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Hypochlorous Acid (hypochlorou + acid)
Selected AbstractsZinc diethyldithiocarbamate allergenicity: potential haptenation mechanismsCONTACT DERMATITIS, Issue 2 2008Itai Chipinda Background:, Zinc diethyldithiocarbamate (ZDEC) and its disulfide, tetraethylthiuram disulfide (TETD), are rubber accelerators and contact allergens that cross-react in some individuals. Objective:, This study explored potential protein haptenation mechanisms of ZDEC and its oxidation products. Methods:, ZDEC oxidation/reduction products and sites of protein binding were assessed using high-performance liquid chromatography and mass spectrometry. The murine local lymph node assay (LLNA) was employed to probe haptenation mechanisms of ZDEC by examining its allergenicity along with its oxidation products and through elimination of oxidation and chelation mechanisms by substituting cobalt for zinc [cobalt (II) dithiocarbamate, CoDEC]. Results:, Oxidation of ZDEC by hypochlorous acid (bleach, HOCl), iodine, or hydrogen peroxide resulted in production of TETD, tetraethylthiocarbamoyl disulfide, and tetraethyldicarbamoyl disulfide (TEDCD). Albumin thiols reduced TETD with subsequent mixed disulfide formation/haptenation. ZDEC directly chelated the copper ion on the active site of the superoxide dismutase, whereas CoDEC did not bind to Cu proteins or form mixed disulfides with free thiols. ZDEC, sodium diethyldithiocarbamate, TEDCD, and TETD were all positive in the LLNA except CoDEC, which was non-allergenic. Conclusion:, The thiol is the critical functional group in ZDEC's allergenicity, and haptenation is predominantly through chelation of metalloproteins and formation of mixed disulfides. [source] The role of taurine in diabetes and the development of diabetic complicationsDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 5 2001Svend Høime Hansen Abstract The ubiquitously found ,-amino acid taurine has several physiological functions, e.g. in bile acid formation, as an osmolyte by cell volume regulation, in the heart, in the retina, in the formation of N -chlorotaurine by reaction with hypochlorous acid in leucocytes, and possibly for intracellular scavenging of carbonyl groups. Some animals, such as the cat and the C57BL/6 mouse, have disturbances in taurine homeostasis. The C57BL/6 mouse strain is widely used in diabetic and atherosclerotic animal models. In diabetes, the high extracellular levels of glucose disturb the cellular osmoregulation and sorbitol is formed intracellularly due to the intracellular polyol pathway, which is suspected to be one of the key processes in the development of diabetic late complications and associated cellular dysfunctions. Intracellular accumulation of sorbitol is most likely to cause depletion of other intracellular compounds including osmolytes such as myo -inositol and taurine. When considering the clinical complications in diabetes, several links can be established between altered taurine metabolism and the development of cellular dysfunctions in diabetes which cause the clinical complications observed in diabetes, e.g. retinopathy, neuropathy, nephropathy, cardiomyopathy, platelet aggregation, endothelial dysfunction and atherosclerosis. Possible therapeutic perspectives could be a supplementation with taurine and other osmolytes and low-molecular compounds, perhaps in a combinational therapy with aldose reductase inhibitors. Copyright © 2001 John Wiley & Sons, Ltd. [source] Redox properties of the couple compound I/native enzyme of myeloperoxidase and eosinophil peroxidaseFEBS JOURNAL, Issue 19 2001Jürgen Arnhold The standard reduction potential of the redox couple compound I/native enzyme has been determined for human myeloperoxidase (MPO) and eosinophil peroxidase (EPO) at pH 7.0 and 25 °C. This was achieved by rapid mixing of peroxidases with either hydrogen peroxide or hypochlorous acid and measuring spectrophotometrically concentrations of the reacting species and products at equilibrium. By using hydrogen peroxide, the standard reduction potential at pH 7.0 and 25 °C was 1.16 ± 0.01 V for MPO and 1.10 ± 0.01 V for EPO, independently of the concentration of hydrogen peroxide and peroxidases. In the case of hypochlorous acid, standard reduction potentials were dependent on the hypochlorous acid concentration used. They ranged from 1.16 V at low hypochlorous acid to 1.09 V at higher hypochlorous acid for MPO and from 1.10 V to 1.03 V for EPO. Thus, consistent results for the standard reduction potentials of redox couple compound I/native enzyme of both peroxidases were obtained with all hydrogen peroxide and at low hypochlorous acid concentrations: possible reasons for the deviation at higher concentrations of hypochlorous acid are discussed. They include instability of hypochlorous acid, reactions of hypochlorous acid with different amino-acid side chains in peroxidases as well as the appearance of a compound I,chloride complex. [source] Biological hydroperoxides and singlet molecular oxygen generationIUBMB LIFE, Issue 4-5 2007Sayuri Miyamoto Abstract The decomposition of lipid hydroperoxides (LOOH) into peroxyl radicals is a potential source of singlet molecular oxygen (1O2) in biological systems. Recently, we have clearly demonstrated the generation of 1O2 in the reaction of lipid hydroperoxides with biologically important oxidants such as metal ions, peroxynitrite and hypochlorous acid. The approach used to unequivocally demonstrate the generation of 1O2 in these reactions was the use of an isotopic labeled hydroperoxide, the 18O-labeled linoleic acid hydroperoxide, the detection of labeled compounds by HPLC coupled to tandem mass spectrometry (HPLC-MS/MS) and the direct spectroscopic detection and characterization of 1O2 light emission. Using this approach we have observed the formation of 18O-labeled 1O2 by chemical trapping of 1O2 with anthracene derivatives and detection of the corresponding labeled endoperoxide by HPLC-MS/MS. The generation of 1O2 was also demonstrated by direct spectral characterization of 1O2 monomol light emission in the near-infrared region (, = 1270 nm). In summary, our studies demonstrated that LOOH can originate 1O2. The experimental evidences indicate that 1O2 is generated at a yield close to 10% by the Russell mechanism, where a linear tetraoxide intermediate is formed in the combination of two peroxyl radicals. In addition to LOOH, other biological hydroperoxides, including hydroperoxides formed in proteins and nucleic acids, may also participate in reactions leading to the generation 1O2. This hypothesis is currently being investigated in our laboratory. [source] Electrolytic removal of ammonia from brine wastewater: scale-up, operation and pilot-scale evaluationJOURNAL OF CHEMICAL TECHNOLOGY & BIOTECHNOLOGY, Issue 3 2004Catalino G Alfafara Abstract Brine wastewater with a high ammonia content from an iodine processing plant (commonly called kansui in Japan) was treated by electrolysis. The system, which can be considered as an indirect electrolytic treatment process, generates chlorine at the anodes and initiates the formation of mixed oxidants like hypochlorous acid. The oxidants then act as agents for ammonia destruction. Laboratory-scale experiments showed that high ammonia concentrations (as much as 200 mg dm,3) could be completely removed within a few minutes, and could be considered a good alternative for efficient ammonia removal from saline wastewaters. From laboratory-scale experiments in the batch and continuous modes, the charge dose was analyzed and used as the operating and scale-up factor. The value of the charge dose was not severely affected by changes in operating conditions such as electrode spacing and temperature. The charge dose from batch and continuous runs was found to be in the range of 23 C (mg NH4 -N removed),1 to 29 C (mg NH4 -N removed),1. Using the charge dose obtained from laboratory-scale continuous electrolysis experiments as the scale-up factor, a pilot-scale reactor was designed, and the operating conditions were calculated. In the pilot-scale reactor tests at different flow rates, the effluent ammonia concentrations were reasonably close to the calculated values predicted from the charge dose equation. Copyright © 2004 Society of Chemical Industry [source] Myeloperoxidase and chlorinated peptides in osteoarthritis: potential biomarkers of the diseaseJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 9 2007Marla J. Steinbeck Abstract Osteoarthritis (OA) is a disabling condition in which multiple initiating events or conditions (heritable and nonheritable) result in eventual loss of articular cartilage. However, the etiology of OA remains poorly understood, and diagnosis of early disease is difficult due to the lack of specific identifiers. Recent literature suggests that a series of inflammatory processes may be involved in initiating and propagating OA. We hypothesized that products of neutrophils and macrophages, namely myeloperoxidase (MPO), a specific enzyme responsible for the production of both highly reactive hypochlorous acid (HOCl) and chlorine gas (Cl2) and chlorinated peptides, may be present in the synovial fluid of patients with OA. We examined the synovial fluid from 30 patients to identify and profile the presence of MPO. We divided the samples into three groups using radiographic and clinical assessment: (1) control, patients with acute knee injury with no history of OA and no radiographic evidence of OA; (2) early OA, patients with a mild OA based on radiographs; and (3) late OA, patients with a longstanding history of OA and with radiographic evidence of complete joint loss. Patients with early OA demonstrated significantly elevated levels of MPO. We also demonstrated the presence of HOCl and Cl2 modified proteins (Cl-peptides) in early OA synovial fluid samples by liquid chromatography and mass spectrometry. Patients in the control and advanced OA groups demonstrated little elevation in MPO levels and Cl-peptides were undetectable. These results indicate that MPO and Cl-peptides may serve as diagnostic markers for the detection of early OA. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1128,1135, 2007 [source] In situ hypochlorous acid generation for the treatment of brackish shrimp aquaculture wastewaterAQUACULTURE RESEARCH, Issue 5 2008Krishnan Vijayaraghavan Abstract This study presents an unconventional framework for treating shrimp aquaculture wastewater based on in situ hypochlorous acid (HOCl) oxidation. The in situ oxidation process makes use of the salinity present in aquaculture wastewater to generate HOCl. The undivided electrolytic cell consisted of two sets of graphite as the anode and stainless sheets as the cathode. The electrochemical oxidation of shrimp aquaculture wastewater was carried out for an influent COD concentration of 1730 mg L,1 at current densities of 37.2 and 74.5 mA cm,2. The results showed that in order to achieve a residual COD concentration of 50±5 mg L,1 at current densities of 37.2 and 74.5 mA cm,2, electrolysis periods of 60 and 30 min are required respectively. Hence, for the above-mentioned current densities, the corresponding energy requirements were found to be 19.4 and 13.3 W h L,1. The cost incurred in treating 1 m3 of shrimp aquaculture wastewater was found to be RM 4 and 3 when the electrolytic reactor was operated at a current density of 37.2 and 74.5 mA cm,2 with a salinity of 23,. The foregoing study highlights the potential of in situ HOCl oxidation in treating brackish shrimp aquaculture wastewater. [source] Nitrite-mediated protection against hypochlorous acid,induced chondrocyte toxicity: A novel cytoprotective role of nitric oxide in the inflamed joint?ARTHRITIS & RHEUMATISM, Issue 11 2003Matthew Whiteman Objective To examine the potential consequences of overproduction of nitric oxide (NO) and nitrite (NO) in the inflamed rheumatoid joint. Methods Human articular chondrocytes in culture were exposed to HOCl (hypochlorous acid, a physiologic oxidant formed in increased amounts at sites of chronic inflammation), and assays of cell viability, intracellular ATP and glutathione (GSH), and lactate dehydrogenase (LDH) were performed. HOCl-induced lipid peroxidation and activation of the MAP kinases ERK-1/2, JNK-1/2, and p38 were also measured. The modulatory effects of NO-derived nitrite (NO) and nitrate (NO) on HOCl-mediated chondrocyte toxicity were investigated. Results Exposure of human articular chondrocytes to HOCl resulted in a concentration- and time-dependent loss of viability, decrease in ATP and GSH levels, LDH leakage, and cell death. HOCl induced significant lipid peroxidation as well as activation of the MAP kinases ERK-1/2 and p38 but not JNK-1/2. However, the presence of NO but not NO substantially decreased HOCl-dependent cellular toxicity even when NO was added at low (,M) concentrations. In sharp contrast, NO (1 mM) did not inhibit superoxide-, hydroxyl radical,, H2O2 -, or peroxynitrite-mediated cytotoxicity. Furthermore, culture media from cells treated with interleukin-1, (to generate NO and NO) offered significantly more protection against HOCl-mediated cytotoxicity than culture media from untreated cells. Conclusion These data suggest that NO accumulation at chronically inflamed sites where both HOCl and NO are overproduced may be cytoprotective against damage induced by HOCl. Accumulation of NO could represent a novel cytoprotective role of NO in inflamed joints. A mechanism for this is suggested. [source] In vitro protective effect of Rhodiola rosea extract against hypochlorous acid-induced oxidative damage in human erythrocytesBIOFACTORS, Issue 3 2004Roberta De Sanctis Abstract Rhodiola rosea L. (Crassulaceae) is a plant living at high altitudes in Europe and Asia. Its roots have long been used in the traditional medical system of these geographical areas to increase the organism resistance to physical stress; today, it has become an important component of many dietary supplements. In this study we investigate the antioxidant capacity of the R. rosea aqueous extract evaluating its ability to counteract some of the main damages induced by hypochlorous acid (HOCl), a powerful oxidant generated by activated phagocytes, to human erythrocytes. Ascorbic acid was used as a reference substance because of its physiological HOCl-scavenging ability. Our study demonstrates that R. rosea is able to significantly protect, in a dose-dependent manner, human RBC from glutathione (GSH) depletion, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) inactivation and hemolysis induced by the oxidant. Furthermore, we demonstrate that R. rosea aqueous extract acts from the inside of the erythrocyte suggesting a probable involving of cell components. The protection on GSH afforded by the R. rosea extract with respect to ascorbic acid, occurred also if added 2 or 5 min. later than the oxidant, suggesting a more rapid or powerful effect. [source] | ||||||||||||||||