Generation Of Hypochlorous Acid Research Articles

An Oxidative Cleavage-Based Cruciform DNA Nanostructure for In Vivo Hypochlorous Acid Visualization to Monitor Intestinal Inflammation.

Ulcerative colitis is a persistent inflammatory bowel disease characterized by inflammation and ulceration in the colon and gastrointestinal tract. It was indicated that the generation of hypochlorous acid (HClO) through the enzymatic activity of myeloperoxidase is significantly linked to ulcerative colitis. In this study, by assembling two hairpins (Hpa and Hpb) onto a quadrivalent cruciform DNA nanostructure, a novel HClO-activatable fluorescent probe was developed based on DNA nanomaterials (denoted MHDNA), which is sensitive, economic, simple, and stable. In the presence of HClO, the Trigger (T) was liberated from the MHDNA probe through a hydrolysis reaction between HClO and phosphorothioate (PS), which is modified on the MHDNA probe and has proved to exhibit particular susceptibility to the HClO. The liberated T subsequently initiated the opening of Hpa and Hpb to facilitate the catalyzed hairpin assembly (CHA) reaction, resulting in the changes of fluorescence and releasing T for recycled signal amplification to achieve sensitive detection of HClO (with a limit of detection 9.83 nM). Additionally, the MHDNA-based spatial-confinement effect shortens the physical distance between Hpa and Hpb and yields a high local concentration of the two reactive hairpins, achieving more rapid reaction kinetics in comparison to conventional CHA methods. Inspirationally, the MHDNA probe was effectively utilized for imaging HClO in ulcerative colitis mice, yielding valuable diagnostic insights for ulcerative colitis.

Sunlight-Driven Generation of Hypochlorous Acid on Plasmonic Au/AgCl Catalysts in Aerated Chloride Solution.

HClO is typically manufactured from Cl2 gas generated by the electrochemical oxidation of Cl- using considerable electrical energy with a large concomitant emission of CO2. Therefore, renewable energy-driven HClO generation is desirable. In this study, we developed a strategy for stable HClO generation by sunlight irradiation of a plasmonic Au/AgCl photocatalyst in an aerated Cl- solution at ambient temperature. Plasmon-activated Au particles by visible light generate hot electrons, which are consumed by O2 reduction, and hot holes, which oxidize the lattice Cl- of AgCl adjacent to the Au particles. The formed Cl2 is disproportionated to afford HClO, and the removed lattice Cl- are compensated by the Cl- in the solution, thus promoting a catalytic HClO generation cycle. A solar-to-HClO conversion efficiency of ∼0.03% was achieved by simulated sunlight irradiation, where the resultant solution contained >38 ppm (>0.73 mM) of HClO and exhibited bactericidal and bleaching activities. The strategy based on the Cl- oxidation/compensation cycles will pave the way for sunlight-driven clean, sustainable HClO generation.

Effective inactivation of Escherichia coli, Staphylococcus aureus, and Pseudomonas aeruginosa sp. in high‐frequency driven electrosurgery

AbstractWound infection must be avoided in high‐frequency (HF) driven electrosurgery. In this study, the plasma treatment of bacterial solution is characterized by means of voltage‐current measurements, chemical activity analysis, microphotography, and numerical simulation. Here, we have found that the plasma‐activated physiological saline in HF‐driven electrosurgery is very effective in the inactivation of main human pathogenic bacteria. Our analysis shows that the effective inactivation of Escherichia coli, Staphylococcus aureus, and Pseudomonas aeruginosa sp. in the HF‐driven electrosurgery is due to the generation of hypochlorous acid (HClO) by the electrolysis of saline solution in the electrosurgery. The simulation indicates the very effective inactivation of human pathogenic bacteria by HClO in HF‐driven electrosurgery.

RLS-0071, a dual-targeting anti-inflammatory peptide - biomarker findings from a first in human clinical trial

BackgroundRLS-0071 is a novel 15 amino acid peptide dual-targeting anti-inflammatory inhibitor of complement and neutrophil effectors. RLS-0071 inhibits classical complement pathway activation at C1 and blocks the enzymatic activity of myeloperoxidase that leads to the generation of hypochlorous acid and induces NETosis. This peptide is being developed for the treatment of neonatal hypoxic ischemic encephalopathy (HIE) and neutrophilic pulmonary diseases.MethodsThis was a first in human clinical trial in healthy volunteers to assess safety and pharmacokinetics of single and multiple ascending doses of RLS-0071.ResultsRLS-0071 single and multiple doses were not associated with any clinically significant changes in safety parameters, laboratory test results or ECG measurements. Adverse events were similar between active drug and placebo groups. The pharmacokinetic profile demonstrated dose proportionality and two-compartment kinetics with rapid tissue distribution. Exploratory biomarker and target engagement assays demonstrated dose dependent classical complement pathway inhibition and myeloperoxidase binding.Discussion/ConclusionRLS-0071 was shown to be safe and well-tolerated at all doses tested with rapid tissue distribution and target engagement for both the classical complement pathway and myeloperoxidase. The findings are supportive of further clinical development and evaluation of RLS-0071 in conditions such as HIE and acute pulmonary diseases.Trial registrationClinicalTrials.gov Identifier: NCT05298787 March 28, 2022. Retrospectively registered.

In Vitro and In Vivo Antimicrobial Activity of Hypochlorous Acid against Drug-Resistant and Biofilm-Producing Strains.

ABSTRACTThe aims of this study were as follows. First, we determined the antimicrobial efficacy of hypochlorous acid (HClO) against bacterial, fungal, and yeast strains growing planktonically and growing in biofilms. Second, we sought to compare the activity of the combination of daptomycin and HClO versus those of the antimicrobial agents alone for the treatment of experimental catheter-related Staphylococcus epidermidis infection (CRI) using the antibiotic lock technique (ALT) in a rabbit model. HClO was generated through direct electric current (DC) shots at determined amperages and times. For planktonic susceptibility studies, 1 to 3 DC shots of 2, 5, and 10 mA from 0 to 300 s were applied. A DC shot of 20 mA from 0 to 20 min was applied to biofilm-producing strains. Central venous catheters were inserted into New Zealand White rabbits, inoculated with an S. epidermidis strain, and treated with saline solution or ALT using daptomycin (50 mg/mL), HClO (20 mA for 45 min), or daptomycin plus HClO. One hundred percent of the planktonic bacterial, fungal, and yeast strains were killed by applying one DC shot of 2, 5, and 10 mA, respectively. One DC shot of 20 mA for 20 min was sufficient to eradicate 100% of the tested biofilm-producing strains. Daptomycin plus HClO lock therapy showed the highest activity for experimental CRI with S. epidermidis. HClO could be an effective strategy for treating infections caused by extensively drug-resistant or multidrug-resistant and biofilm-producing strains in medical devices and chronic wounds. The results of the ALT using daptomycin plus HClO may be promising.IMPORTANCE Currently, drug-resistant infections are increasing and there are fewer antibiotics available to treat them. Therefore, there is an urgent need to find new antibiotics and nonantimicrobial strategies to treat these infections. We present a new nonantibiotic strategy based on hypochlorous acid generation to treat long-term catheter-related and chronic wounds infections.

Synthesis of Sulfonyl Halides from Disulfides or Thiols Using Sodium Hypochlorite Pentahydrate (NaOCl·5H2O) Crystals

AbstractSynthesis of sulfonyl halides using sodium hypochlorite pentahydrate (NaOCl·5H2O) crystals was studied in detail, considering the reaction rate and yield of the desired product. NaOCl·5H2O reacted with disulfides or thiols in acetic acid to produce sulfonyl chlorides. The yields of the desired sulfonyl chlorides were enhanced when the reaction was performed in (trifluoromethyl)benzene under a CO2 atmosphere. The generation of hypochlorous acid (HOCl) was essential for both reactions. Similarly, sulfonyl bromides were prepared via the reaction of disulfides or thiols with sodium bromide and NaOCl·5H2O crystals in acetic acid owing to the generation of hypobromous acid (HOBr). However, the reaction could not proceed in (trifluoromethyl)benzene under a CO2 atmosphere because bromine was produced instead of HOBr.

Allopurinol attenuates oxidative injury in rat hearts suffered ischemia/reperfusion via suppressing the xanthine oxidase/vascular peroxidase 1 pathway

Allopurinol, a xanthine oxidase (XO) inhibitor, is reported to alleviate myocardial ischemia/reperfusion (I/R) injury by reducing the production of reactive oxygen species (ROS). As an XO-derived product, H2O2 can act as a substrate of vascular peroxidase 1 (VPO1) to induce the generation of hypochlorous acid (HOCl), a potent oxidant. This study aims to explore whether the XO/VPO1 pathway is involved in the anti-oxidative effects of allopurinol on the myocardial I/R injury. In a rat heart model of I/R, allopurinol alleviated I/R oxidative injury accompanied by decreased XO activity, XO-derived products (H2O2 and uric acid), and VPO1 expression (mRNA and protein). In a cardiac cell model of hypoxia/reoxygenation (H/R), allopurinol or XO siRNA reduced H/R injury concomitant with decreased XO activity, VPO1 expression as well as the XO and VPO1-derived products (H2O2, uric acid, and HOCl). Although knockdown of VPO1 could also exert a beneficial effect on H/R injury, it did not affect XO activity, XO expression, and XO-derived products. Based on these observations, we conclude that the novel pathway of XO/VPO1 is responsible for, at least partly, myocardial I/R-induced oxidative injury, and allopurinol exerted the cardioprotective effects on myocardial I/R injury via inhibiting the XO/VPO1 pathway.

Peptide inhibition of neutrophil-mediated injury after in vivo challenge with supernatant of Pseudomonas aeruginosa and immune-complexes.

Neutrophils are recognized for their role in host defense against pathogens as well as inflammatory conditions mediated through many mechanisms including neutrophil extracellular trap (NET) formation and generation of reactive oxygen species (ROS). NETs are increasingly appreciated as a major contributor in autoimmune and inflammatory diseases such as cystic fibrosis. Myeloperoxidase (MPO), a key neutrophil granule enzyme mediates generation of hypochlorous acid which, when extracellular, can cause host tissue damage. To better understand the role played by neutrophils in inflammatory diseases, we measured and modulated myeloperoxidase activity and NETs in vivo, utilizing a rat peritonitis model. RLS-0071 is a 15 amino acid peptide that has been shown to inhibit myeloperoxidase activity and NET formation in vitro. The rat model of inflammatory peritonitis was induced with intraperitoneal injection of either P. aeruginosa supernatant or immune-complexes. After euthanasia, a peritoneal wash was performed and measured for myeloperoxidase activity and free DNA as a surrogate for measurement of NETs. P. aeruginosa supernatant caused a 2-fold increase in MPO activity and free DNA when injected IP. Immune-complexes injected IP increased myeloperoxidase activity and free DNA 2- fold. RLS-0071 injection decreased myeloperoxidase activity and NETs in the peritoneal fluid generally to baseline levels in the presence of P. aeruginosa supernatant or immune-complexes. Taken together, RLS-0071 demonstrated the ability to inhibit myeloperoxidase activity and NET formation in vivo when initiated by different inflammatory stimuli including shed or secreted bacterial constituents as well as immune-complexes.

Optimization of hypochlorous acid generation by HCl electrolysis through response surface methodology and artificial neural networks

Hypochlorous acid (HOCl), also known as electrolyzed water (EW), is a sustainable and environment-friendly disinfectant, which can comply with food safety regulations. In this study, HOCl was produced through HCl electrolysis using an acrylic electrolyzing reactor without a diaphragm between iridium oxide electrodes coated with titanium. The Box–Behnken design (BBD) was adopted to study the effects of feed water flow rate (FR), pH, temperature, electric voltage, acid concentration (AC), and acid dosing pump stroke (APS) on HOCl production measured as available chlorine concentration (ACC). Then, optimum parameters were explored using response surface methodology (RSM). The proposed quadratic models defined the relationship between HOCl production and the process variables. The models were statistically significant as shown by analysis of variance. The optimum operating parameters for HOCl production were 6.5 L/min, pH 7.5 at 20 °C, 3.8 volts, 6% AC, and APS at 3%. The FR, AC, and APS were significant parameters, and no substantial effect was observed for pH and temperature of feed water or the variation in current–voltage. High FR caused a conspicuous drop, and the high voltage showed a slight increase in ACC. However, an increase in AC and APS significantly enhanced the ACC, although the pH dropped below 5.0–6.5, indicating the presence of other chlorine-based compounds apart from HOCl. RSM model validation through experimental results indicated that the proposed model could effectively provide a relationship between ACC and process variables. Additionally, an artificial neural network model was tested to predict the ACC that showed good fitness to the experimental results.

Microbial-derived indoles inhibit neutrophil myeloperoxidase to diminish bystander tissue damage.

During episodes of acute inflammation, polymorphonuclear leukocytes (PMNs) are actively recruited to sites of inflammation or injury where they provide anti-microbial and wound-healing functions. One enzyme crucial for fulfilling these functions is myeloperoxidase (MPO), which generates hypochlorous acid from Cl- and hydrogen peroxide. The potential exists, however, that uncontrolled the extracellular generation of hypochlorous acid by MPO can cause bystander tissue damage and inhibit the healing response. Previous work suggests that the microbiota-derived tryptophan metabolites 1H-indole and related molecules ("indoles") are protective during intestinal inflammation, although their precise mechanism of action is unclear. In the present work, we serendipitously discovered that indoles are potent and selective inhibitors of MPO. Using both primary human PMNs and recombinant human MPO in a cell-free system, we revealed that indoles inhibit MPO at physiologic concentrations. Particularly, indoles block the chlorinating activity of MPO, a reliable marker for MPO-associated tissue damage, as measured by coulometric-coupled HPLC. Further, we observed direct interaction between indoles and MPO using the established biochemical techniques microscale thermophoresis and STD-NMR. Utilizing a murine colitis model, we demonstrate that indoles inhibit bystander tissue damage, reflected in decreased colon 3-chlorotyrosine and pro-inflammatory chemokine expression in vivo. Taken together, these results identify microbiota-derived indoles that acts as endogenous immunomodulatory compounds through their actions on MPO, suggesting a symbiotic association between the gut microbiota and host innate immune system. Such findings offer exciting new targets for future pharmacological intervention.

Discovery of a novel indole pharmacophore for the irreversible inhibition of myeloperoxidase (MPO)

Myeloperoxidase (MPO) activity and subsequent generation of hypochlorous acid has been associated with the killing of host-invading microorganisms (e.g. bacteria, viruses, and fungi). However, during oxidative stress, high MPO activity can damage host tissue and is linked to several chronic inflammatory conditions. Herein, we describe the development of a novel biaryl, indole-pyrazole series of irreversible mechanism-based inhibitors of MPO. Derived from an indole-containing high-throughput screen hit, optimization efforts resulted in potent and selective 6-substituted indoles with good oral bioavailability and in vivo activity.

Highly efficient removal of organic pollutants via a green catalytic oxidation system based on sodium metaborate and peroxymonosulfate

The development of highly efficient and green catalytic oxidation process based on peroxymonosulfate (PMS) activation has been identified to be a significant yet challenging objective in the environmental catalysis field. A simple, environmentally benign and highly effective catalytic oxidation system was innovatively constructed by coupling NaBO2 and PMS for the removal of Acid Red 1. The catalytic mechanism in the NaBO2/PMS system was elucidated by electron paramagnetic resonance (EPR) combined with several radical capture reagents (ascorbic acid, methanol, tert-butyl alcohol, ethanol and l-histidine). The experimental results indicated that singlet oxygen (1O2) severed as the predominant reactive oxygen species (ROS) rather than the HO or ▪ during the catalytic oxidation process, at variance with the reported radical pathway in the Co2+/PMS system. Inspiringly, p-benzoquinone (p-BQ) as a trapping agent in most advanced oxidation process could be turned into the positive one in the NaBO2/PMS system, achieving a nearly 3-times enhancement in terms of the rate constant for AR1 removal. More interestingly, sodium chloride (NaCl) presented the same enhancement effect as p-benzoquinone due to generation of hypochlorous acid (HOCl) and more 1O2, which was completely different from the reported. This study develops a highly efficient green oxidation process and opens up a new insight in the remediation of contaminated water.

8-Chloroadenosine induces apoptosis in human coronary artery endothelial cells through the activation of the unfolded protein response

Infiltration of leukocytes within the vessel at sites of inflammation and the subsequent generation of myeloperoxidase-derived oxidants, including hypochlorous acid, are key characteristics of atherosclerosis. Hypochlorous acid is a potent oxidant that reacts readily with most biological molecules, including DNA and RNA. This results in nucleic acid modification and the formation of different chlorinated products. These products have been used as biomarkers of inflammation, owing to their presence in elevated amounts in different inflammatory fluids and diseased tissue, including atherosclerotic lesions. However, it is not clear whether these materials are simply biomarkers, or could also play a role in the development of chronic inflammatory pathologies. In this study, we examined the reactivity of different chlorinated nucleosides with human coronary artery endothelial cells (HCAEC). Evidence was obtained for the incorporation of each chlorinated nucleoside into the cellular RNA or DNA. However, only 8-chloro-adenosine (8ClA) had a significant effect on the cell viability and metabolic activity. Exposure of HCAEC to 8ClA decreased glycolysis, and resulted in a reduction in ATP, with a corresponding increase in the chlorinated analogue, 8Cl-ATP in the nucleotide pool. 8ClA also induced sustained endoplasmic reticulum stress within the HCAEC, which resulted in activation of the unfolded protein response, the altered expression of antioxidant genes and culminated in the release of calcium into the cytosol and cell death by apoptosis. Taken together, these data provide new insight into pathways by which myeloperoxidase activity and resultant hypochlorous acid generation could promote endothelial cell damage during chronic inflammation, which could be relevant to the progression of atherosclerosis.

Catalase prevents myeloperoxidase self-destruction in response to oxidative stress

Catalase (CAT) and myeloperoxiase (MPO) are heme-containing enzymes that have attracted attention for their role in the etiology of numerous respiratory disorders such as cystic fibrosis, bronchial asthma, and acute hypoxemic respiratory failure. However, information regarding the interrelationship and competition between the two enzymes, free iron accumulation, and decreased levels of non-enzymatic antioxidants at sites of inflammation is still lacking. Myeloperoxidase catalyzes the generation of hypochlorous acid (HOCl) from the reaction of hydrogen peroxide (H2O2) and chloride (Cl−). Self-generated HOCl has recently been proposed to auto-inhibit MPO through a mechanism that involves MPO heme destruction. Here, we investigate the interplay of MPO, HOCl, and CAT during catalysis, and explore the crucial role of MPO inhibitors and HOCl scavengers in protecting the catalytic site from protein modification of both enzymes against oxidative damage mediated by HOCl. We showed that CAT not only competes with MPO for H2O2 but also scavenges HOCl. The protective role provided by CAT versus the damaging effect provided by HOCl depends in part on the ratio between MPO/CAT and the affinity of the enzymes towards H2O2 versus HOCl. The severity of such damaging effects mainly depends on the ratio of HOCl to enzyme heme content. In addition to its effect in mediating protein modification and aggregation, HOCl oxidatively destroys the catalytic sites of the enzymes, which contain porphyrin rings and iron. Thus, modulation of MPO/CAT activities may be a fundamental feature of catalysis, and functions to down-regulate HOCl synthesis and prevent hemoprotein heme destruction and/or protein modification.

Vascular peroxidase 1 up regulation by angiotensin II attenuates nitric oxide production through increasing asymmetrical dimethylarginine in HUVECs

Asymmetric dimethylarginine (ADMA), the endogenous inhibitor of nitric oxide synthase, contributes to endothelial dysfunction and subsequent cardiovascular events including hypertension. Vascular peroxidase 1 (VPO1) is a novel heme-containing peroxidase that uses hydrogen peroxide (H2O2) generated from co-expressed nicotinamide adenine dinucleotide phosphate (NADPH) oxidase to catalyze peroxidative reactions. Our previous study revealed a clear connection between VPO1 gene expression and endothelial dysfunction in spontaneously hypertensive rats. In the present study, we explored whether VPO1 participates in endothelial dysfunction during hypertension by increasing ADMA production. Spontaneously hypertensive rats displayed impaired endothelium-dependent relaxation, decreased eNOS expression and nitric oxide production, significantly increased VPO1 expression in both plasma and aorta tissue, and an increased ADMA level in plasma. In cultured endothelial cells, angiotensin II increased the ADMA level by inhibiting dimethylarginine dimethylaminohydrolase activity, which was inhibited by knockdown of VPO1 using small hairpin RNA. Moreover, the NADPH oxidase inhibitor and the hydrogen peroxide scavenger attenuated angiotensin II-mediated up-regulation of VPO1 and generation of hypochlorous acid. Furthermore, VPO1-derived hypochlorous acid suppressed recombinant dimethylarginine dimethylaminohydrolase activity and increased ADMA production. VPO1 plays a critical role in ADMA production via H2O2–VPO1–hypochlorous acid pathways, which may contribute to endothelial dysfunction in hypertension.

BioNano engineered hybrids for hypochlorous acid generation

Enzyme-based systems represent a user- and environmentally-friendly alternative to current corrosive and/or toxic decontamination technologies used for microbial decontamination. Herein an easily deployable enzyme-nanosupport hybrid system was developed for in situ generation of hypochlorous acid (HOCl), a strong decontaminant. The user-controlled strategy allowed co-immobilization of two different enzymes at a nanosupport interface and decontaminant generation through a chain reaction. For this, glucose oxidase was used as the working enzyme and co-immobilized onto multi-walled carbon nanotubes along with chloroperoxidase. Our hypothesis was that hydrogen peroxide produced at the nanosupport interface through the glucose oxidase enzymatic reaction can further be used as substrate by the co-immobilized CPO to convert (Cl−) into HOCl. The chemistry of the immobilization method, as well as the enzyme loading, activity, kinetics and enzyme stability at the nanointerface were evaluated. The multi-enzyme system was found to be able to initiate and propagate the chain reaction resulting in decontaminant production. The strong capability of HOCl generation can be viewed as an important first step toward creating self-sustainable microbial decontamination coatings to be used against various pathogens such as bacteria and spores.

Intracellular localization of myeloperoxidase in murine peritoneal B-lymphocytes and macrophages

Generation of hypochlorous acid (HOCl), an important microbicidal agent, is considered to be the main function of myeloperoxidase (MPO), an enzyme present in phagocytes. High amounts of MPO are present in neutrophil azurophilic granules, which are mobilized into the phagolysosome vacuole during phagocytosis. MPO is also present in monocytes and macrophages, although to a lesser degree than in neutrophils. In the present study, we investigated the distribution of MPO in murine peritoneal cells using flow cytometry, confocal microscopy (CM) and transmission electron microscopy (TEM). MPO was observed in macrophages, and surprisingly, we detected MPO in B lymphocytes, specifically in B1-a. MPO was present in cytoplasmic granules, vesicles, mitochondria and the nucleus of murine peritoneal cells. Together, these findings suggest that, in addition to its known microbicidal activity, MPO has a myriad of other unanticipated cellular functions.

好中球機能異常による感染防御能の低下と炎症の誘発

Neutrophil accumulation is a critical event in the pathogenesis of inflammation. The generation of hypochlorous acid by myeloperoxidase (MPO) in neutrophils is crucial to the host defense response. MPO-deficient (MPO-KO) mice showed severely reduced cytotoxicity to Candida albicans, Aspergillus fumigatus, Cryptococcus neoformans and other microorganisms, demonstrating that an MPO-dependent oxidative system is important for in vivo host defense against fungi. On the other hand, impaired reactive oxygen species (ROS) production by neutrophils has previously been shown to cause an abnormal inflammatory response. In the present study, we have found that MPO-KO mice exhibit more severe pulmonary inflammation than wild-type mice when challenged with an intranasal administration of zymosan. In addition to measuring the kinetics of neutrophil accumulation, we also measured the production of macrophage inflammatory protein-2 (MIP-2) in the lung, and we correlate the degree of neutrophil accumulation with the production of this mediator. Our results demonstrate that MPO regulates the production of MIP-2, which may modulate neutrophil accumulation during lung inflammation.

Hypertonic saline increases lung epithelial lining fluid glutathione and thiocyanate: two protective CFTR-dependent thiols against oxidative injury

BackgroundCystic fibrosis is a debilitating lung disease due to mutations in the cystic fibrosis transmembrane conductance regulator protein (CFTR) and is associated with chronic infections resulting in elevated myeloperoxidase activity and generation of hypochlorous acid (HOCl). CFTR mutations lead to decreased levels of glutathione (GSH) and thiocyanate (SCN) in the epithelial lining fluid (ELF). Hypertonic saline is used to improve lung function however the mechanism is uncertain.MethodsIn the present study, the effect of GSH and SCN on HOCl-mediated cell injury and their changes in the ELF after hypertonic saline nebulization in wild type (WT) and CFTR KO mice was examined. CFTR sufficient and deficient lung cells were assessed for GSH, SCN and corresponding sensitivity towards HOCl-mediated injury, in vitro.ResultsCFTR (-) cells had lower extracellular levels of both GSH and SCN and were more sensitive to HOCl-mediated injury. In vivo, hypertonic saline increased ELF GSH in the WT and to a lesser extent in the CFTR KO mice but only SCN in the WT ELF. Finally, potential protective effects of GSH and SCN at concentrations found in the ELF against HOCl toxicity were examined in vitro.ConclusionsWhile the concentrations of GSH and SCN associated with the WT ELF protect against HOCl toxicity, those found in the CFTR KO mice were less sufficient to inhibit cell injury. These data suggests that CFTR has important roles in exporting GSH and SCN which are protective against oxidants and that hypertonic saline treatment may have beneficial effects by increasing their levels in the lung.

In situ hypochlorous acid generation for the treatment of brackish shrimp aquaculture wastewater

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.