Society 126, no. 5 (2004): 1348–49. http://dx.doi.org/10.1021/ja039466i.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Glotzer, Deborah E., and Howard Bauchner. "Management of Childhood Lead Poisoning: A Survey." Pediatrics 89, no. 4 (1992): 614–18. http://dx.doi.org/10.1542/peds.89.4.614.

Full text

Abstract:

Published recommendations (1985) for the management of childhood lead poisoning suggest the use of ethylenediaminetetraacetic acid (EDTA)provocation testing and chelation as the mainstay of treatment for blood lead levels between 25 and 55 μg/dL. Since 1985 evidence has accumulated indicating that (1) levels of blood lead less than 25 μg/dL are detrimental to cognitive development, (2) EDTA provocation testing may result in potentially harmful shifts in the body lead burden, and (3) oral agents such as penicillamine and 2,3-dimercaptosuccinic acid are effective in reducing elevated lead levels. To determine how this evidence impacts on the management of childhood lead poisoning, the authors surveyed the lead poisoning clinics of pediatric departments in the cities estimated by the United States Public Health Service to have the largest number of children affected by lead poisoning. Thirty (70%) of 43 surveys were completed. Respondents indicated that the lowest blood lead level for which they would use a chelating agent to reduce the lead burden was as follows: 50 μg/dL (3%), 45 μg/dL (3%), 40μg/dL (13%) 35 μg/dL (3%), 30 μg/dL (27%), 25 μg/dL (47%) and 20μg/dL (3%). For all blood lead levels from 20 through 55 μg/dL, EDTA was the most frequently recommended chelating agent (chelation and provocation testing). Fifteen percent of responding lead clinics do not use the provocation test under any circumstances. For a child with a negative EDTA provocation test, the percentage of respondents recommending the use of any chelation therapy ranged from 16% for blood lead levels of 25 through 29μg/dL to 66% for levels of 50 through 55 μg/dL. Orally active chelating agents are used by fewer than one third of the responding lead clinics and were selected as the chelating agent of choice at all blood lead levels from 25 through 55 μg/dL by at least one respondent. The results of this survey indicate the following: (1) There is a wide range of blood lead levels for which chelation therapy is recommended. (2) The majority of children with elevated lead burdens are managed using EDTA. (3) The EDTA provocation test continues to be widely used. (4) The majority of children with blood lead levels of 25 through 44 μg/dL with negative provocation tests do not receive chelation therapy. (5) Orally active chelating agents are used in the minority of lead clinics. (6) No common approach for the treatment of lead toxicity appears to exist. (7) In the majority of pediatric centers, current management of blood lead elevation does not appear to reflect new information regarding the effects and treatment of lead poisoning.

APA, Harvard, Vancouver, ISO, and other styles

Zastelo, Elena S., Elvira N. Fedulova, Anastasiya N. Gabrikevich, Tatiana V. Skochilova, and Anatoly I. Khavkin. "Wilson’s Disease. Onset and Complex Diagnosis: Clinical Case." Current Pediatrics 23, no. 6 (2025): 483–88. https://doi.org/10.15690/vsp.v23i6.2834.

Full text

Abstract:

Background. The low prevalence of Wilson’s disease, diversity of clinical signs, long latent course, inheritance features make it difficult to diagnose and require multidisciplinary approach from doctors. Clinical case description. This article describes a clinical case of Wilson’s disease, rare hereditary multisystem disease, diagnosed in patient F., 13 years old. The disease onset was at the age of 6 masked by gastroesophageal reflux disease. Hepatomegaly, cytolysis, and cholestasis were diagnosed 4 years later, thus diagnosis of hepatitis of unknown origin was established requiring further specification. The decrease of free copper level in serum was revealed at the age of 12, penicillamine test was positive. Molecular genetic testing was performed and the pathogenic variant c.3207C>A (heterozygous state) in the ATP7B gene was revealed. We have measured 4 points via the Leipzig score for Wilson’s disease (Leipzig, 2001): serum ceruloplasmin <20 mg/dL — 1 point, increase in urinary copper excretion of more than 5 times at penicillamine test — 2 points, pathogenic variant c.3207C>A (heterozygous state) in the gene ATP7B — 1 point. This score corresponds to the diagnosis of Wilson’s disease. The use of chelation and hepatoprotective therapy has led to positive dynamics. Thus, the disease can debut with nonspecific, asymptomatic increases in transaminases and ultrasound changes in liver at any age. Wilson’s disease is progressive disease and in the absence of timely initiated therapy, patients die due to complications of cirrhosis and/or (less often) progressive neurological symptoms. The prognosis can be favorable with effective chelation therapy or liver transplantation. Conclusion. The described clinical case demonstrates the variability of clinical signs in children with Wilson’s disease that complicates the diagnostic search and early diagnosis

APA, Harvard, Vancouver, ISO, and other styles

Rao, Janapareddy Vijaya Bhaskara, Bhuma Vengamma, Thota Naveen, and Vandanapu Naveen. "Lead encephalopathy in adults." Journal of Neurosciences in Rural Practice 5, no. 02 (2014): 161–63. http://dx.doi.org/10.4103/0976-3147.131665.

Full text

Abstract:

Lead poisoning is a common occupational health hazard in developing countries. We report the varied clinical presentation, diagnostic and management issues in two adult patients with lead encephalopathy. Both patients worked in a battery manufacturing unit. Both patients presented with seizures and one patient also complained of abdominal colic and vomiting. Both were anemic and a lead line was present. Blood lead level in both the patients was greater than 25 μg/dl. Magnetic resonance imaging of brain revealed bilateral symmetric involvement of the thalamus, lentiform nucleus in both patients and also the external capsules, sub-cortical white matter in one patient. All these changes, seen as hyperintensities in T2-weighted images suggested demyelination. They were advised avoidance of further exposure to lead and were treated with anti-epileptics; one patient also received D-penicillamine. They improved well on follow-up. Lead encephalopathy is an uncommon but important manifestation of lead toxicity in adults.

APA, Harvard, Vancouver, ISO, and other styles

Aaseth, Jan, Axel Wannag, and Tor Norseth. "The Effect of N-acetyJated DL-penicillamine and DL-homocysteine Thiolactone on the Mercury Distribution in Adult Rats, Rat Foetuses and Macaca Monkeys after Exposure to Methyl Mercuric Chloride." Acta Pharmacologica et Toxicologica 39, no. 3 (2009): 302–11. http://dx.doi.org/10.1111/j.1600-0773.1976.tb03181.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Shi, Tiesheng, Johan Berglund, and Lars I. Elding. "Kinetics and Mechanism for Reduction oftrans-Dichlorotetracyanoplatinate(IV) by Thioglycolic Acid,l-Cysteine,dl-Penicillamine, and Glutathione in Aqueous Solution." Inorganic Chemistry 35, no. 12 (1996): 3498–503. http://dx.doi.org/10.1021/ic951598s.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Askew, Stuart C., Anthony R. Butler, Frederick W. Flitney, Graham D. Kemp, and Ian L. Megson. "Chemical mechanisms underlying the vasodilator and platelet anti-aggregating properties of S-nitroso-N-acetyl-dl-penicillamine and S-nitrosoglutathione." Bioorganic & Medicinal Chemistry 3, no. 1 (1995): 1–9. http://dx.doi.org/10.1016/0968-0896(94)00139-t.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Pantel, Priya, and Swati Nagpal. "AYURVEDIC PROTOCOL FOR THE MANAGEMENT OF WILSON’S DISEASE – A CASE REPORT." International Ayurvedic Medical Journal 9, no. 7 (2021): 1593–96. http://dx.doi.org/10.46607/iamj4509072021.

Full text

Abstract:

Wilson’s disease (hepatolenticular degeneration) is a rare important autosomal recessive disorder caused by dys- function of the copper transporter ATP7B, which leads to snagging in copper transport by the hepatic lysosomes resulted in the deposition of copper in the brain, liver, kidney, or skeletal system. The symptoms are jaundice, Kayser-Fleischer rings, dysarthria, ataxia, and muscle spasticity etc. Current therapeutic modalities for the manage- ment of Wilson's disease include zinc, trientine, penicillamine etc. In Ayurvedic classics there is no exact correlation is available for this disease entity that exactly matches the feature of Wilson disease, but it can be correlated with Vatavyadhi under the Sahaja Vyadhi (Heredity) or Janamjata Vyadhi (congenital). The treatment1 mentioned for Vatavyadhi is Snehana (oleation), Mrudu Swedana (mild sedation), Anuvasana Basti (oil enema) and Niruha Basti (Decoction Enema). Material and methods: An 18-year-old male patient with Wilson disease complained of short stepping gait, persistent constipation, tremors, changed speech, generalised stiffness, and frequent eye blinking. S. Ceruloplasmin was found to be 18.33 mg/dL (usually 20 mg/dl to 40 mg/dl), S. copper was found to be within normal limits, and a slit lamp assay for the KF ring was negative. Ayurvedic therapy was used in conjunction with oral medicine throughout the treatment. Results: Clinical observations revealed that the patient's earlier symptoms had significantly improved, and he was able to carry out his usual activities with ease. Duration of treatment:three months. Conclusion: From the case study it can be concluded that the Ayurvedic medications and Panchkarma therapy in such patients may help in providing supportive care and improving the quality of life. Keywords: Vatavyadhi, Shaman Chikitsa, Bastikarma, Wilson's disease.

APA, Harvard, Vancouver, ISO, and other styles

Bhushan, Ravi, та Rajender Kumar. "Analytical and preparative enantioseparation of dl-penicillamine and dl-cysteine by high-performance liquid chromatography on α-acid glycoprotein and β-cyclodextrin columns using ninhydrin as a reversible tagging reagent". Journal of Chromatography A 1216, № 15 (2009): 3413–17. http://dx.doi.org/10.1016/j.chroma.2009.02.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Pope, M., P. A. Marsden, E. Cole, et al. "Resistance to Murine Hepatitis Virus Strain 3 Is Dependent on Production of Nitric Oxide." Journal of Virology 72, no. 9 (1998): 7084–90. http://dx.doi.org/10.1128/jvi.72.9.7084-7090.1998.

Full text

Abstract:

ABSTRACT The strain-specific spectrum of liver disease following murine hepatitis virus type 3 (MHV-3) infection is dependent on inflammatory mediators released by macrophages. Production of nitric oxide (NO) by macrophages has been implicated in resistance to a number of viruses, including ectromelia virus, vaccinia virus, and herpes simplex virus type 1. This study was undertaken to define the role of NO in MHV-3 infection. Gamma interferon-induced production of NO inhibited growth of MHV-3 in a murine macrophage cell line (RAW 264.7). Viral inhibitory activity was reproduced by the NO donorS-nitroso-N-acetyl-dl-penicillamine (SNAP), whereas N-acetyl-dl-pencillamine (NAP), an inactive analog of SNAP, had no effect. Electron microscopy studies confirmed the inhibitory effects of NO on viral replication. Peritoneal macrophages isolated from A/J mice known to be resistant to MHV-3 produced a fivefold-higher level of NO and higher levels of mRNA transcripts of inducible NO synthase in response to gamma interferon than macrophages from susceptible BALB/cJ mice. SNAP inhibited growth of MHV-3 in macrophages from both strains of mice to similar degrees. In vivo inhibition of NO byN-monomethyl-l-arginine resulted in loss of resistance to MHV-3 in A/J mice. These results collectively demonstrate a defect in the production of NO in macrophages from susceptible BALB/cJ mice and define the importance of endogenous NO in resistance to MHV-3 infection in resistant A/J mice.

APA, Harvard, Vancouver, ISO, and other styles

Mang, Christian F., and Heinz Kilbinger. "Modulation of acetylcholine release in the guinea-pig trachea by the nitric oxide donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP)." British Journal of Pharmacology 131, no. 1 (2000): 94–98. http://dx.doi.org/10.1038/sj.bjp.0703531.

Full text

APA, Harvard, Vancouver, ISO, and other styles

IOANNIDIS, Iosif, Michael BÄTZ, Thomas PAUL, Hans-Gert KORTH, Reiner SUSTMANN, and Herbert de GROOT. "Enhanced release of nitric oxide causes increased cytotoxicity of S-nitroso-N-acetyl-dl-penicillamine and sodium nitroprusside under hypoxic conditions." Biochemical Journal 318, no. 3 (1996): 789–95. http://dx.doi.org/10.1042/bj3180789.

Full text

Abstract:

S-Nitroso-N-acetyl-dl-penicillamine (SNAP) and sodium nitroprusside (SNP), both of which are known to release nitric oxide (•NO), exhibited cytotoxicity against cultivated endothelial cells. Under hypoxic conditions 5 mM SNAP and 20 mM SNP induced a loss in cell viability of about 90% and 80% respectively, after an 8 h incubation. Under normoxic conditions, cell death was only 45% and 42% respectively within the same time period. Concentrations of •NO liberated from SNAP and SNP were measured by the oxyhaemoglobin method and by two of the recently developed nitric oxide cheletropic traps (NOCTs). The •NO concentrations from SNAP and SNP increased from 74 µM and 28 µM to 136 µM and 66 µM respectively within 15 min of hypoxic incubation, and then decreased to 36 µM and 28 µM. In the respective normoxic incubations the •NO levels from SNAP and SNP remained in the region of about 30 µM and 20 µM respectively. In contrast, spermine/NO adduct (spermineNONOate) was shown to be more toxic under normoxic than under hypoxic conditions. Under either of these conditions, the concentration of •NO liberated from 2 mM spermineNONOate was about 20 µM. The results demonstrate that the cytotoxicity of SNAP and SNP, but not of spermineNONOate, is significantly enhanced under hypoxic compared with normoxic incubations. Studies on the •NO-releasing behaviour of these compounds indicate that the increased toxicity of SNAP and SNP under hypoxic conditions is related to the influence of O2 on the chemical processes by which •NO is produced from the precursors, rather than to an increased sensitivity of the hypoxic cells towards •NO.

APA, Harvard, Vancouver, ISO, and other styles

Pravdic, Danijel, Nikolina Vladic, Ivan Cavar, and Zeljko J. Bosnjak. "Effect of nitric oxide donorsS-nitroso-N-acetyl-dl-penicillamine, spermine NONOate and propylamine propylamine NONOate on intracellular pH in cardiomyocytes." Clinical and Experimental Pharmacology and Physiology 39, no. 9 (2012): 772–78. http://dx.doi.org/10.1111/j.1440-1681.2012.05734.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Shi, Tiesheng, Johan Berglund, and Lars I. Elding. "Kinetics and mechanisms for reduction of trans-dichlorotetracyanoplatinate(IV) by thioglycolic acid, L-cysteine, DL-penicillamine and glutathione in aqueous solution." Journal of Inorganic Biochemistry 59, no. 2-3 (1995): 277. http://dx.doi.org/10.1016/0162-0134(95)97380-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Karmakar, Parnajyoti, Biplab K. Bera, Kanai L. Barik, Sudip K. Mukhopadhyay, and Alak K. Ghosh. "Kinetics and mechanism of the interaction of DL-penicillamine with cis-diaqua(cis-1,2-diaminocyclohexane)platinum(II) perchlorate in aqueous medium." Journal of Coordination Chemistry 63, no. 12 (2010): 2158–71. http://dx.doi.org/10.1080/00958972.2010.498910.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Fa, Xinmeng, Shaowei Lin, Jianghua Yang, et al. "−808 nm-activated Ca²⁺ doped up-conversion nanoparticles that release no inducing liver cancer cell (HepG2) apoptosis." Methods and Applications in Fluorescence 10, no. 2 (2022): 024003. http://dx.doi.org/10.1088/2050-6120/ac5524.

Full text

Abstract:

Abstract A near-infrared (NIR) light-triggered release method for nitric oxide (NO) was developed utilizing core/shell NaYF4: Tm/Yb/Ca@NaGdF4: Nd/Yb up-conversion nanoparticles (UCNPs) bearing a mesoporous silica (mSiO2) shell loaded with the NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP). To avoid overheating in biological samples, Nd3+ was chosen as a sensitizer, Yb3+ ions as the bridging sensitizer, and Tm3+ ions as UV-emissive activator while co-doping with Ca2+ was done to enhance the luminescence of the activator Tm3+. NO release from SNAP was triggered by an NIR-UV up-conversion process, initiated by 808 nm light absorbed by the Nd3+ ions. NO release was confirmed by the Griess method. Under 808 nm irradiation, the viability of the liver cancer cell line HepG2 significantly decreased with increasing UCNPs@mSiO2-SNAP concentration. For a UCNPs@mSiO2-SNAP concentration of 200 μg ml−1, the cell survival probability was 47%. These results demonstrate that UCNPs@mSiO2-SNAP can induce the release of apoptosis-inducing NO by NIR irradiation.

APA, Harvard, Vancouver, ISO, and other styles

Yeh, Jui-Ning. "Combination of melatonin-delivered endothelial progenitor cells with S-nitroso-N-acetyl-DL-penicillamine for improving critical limb ischemia in the rat." American Journal of Translational Research 16, no. 9 (2024): 5020–37. http://dx.doi.org/10.62347/ocft1003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Hua, Jinsheng, Hui Yang, Xiufang Li, et al. "Cu(II)-functionalized silk fibroin films for the catalytic generation of nitric oxide." Biointerphases 17, no. 3 (2022): 031001. http://dx.doi.org/10.1116/6.0001690.

Full text

Abstract:

In situ release of nitric oxide (NO) has been suggested to be a potential functionalization strategy for blood-contacting implants. In this study, the NO generation capability catalyzed by the copper ion-incorporated silk fibroin (SF) films in the presence of S-nitroso- N-acetyl-dl-penicillamine (SNAP) is demonstrated. Cu(II) is effectively bound to the surface of the SF film based on metal–protein coordination. The x-ray photoelectron spectroscopy results indicate that copper ions may exist on the surface of the SF film in the form of Cu(II)/Cu(I) coexistence. The degradation behavior showed that the bound copper ions on the surface of the SF films can maintain a slow release in phosphate-buffered saline (PBS) or collagenase IA solution for 7 days. There was no significant difference in the release of copper ions between PBS degradation and enzyme degradation. The loading of copper ions significantly improved the release of NO from SNAP through catalysis. Based on the biological effects of copper ions and the ability to catalyze the release of NO from S-nitrosothiols, copper ion loading provides an option for the construction of bioactive SF biomaterials.

APA, Harvard, Vancouver, ISO, and other styles

Takhampunya, Ratree, R. Padmanabhan, and Sukathida Ubol. "Antiviral action of nitric oxide on dengue virus type 2 replication." Journal of General Virology 87, no. 10 (2006): 3003–11. http://dx.doi.org/10.1099/vir.0.81880-0.

Full text

Abstract:

Recently, nitric oxide (NO) has been shown to suppress dengue virus (DENV) RNA and protein accumulation in infected cells. In this report, the potential target of the inhibitory effect of NO was studied at the molecular level. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP), showed an inhibitory effect on RNA accumulation at around 8–14 h post-infection, which corresponded to the step of viral RNA synthesis in the DENV life cycle. The activity of the viral replicase isolated from SNAP-treated DENV-2-infected cells was suppressed significantly compared with that of the negative-control N-acetyl-dl-penicillamine (NAP)-treated cells. Further investigations on the molecular target of NO action showed that the activity of recombinant DENV-2 NS5 in negative-strand RNA synthesis was affected in the presence of 5 mM SNAP in in vitro RNA-dependent RNA polymerase (RdRp) assays, whereas the RNA helicase activity of DENV-2 NS3 was not inhibited up to a concentration of 15 mM SNAP. These results suggest that the inhibitory effect of NO on DENV infection is partly via inhibition of the RdRp activity, which then downregulates viral RNA synthesis.

APA, Harvard, Vancouver, ISO, and other styles

Bayes, Farhana, ASM Bazlul Karim, Laila Helaly, et al. "Spectrum of Hepatic Presentation of Wilsons Disease in Children Attending A Tertiary Care Centre of Dhaka City." Bangladesh Journal of Child Health 38, no. 2 (2014): 86–93. http://dx.doi.org/10.3329/bjch.v38i2.21142.

Full text

Abstract:

Background: The incidence of Wilsons disease (WD) is increasing day by day in every ethnic group worldwide. WD has been found as a common cause of chronic liver disease in children. This study was undertaken to find out the occurrence and different types of hepatic presentation of Wilsons disease in children admitted with liver diseases at a tertiary care centre of Bangladesh. Methodology: This cross sectional descriptive study was carried out at the department of Paediatric Gastroenterology and Nutrition, BSMMU during the period from March 2008 through April 2010. A total number of 71 children of both sexes aged 3-15 years, who had the features of liver disease (jaundice with or without hepatomegaly / splenomegaly and / or raised serum ALT), were enrolled in this study. For the purpose of the study, the diagnosis of WD was made by the presence of any 2 of the 3 features: presence of K-F ring by slit lamp examination, low serum ceruloplasmin level (<20 mg/dL) and urinary copper excretion of >1600 ?gm /24 hours after penicillamine challenge. Results: Wilsons disease was found in 31 (43.7%) of 71 children. Among them chronic liver diseases were 18 (58%), acute hepatitis 6 (19.4%), acute liver failure 6 (19.4%) and asymptomatic WD case was 1 (3.2%). The mean age ±SD of WD cases at presentation was 9.87±2.6 years and 22 (70%) cases were male. Maximum numbers of WD cases were found in children below 10 year of age. The two common presenting features of WD cases were jaundice 28 (90.3%) and ascitis (58.1%). Other features were K-F ring, 25 (80.6%) and hepatomegaly, 24 (77.4%). Biochemical findings showed low serum ceruloplasmin level (done in 20 patients) in 20 cases and 24 hours urinary copper excretion of >1600 mg/day in 23 cases. About one third of children presented with liver diseases were diagnosed as Wilsons disease and about 50% of WD cases presented with chronic liver diseases. Conclusion: Wilsons disease is a common cause of chronic liver disease. Penicillamine challenge is a reliable diagnostic test for Wilsons disease. DOI: http://dx.doi.org/10.3329/bjch.v38i2.21142 Bangladesh J Child Health 2014; VOL 38 (2) : 79-85

APA, Harvard, Vancouver, ISO, and other styles

Haftu, Hansa, Mohammed Mustefa, and Teklu Gebrehiwot. "Zinc Monotherapy as an Alternative Treatment Option for Decompensated Liver Disease due to Wilson Disease?" Case Reports in Hepatology 2020 (January 14, 2020): 1–5. http://dx.doi.org/10.1155/2020/1275940.

Full text

Abstract:

Background. Wilson disease is a rare metabolic disorder involving copper metabolism, and patients may present with a variable degree of hepatic, neurologic, and psychiatric manifestations. In the case of hepatic presentation, treatment is usually initiated with potentially toxic copper chelators (D-penicillamine or Trenton). Although zinc is of low toxicity and low cost for treatment of Wilson disease, it has been limited to the adjunctive as a single maintenance drug or for asymptomatic patients. The use of zinc monotherapy in patients suffering from a severe liver disease was not well studied. In our case report, we describe a pediatric patient who presented with liver failure and the use of zinc monotherapy in patients with severe hepatic manifestations. Case presentation. A 15-year-old male patient from Ethiopia presented with generalized body swelling (edema and ascites) with yellowish discoloration of his eyes and easy fatigability. He had hyperbilirubinemia, coagulopathy, hypoalbuminemia, and deranged liver enzymes. He had a Keyser–Fleischer ring visible with the naked eye, which was confirmed by slit-lamp examination. He had very low serum ceruloplasmin (<8 mg/L) and high 24-hour urine copper (150 mcg/dl). In accordance with the scoring system proposed by the 8th International Meeting on Wilson Disease and Menkes Disease, a diagnosis of Wilson disease was made. Zinc monotherapy with low copper diet was initiated for decompensated liver disease due to Wilson disease because of the inaccessibility of chelators (D-penicillamine or Trientine). After months of treatment with zinc, the patient experienced normalization of hepatic synthetic function and resolution of hypoalbuminemia and coagulopathy. The patient had also clinically stabilized (ascites, lower extremity swelling, edema, and jaundice were improved. Currently, the patient is on follow-up almost for the last four years in the gastrointestinal clinic. Conclusion. Our case shows that zinc has the potential for treatment in improving liver function. Though zinc has its own side effects, it is important and maybe an alternative treatment option in those with limited resources (not able to access chelators). This example hopefully will encourage future investigations and researches on zinc monotherapy for treating symptomatic decompensated hepatic Wilson disease.

APA, Harvard, Vancouver, ISO, and other styles

‘t Hart, Daan, Jinhua Li, Johan van der Vlag, and Tom Nijenhuis. "Repurposing Riociguat to Target a Novel Paracrine Nitric Oxide-TRPC6 Pathway to Prevent Podocyte Injury." International Journal of Molecular Sciences 22, no. 22 (2021): 12485. http://dx.doi.org/10.3390/ijms222212485.

Full text

Abstract:

Increased expression and activity of the Ca2+ channel transient receptor potential channel 6 (TRPC6) is associated with focal segmental glomerulosclerosis, but therapeutic strategies to target TRPC6 are currently lacking. Nitric oxide (NO) is crucial for normal glomerular function and plays a protective role in preventing glomerular diseases. We investigated if NO prevents podocyte injury by inhibiting injurious TRPC6-mediated signaling in a soluble guanylate cyclase (sGC)-dependent manner and studied the therapeutic potential of the sGC stimulator Riociguat. Experiments were performed using human glomerular endothelial cells and podocytes. Podocyte injury was induced by Adriamycin incubation for 24 h, with or without the NO-donor S-Nitroso-N-acetyl-DL-penicillamine (SNAP), the sGC stimulator Riociguat or the TRPC6 inhibitor Larixyl Acetate (LA). NO and Riociguat stimulated cGMP synthesis in podocytes, decreased Adriamycin-induced TRPC6 expression, inhibited the Adriamycin-induced TRPC6-mediated Ca2+ influx and reduced podocyte injury. The protective effects of Riociguat and NO were blocked when sGC activity was inhibited with 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or when TRPC6 activity was inhibited by LA. Our data demonstrate a glomerular (e)NOS-NO-sGC-cGMP-TRPC6 pathway that prevents podocyte injury, which can be translated to future clinical use by, e.g., repurposing the market-approved drug Riociguat.

APA, Harvard, Vancouver, ISO, and other styles

Aleksandrowicz, Marta, Beata Dworakowska, Krzysztof Dolowy, and Ewa Kozniewska. "Restoration of the response of the middle cerebral artery of the rat to acidosis in hyposmotic hyponatremia by the opener of large-conductance calcium sensitive potassium channels (BKCa)." Journal of Cerebral Blood Flow & Metabolism 37, no. 9 (2017): 3219–30. http://dx.doi.org/10.1177/0271678x16685575.

Full text

Abstract:

Hyposmotic hyponatremia (the decrease of extracellular concentration of sodium ions from 145 to 121 mM and the decrease of hyposmolality from 300 to 250 mOsm/kg H2O) impairs response of the middle cerebral artery (MCA) to acetylcholine and NO donor (S-nitroso-N-acetyl-DL-penicillamine). Since acidosis activates a similar intracellular signaling pathway, the present study was designed to verify the hypothesis that the response of the MCA to acidosis is impaired during acute hyposmotic hyponatremia due to abnormal NO-related signal transduction in vascular smooth muscle cells. Studies performed on isolated, cannulated, and pressurized rat MCA revealed that hyposmotic hyponatremia impaired the response of the MCA to acidosis and this was associated with hyposmolality rather than with decreased sodium ion concentration. Response to acidosis was restored by the BKCa but not by the KATP channel activator. Patch-clamp electrophysiology performed on myocytes freshly isolated from MCAs, demonstrated that hyposmotic hyponatremia does not affect BKCa currents but decreases the voltage-dependency of the activation of the BKCa channels in the presence of a specific opener of these channels. Our study suggests that reduced sensitivity of BKCa channels in the MCA to agonists results in the lack of response of this artery to acidosis during acute hyposmotic hyponatremia.

APA, Harvard, Vancouver, ISO, and other styles

Holliday, L. S., A. D. Dean, R. H. Lin, J. E. Greenwald, and S. L. Gluck. "Low NO concentrations inhibit osteoclast formation in mouse marrow cultures by cGMP-dependent mechanism." American Journal of Physiology-Renal Physiology 272, no. 3 (1997): F283—F291. http://dx.doi.org/10.1152/ajprenal.1997.272.3.f283.

Full text

Abstract:

High concentrations of nitric oxide (NO) inhibit bone resorption by mature osteoclasts. We examined the effects of low NO concentrations on osteoclast formation in mouse bone marrow cultures. The NO releasers sodium nitroprusside (SNP) and S-nitroso-N-acetyl-DL-penicillamine inhibited the formation of multinucleated cells expressing tartrate-resistant acid phosphatase (a marker for osteoclasts) when administered during the last 3 days of 6-day cultures (differentiation stage) but not during the first 3 days (proliferation stage). SNP (1 microM) completely inhibited pit formation on dentine wafers when added to cultures during osteoclast formation, but 100 microM SNP was required to inhibit pitting by mature osteoclasts. Conversely, the NO synthase inhibitors aminoguanidine and nitro-L-arginine methyl ester both increased osteoclast formation. Inhibition of osteoclast formation by NO likely was guanosine 3',5'-cyclic monophosphate (cGMP) dependent, as SNP increased cGMP in marrow cultures, and 1 mM 8-bromo-cGMP or dibutyryl-cGMP reduced osteoclast formation when administered during the differentiation stage. The cGMP-specific type V phosphodiesterase inhibitor, zaprinast (M & B 22948) also inhibited osteoclast formation (half-maximal inhibitory constant, 100 microM) only when added during the differentiation stage. We conclude that the differentiation stage of osteoclast formation is inhibited by increases in cGMP levels elicited by NO.

APA, Harvard, Vancouver, ISO, and other styles

Harraz, Osama F., Suzanne E. Brett, and Donald G. Welsh. "Nitric oxide suppresses vascular voltage-gated T-type Ca2+ channels through cGMP/PKG signaling." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 2 (2014): H279—H285. http://dx.doi.org/10.1152/ajpheart.00743.2013.

Full text

Abstract:

Recent reports have noted that T-type Ca2+ channels (CaV3.x) are expressed in vascular smooth muscle and are potential targets of regulation. In this study, we examined whether and by what mechanism nitric oxide (NO), a key vasodilator, influences this conductance. Using patch-clamp electrophysiology and rat cerebral arterial smooth muscle cells, we monitored an inward Ba2+ current that was divisible into a nifedipine-sensitive and -insensitive component. The latter was abolished by T-type channel blocker and displayed classic T-type properties including faster activation and steady-state inactivation at hyperpolarized potentials. NO donors (sodium nitroprusside, S-nitroso- N-acetyl- dl-penicillamine), along with activators of protein kinase G (PKG) signaling, suppressed T-type currents. Inhibitors of guanylyl cyclase/PKG {1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and KT5823, respectively}, had no effect on basal currents; KT5823 did, however, mask T-type Ca2+ channel current inhibition by NO/PKG. Functional experiments confirmed an inhibitory effect for NO on the T-type contribution to cerebral arterial myogenic tone. Cumulatively, our findings support the view that T-type Ca2+ channels are a regulatory target of vasodilatory signaling pathways. This targeting will influence Ca2+ dynamics and consequent tone development in the cerebral circulation.

APA, Harvard, Vancouver, ISO, and other styles

Ungvari, Zoltan, and Akos Koller. "Selected Contribution: NO released to flow reduces myogenic tone of skeletal muscle arterioles by decreasing smooth muscle Ca2+sensitivity." Journal of Applied Physiology 91, no. 1 (2001): 522–27. http://dx.doi.org/10.1152/jappl.2001.91.1.522.

Full text

Abstract:

To clarify the contribution of intracellular Ca2+ concentration ([Ca2+]i)-dependent and -independent signaling mechanisms in arteriolar smooth muscle (aSM) to modulation of arteriolar myogenic tone by nitric oxide (NO), released in response to increases in intraluminal flow from the endothelium, changes in aSM [Ca2+]i and diameter of isolated rat gracilis muscle arterioles (pretreated with indomethacin) were studied by fluorescent videomicroscopy. At an intraluminal pressure of 80 mmHg, [Ca2+]i significantly increased and myogenic tone developed in response to elevations of extracellular Ca2+ concentration. The Ca2+ channel inhibitor nimodipine substantially decreased [Ca2+]i and completely inhibited myogenic tone. Dilations to intraluminal flow (that were inhibited by N ω-nitro-l-arginine methyl ester) or dilations to the NO donor S-nitroso- N-acetyl-dl-penicillamine (that were inhibited by the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) were not accompanied by substantial decreases in aSM [Ca2+]i. 8-Bromoguanosine cGMP and the cGMP-specific phosphodiesterase inhibitor zaprinast significantly dilated arterioles yet elicited only minimal decreases in [Ca2+]i. Thus flow-induced endothelial release of NO elicits relaxation of arteriolar smooth muscle by a cGMP-dependent decrease of the Ca2+ sensitivity of the contractile apparatus without substantial changes in the pressure-induced level of [Ca2+]i.

APA, Harvard, Vancouver, ISO, and other styles

Ioannidis, I., and H. de Groot. "Cytotoxicity of nitric oxide in Fu5 rat hepatoma cells: evidence for co-operative action with hydrogen peroxide." Biochemical Journal 296, no. 2 (1993): 341–45. http://dx.doi.org/10.1042/bj2960341.

Full text

Abstract:

The NO-releasing compounds 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1), sodium nitroprusside (SNP) and S-nitroso-N-acetyl-DL-penicillamine (SNAP) mediated a rapid loss of viability of Fu5 rat hepatoma cells. SIN-1 in addition to NO also released the superoxide anion radical (O2-.). Its cytotoxicity, however, was not affected by superoxide dismutase. In contrast, the H2O2-converting enzyme catalase significantly, but not completely, diminished cell damage, indicating participation of H2O2 in the tumoricidal activity of SIN-1. Glucose oxidase (5 m-units/ml), producing similar amounts of H2O2 to 5 mM SIN-1, had no effect on cell viability. When 5 m-units/ml glucose oxidase was added to incubations with 5 mM SNP, which alone initiated cell injury of about 40%, cell damage was significantly increased up to 95%. Similar results were observed with 1 mM SNAP and 20 m-units/ml xanthine oxidase, which mediated cytotoxicity of about 90% when both compounds were added together, compared with 35% and 55% cell injury, respectively, induced by the single compounds. The results indicate that a co-operative action with H2O2 enhances the tumoricidal activity of NO in Fu5 cells. No evidence for an interplay of NO with O2-. in cytotoxicity, e.g. via the peroxynitrite anion (ONOO-), was found.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!