Acquired sensorineural hearing loss,oxidative stress,and microRNAs

Hearing loss is the third leading cause of human disability.Age-related hearing loss,one type of acquired sensorineural hearing loss,is largely responsible for this escalating global health burden.Noise-induced,ototoxic,and idiopathic sudden sensorineural are other less common types of acquired hearing loss.The etiology of these conditions is complex and multi-fa ctorial involving an interplay of genetic and environmental factors.Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss.Short non-coding RNA sequences known as microRNAs(miRNAs)have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response.Sensory hair cell death is a central histopathological finding in sensorineural hearing loss.As these cells do not regenerate in humans,it underlies the irreversibility of human age-related hearing loss.Ovid EMBASE,Ovid MEDLINE,Web of Science Core Collection,and ClinicalTrials.gov databases over the period August 1,2018 to July 31,2023 were searched with"hearing loss,""hypoxamiRs,""hypoxia,""microRNAs,""ischemia,"and"oxidative stress"text words for English language primary study publications or registered clinical trials.Registe red clinical trials known to the senior author we re also assessed.A total of 222studies were thus identified.After excluding duplicates,editorials,retra ctions,secondary research studies,and non-English language articles,39 primary studies and clinical trials underwent full-text screening.This resulted in 11 animal,in vitro,and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review.MiRNAs miR-34a and miR-29b levels increase with age in mice.These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferato r-activated receptor gamma coactivator-1-alpha(SIRT1/P GC-1α),SIRT1p53,and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis.Furthermore,hypoxia and oxidative stress had a similar adve rse apoptotic effect,which was inhibited by resve ratrol and a myocardial inhibitorassociated transcript,a miR-29b competing endogenous mRNA.Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice-an effect that was corrected by inner ear stem cell-derived exosomes.There is ongoing work seeking to determine if these findings can be effectively translated to humans.

Targeting sepsis through inflammation and oxidative metabolism

Infection is a public health problem and represents a spectrum of disease that can result in sepsis and septic shock.Sepsis is characterized by a dysregulated immune response to infection.Septic shock is the most severe form of sepsis which leads to distributive shock and high mortality rates.There have been significant advances in sepsis management mainly focusing on early identification and therapy.However,complicating matters is the lack of reliable diagnostic tools and the poor specificity and sensitivity of existing scoring tools i.e.,systemic inflammatory response syndrome criteria,sequential organ failure assessment(SOFA),or quick SOFA.These limitations have underscored the modest progress in reducing sepsis-related mortality.This review will focus on novel therapeutics such as oxidative stress targets,cytokine modulation,endothelial cell modulation,etc.,that are being conceptualized for the management of sepsis and septic shock.

Diabetes mellitus and glymphatic dysfunction:Roles for oxidative stress,mitochondria,circadian rhythm,artificial intelligence,and imaging

Diabetes mellitus(DM)is a debilitating disorder that impacts all systems of the body and has been increasing in prevalence throughout the globe.DM represents a significant clinical challenge to care for individuals and prevent the onset of chronic disability and ultimately death.Underlying cellular mechanisms for the onset and development of DM are multi-factorial in origin and involve pathways associated with the production of reactive oxygen species and the generation of oxidative stress as well as the dysfunction of mitochondrial cellular organelles,programmed cell death,and circadian rhythm impairments.These pathways can ultimately involve failure in the glymphatic pathway of the brain that is linked to circadian rhythms disorders during the loss of metabolic homeostasis.New studies incorporate a number of promising techniques to examine patients with metabolic disorders that can include machine learning and artificial intelligence pathways to potentially predict the onset of metabolic dysfunction.

Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

Antioxidative effects of berberine pre-treatment on hydrogen peroxide-induced PC12 cell toxicity

Oxidative stress has been implicated in the pathogenesis of Alzheimer＇s disease. Oxidative damage could be prevented by augmenting the endogenous defense capacity against oxidative stress by antioxidant intake. As an effective alkaloid component of Chinese herbal medicine Rhizoma coptidis extract, berberine exhibits antioxidative properties and ameliorates memory impairment in a rat model of Alzheimer＇s disease. The present study investigated the protective effects of berberine on H2O2-induced PC12 cell toxicity. Results demonstrated that berberine protects PC12 cells from H2O2-induced apoptosis and increases PC12 cell viability. Lactate dehydrogenase release, reactive oxygen content, and malonyl dialdehyde levels were significantly decreased （P 〈 0.01）. The protective effects of berberine on H2O2-induced PC12 cell toxicity were achieved via the antioxidative effects of berberine.

Synergistic catalysis of the N-hydroxyphthalimide on flower-like bimetallic metal-organic frameworks for boosting oxidative desulfurization

Synergic catalytic effect between active sites and supports greatly determines the catalytic activity for the aerobic oxidative desulfurization of fuel oils.In this work,Ni-doped Co-based bimetallic metal-organic framework(CoNi-MOF)is fabricated to disperse N-hydroxyphthalimide(NHPI),in which the whole catalyst provides plentiful synergic catalytic effect to improve the performance of oxidative desulfurization(ODS).As a bimetallic MOF,the second metal Ni doping results in the flower-like morphology and the modification of electronic properties,which ensure the exposure of NHPI and strengthen the synergistic effect of the overall catalyst.Compared with the monometallic Co-MOF and naked NHPI,the NHPI@CoNi-MOF triggers the efficient activation of molecular oxygen and improves the ODS performance without an initiator.The sulfur removal of dibenzothiophene-based model oil reaches 96.4%over the NHPI@CoNi-MOF catalyst in 8 h of reaction.Furthermore,the catalytic product of this aerobic ODS reaction is sulfone,which is adsorbed on the catalyst surface due to the difference in polarity.This work provides new insight and strategy for the design of a strong synergic catalytic effect between NHPI and bimetallic supports toward high-activity aerobic ODS materials.

Effects of Tongluo Jiedu prescription on immune function and oxidative stress in patients with oral cancer

BACKGROUND Oral cancer,which is caused by mucous membrane variation,represents a prevalent malignant tumor in the oral and maxillofacial region,posing a significant threat to patients’lives and safety.While surgical intervention stands as a cornerstone treatment for oral cancer patients,it carries the risk of incomplete treatment or high rates of postoperative recurrence.Hence,a multifaceted approach incorporating diverse treatment modalities is essential to enhance patient prognosis.AIM To analyze the application effect of Tongluo Jiedu prescription as adjuvant therapy and its influence on patient prognosis in patients with oral cancer.METHODS Eighty oral cancer patients in our hospital were selected and divided into the observation group and control group by a random number table.The control group was treated with continuous arterial infusion chemotherapy of cisplatin and 5-fluorouracil.The observation group was additionally given Tongluo Jiadu prescription.The inflammatory stress level,peripheral blood T-cell subsets,and immune function of the two groups were subsequently observed.SPSS 21.0 was used for data analysis.RESULTS The observation group demonstrated lower levels of interleukin-6 and C-reactive protein,and a higher level of tumor necrosis factor in comparison to the control group.After treatment,the immune function in the observation group was significantly better than in the control group.CONCLUSION Tongluo Jiedu prescription can improve the immune function and oxidative stress level of patients with oral cancer and accelerate the recovery process.

Ethyl acetate fraction of Sargassum pallidum extract attenuates particulate matter-induced oxidative stress and inflammation in keratinocytes and zebrafish

Objective:To evaluate the effect of the ethyl acetate fraction derived from Sargassum pallidum extract against particulate matter(PM)-induced oxidative stress and inflammation in HaCaT cells and zebrafish.Methods:HaCaT cells and zebrafish were used to evaluate the protective effects of the ethyl acetate fraction of Sargassum pallidum extract against PM-induced oxidative stress and inflammation.The production of nitric oxide(NO),intracellular ROS,prostaglandin E_(2)(PGE_(2)),and pro-inflammatory cytokines,and the expression levels of COX-2,iNOS,and NF-κB were evaluated in PM-induced HaCaT cells.Furthermore,the levels of ROS,NO,and lipid peroxidation were assessed in the PM-exposed zebrafish model.Results:The ethyl acetate fraction of Sargassum pallidum extract significantly decreased the production of NO,intracellular ROS,and PGE_(2) in PM-induced HaCaT cells.In addition,the fraction markedly suppressed the levels of pro-inflammatory cytokines and inhibited the expression levels of COX-2,iNOS,and NF-κB.Furthermore,it displayed remarkable protective effects against PM-induced inflammatory response and oxidative stress,represented by the reduction of NO,ROS,and lipid peroxidation in zebrafish.Conclusions:The ethyl acetate fraction of Sargassum pallidum extract exhibits a protective effect against PM-induced oxidative stress and inflammation both in vitro and in vivo and has the potential as a candidate for the development of pharmaceutical and cosmeceutical products.

Effect of organic mineral supplementation in reducing oxidative stress in Holstein calves during short‑term heat stress and recovery conditions

Background This study investigated the effects of inorganic and organic minerals on physiological responses,oxidative stress reduction,and rumen microbiota in Holstein bull calves(123.81±9.76 kg;5 months old)during short-term heat stress(HS)and recovery periods.Eight Holstein calves were randomly assigned to four treatment groups:no mineral supplementation(Con),inorganic minerals(IM),organic minerals(OM),and high-concentration organic minerals(HOM)and two thermal environments(HS and recovery)using 4×2 factorial arrangement in a crossover design of four periods of 35 d.Calves were maintained in a temperature-controlled barn.The experimental period consisted of 14 d of HS,14 d of recovery condititon,and a 7-d washing period.Results Body temperature and respiration rate were higher in HS than in the recovery conditions(P<0.05).Selenium concentration in serum was high in the HOM-supplemented calves in both HS(90.38μg/dL)and recovery periods(102.00μg/dL)(P<0.05).During the HS period,the serum cortisol was 20.26 ng/mL in the HOM group,which was 5.60 ng/mL lower than in the control group(P<0.05).The total antioxidant status was the highest in the OM group(2.71 mmol Trolox equivalent/L),followed by the HOM group during HS,whereas it was highest in the HOM group(2.58 mmol Trolox equivalent/L)during the recovery period(P<0.05).Plasma malondialdehyde and HSP70 levels were decreased by HOM supplementation during the HS and recovery periods,whereas SOD and GPX levels were not significantly affected(P>0.05).The principal coordinate analysis represented that the overall rumen microbiota was not influenced by mineral supplementation;however,temperature-induced microbial structure shifts were indicated(PERMANOVA:P<0.05).At the phylum level,Firmicutes and Actinobacteria decreased,whereas Fibrobacteres,Spirochaetes,and Tenericutes increased(P<0.05),under HS conditions.The genus Treponema increased under HS conditions,while Christensenella was higher in recovery conditions(P<0.05).Conclusion HOM supplementation during HS reduced cortisol concentrations and increased total antioxidant status in Holstein bull calves,suggesting that high organic mineral supplementation may alleviate the adverse effects of HS.

Activation of the wnt/β-catenin/CYP1B1 pathway alleviates oxidative stress and protects the blood-brain barrier under cerebral ischemia/reperfusion conditions

Accumulating evidence suggests that oxidative stress and the Wnt/β-catenin pathway participate in stroke-induced disruption of the blood-brain barrier.However,the potential links between them following ischemic stroke remain largely unknown.The present study found that cerebral ischemia leads to oxidative stress and repression of the Wnt/β-catenin pathway.Meanwhile,Wnt/β-catenin pathway activation by the pharmacological inhibito r,TWS119,relieved oxidative stress,increased the levels of cytochrome P4501B1(CYP1B1)and tight junction-associated proteins(zonula occludens-1[ZO-1],occludin and claudin-5),as well as brain microvascular density in cerebral ischemia rats.Moreove r,rat brain microvascular endothelial cells that underwent oxygen glucose deprivation/reoxygenation displayed intense oxidative stress,suppression of the Wnt/β-catenin pathway,aggravated cell apoptosis,downregulated CYP1B1and tight junction protein levels,and inhibited cell prolife ration and migration.Overexpression ofβ-catenin or knockdown ofβ-catenin and CYP1B1 genes in rat brain mic rovascular endothelial cells at least partly ameliorated or exacerbated these effects,respectively.In addition,small interfering RNA-mediatedβ-catenin silencing decreased CYP1B1 expression,whereas CYP1B1 knoc kdown did not change the levels of glycogen synthase kinase 3β,Wnt-3a,andβ-catenin proteins in rat brain microvascular endothelial cells after oxygen glucose deprivatio n/reoxygenation.Thus,the data suggest that CYP1B1 can be regulated by Wnt/β-catenin signaling,and activation of the Wnt/β-catenin/CYP1B1 pathway contributes to alleviation of oxidative stress,increased tight junction levels,and protection of the blood-brain barrier against ischemia/hypoxia-induced injury.

Biochanin A attenuates spinal cord injury in rats during early stages by inhibiting oxidative stress and inflammasome activation

Previous studies have shown that Biochanin A,a flavonoid compound with estrogenic effects,can serve as a neuroprotective agent in the context of cerebral ischemia/reperfusion injury;howeve r,its effect on spinal cord injury is still unclea r. In this study,a rat model of spinal cord injury was established using the heavy o bject impact method,and the rats were then treated with Biochanin A(40 mg/kg) via intrape ritoneal injection for 14 consecutive days.The res ults showed that Biochanin A effectively alleviated spinal cord neuronal injury and spinal co rd tissue injury,reduced inflammation and oxidative stress in spinal cord neuro ns,and reduced apoptosis and pyroptosis.In addition,Biochanin A inhibited the expression of inflammasome-related proteins(ASC,NLRP3,and GSDMD)and the Toll-like receptor 4/nuclear factor-κB pathway,activated the Nrf2/heme oxygenase 1 signaling pathway,and increased the expression of the autophagy markers LC3 Ⅱ,Beclin-1,and P62.Moreove r,the therapeutic effects of Biochanin A on early post-s pinal cord injury were similar to those of methylprednisolone.These findings suggest that Biochanin A protected neurons in the injured spinal cord through the Toll-like receptor 4/nuclear factor κB and Nrf2/heme oxygenase 1 signaling pathways.These findings suggest that Biochanin A can alleviate post-spinal cord injury at an early stage.

Inflammatory markers,oxidative stress,and mitochondrial dynamics:Repercussions on coronary artery disease in diabetes

Inflammatory markers and mediators that affect the development of cardiovascular diseases have been the focus of recent scientific work.Thus,the purpose of this editorial is to promote a critical debate about the article titled“Nε-carboxymethyl-lysine and inflammatory cytokines,markers,and mediators of coronary artery disease progression in diabetes”,published in the World Journal of Diabetes in 2024.This work directs us to reflect on the role of advanced glycation end products,which are pro-inflammatory products arising from the metabolism of fatty acids and sugars whose main marker in tissues is Nε-carboxymethyllysine(NML).Recent studies have linked high levels of pro-inflammatory agents with the development of coronary artery disease(CAD),especially tumor necrosis factor alpha,interleukins,and C-reactive protein.These inflammatory agents increase the production of reactive oxygen species(ROS),of which people with diabetes are known to have an increased production.The increase in ROS promotes lipid peroxidation,which causes damage to myocytes,promoting myocardial damage.Furthermore,oxidative stress induces the binding of NML to its receptor RAGE,which in turn activates the nuclear factor-kB,and consequently,inflammatory cytokines.These inflammatory cytokines induce endothelial dysfunction,with increased expression of adhesion molecules,changes in endothelial permeability and changes in the expression of nitric oxide.In this sense,the therapeutic use of monoclonal antibodies(inflammatory reducers such as statins and sodium-glucose transport inhibitors)has demonstrated positive results in the regression of atherogenic plaques and consequently CAD.On the other hand,many studies have demonstrated a relationship between mitochondrial dynamics,diabetes,and cardiovascular diseases.This link occurs since ROS have their origin in the imbalance in glucose metabolism that occurs in the mitochondrial matrix,and this imbalance can have its origin in inadequate diet as well as some pathologies.Photobiomodulation(PBM)has recently been considered a possible therapeutic agent for cardiovascular diseases due to its effects on mitochondrial dynamics and oxidative stress.In this sense,therapies such as PBM that act on pro-inflammatory mediators and mitochondrial modulation could benefit those with cardiovascular diseases.

Crosstalk among Oxidative Stress,Autophagy,and Apoptosis in the Protective Effects of Ginsenoside Rb1 on Brain Microvascular Endothelial Cells:A Mixed Computational and Experimental Study

Objective Brain microvascular endothelial cells (BMECs) were found to shift from their usually inactive state to an active state in ischemic stroke (IS) and cause neuronal damage. Ginsenoside Rb1 (GRb1),a component derived from medicinal plants,is known for its pharmacological benefits in IS,but its protective effects on BMECs have yet to be explored. This study aimed to investigate the potential protective effects of GRb1 on BMECs. Methods An in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model was established to mimic ischemia-reperfusion (I/R) injury. Bulk RNA-sequencing data were analyzed by using the Human Autophagy Database and various bioinformatic tools,including gene set enrichment analysis (GSEA),Gene Ontology (GO) classification and enrichment analysis,Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis,protein-protein interaction network analysis,and molecular docking. Experimental validation was also performed to ensure the reliability of our findings. Results Rb1 had a protective effect on BMECs subjected to OGD/R injury. Specifically,GRb1 was found to modulate the interplay between oxidative stress,apoptosis,and autophagy in BMECs. Key targets such as sequestosome 1 (SQSTM1/p62),autophagy related 5 (ATG5),and hypoxia-inducible factor 1-alpha (HIF-1α) were identified,highlighting their potential roles in mediating the protective effects of GRb1 against IS-induced damage. Conclusion GRbl protects BMECs against OGD/R injury by influencing oxidative stress,apoptosis,and autophagy. The identification of SQSTM1/p62,ATG5,and HIF-1α as promising targets further supports the potential of GRb1 as a therapeutic agent for IS,providing a foundation for future research into its mechanisms and applications in IS treatment.

Duodenal-jejunal bypass improves hypothalamic oxidative stress and inflammation in diabetic rats via glucagon-like peptide 1-mediated Nrf2/HO-1 signaling

BACKGROUND Type 2 diabetes mellitus(T2DM)is often accompanied by impaired glucose utilization in the brain,leading to oxidative stress,neuronal cell injury and inflammation.Previous studies have shown that duodenal jejunal bypass(DJB)surgery significantly improves brain glucose metabolism in T2DM rats,the role and the metabolism of DJB in improving brain oxidative stress and inflammation condition in T2DM rats remain unclear.AIM To investigate the role and metabolism of DJB in improving hypothalamic oxidative stress and inflammation condition in T2DM rats.METHODS A T2DM rat model was induced via a high-glucose and high-fat diet,combined with a low-dose streptozotocin injection.T2DM rats were divided into DJB operation and Sham operation groups.DJB surgical intervention was carried out on T2DM rats.The differential expression of hypothalamic proteins was analyzed using quantitative proteomics analysis.Proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of T2DM rats were analyzed by flow cytometry,quantitative real-time PCR,Western blotting,and immunofluorescence.RESULTS Quantitative proteomics analysis showed significant differences in proteins related to oxidative stress,inflammation,and neuronal injury in the hypothalamus of rats with T2DM-DJB after DJB surgery,compared to the T2DM-Sham groups of rats.Oxidative stress-related proteins(glucagon-like peptide 1 receptor,Nrf2,and HO-1)were significantly increased(P<0.05)in the hypothalamus of rats with T2DM after DJB surgery.DJB surgery significantly reduced(P<0.05)hypothalamic inflammation in T2DM rats by inhibiting the activation of NF-κB and decreasing the expression of interleukin(IL)-1βand IL-6.DJB surgery significantly reduced(P<0.05)the expression of factors related to neuronal injury(glial fibrillary acidic protein and Caspase-3)in the hypothalamus of T2DM rats and upregulated(P<0.05)the expression of neuroprotective factors(C-fos,Ki67,Bcl-2,and BDNF),thereby reducing hypothalamic injury in T2DM rats.CONCLUSION DJB surgery improve oxidative stress and inflammation in the hypothalamus of T2DM rats and reduce neuronal cell injury by activating the glucagon-like peptide 1 receptor-mediated Nrf2/HO-1 signaling pathway.

Cosmetic or Dietary Vegetable Oils Sampled in the Cameroonian Market May Not Expose Consumers to Lipid Oxidation Products Generating Oxidative Stress and Inflammation

Vegetable oils are a source of energy, essential fatty acids, antioxidants and fat-soluble vitamins useful for human health care and development. These oils also contribute to organoleptic quality of their products’ derivatives. However, their chemical and physical properties can be modified by the mode of their extraction, storage and distribution. These modifications might negatively affect the nutritional quality of the oils. The goals of this study were to: sample different vegetable oils for cosmetic or dietary use marketed in Cameroon, and verify purity and oxidation states of each kind of oil through determination of its acidity, iodine, peroxide, saponification, refractive indexes and the conformity of the labeling. The carotene content, the level of polar components and specific absorbance were also determined. As the result, six oils namely palm, palm kernel, coconut, black cumin, peanut and shea butter were collected. Apart from labeling, chemicals and physicals parameters analyzed were generally in accordance with the Cameroonian and Codex Alimentarius standard. This study suggests that vegetable oils sampled in the Cameroonian market may not expose consumers to lipid oxidation products generating pathological oxidative stress and inflammation. However, efforts in application of existing standard need to be done as far as labeling are concerned.

Enhancing lead-free photovoltaic performance:Minimizing buried surface voids in tin perovskite films through weakly polar solvent pre-treatment strategy

Buried interfacial voids have always been a notorious phenomenon observed in the fabrication of lead perovskite films. The existence of interfacial voids at the buried interface will capture the carrier, suppress carrier transport efficiencies, and affect the stability of photovoltaic devices. However, the impact of these buried interfacial voids on tin perovskites, a promising avenue for advancing lead-free photovoltaics, has been largely overlooked. Here, we utilize an innovative weakly polar solvent pretreatment strategy(WPSPS) to mitigate buried interfacial voids of tin perovskites. Our investigation reveals the presence of numerous voids in tin perovskites during annealing, attributed to trapped dimethyl sulfoxide(DMSO) used in film formation. The WPSPS method facilitates accelerated DMSO evaporation, effectively reducing residual DMSO. Interestingly, the WPSPS shifts the energy level of PEDOT:PSS downward, making it more aligned with the perovskite. This alignment enhances the efficiency of charge carrier transport. As the result, tin perovskite film quality is significantly improved,achieving a maximum power conversion efficiency approaching 12% with only an 8.3% efficiency loss after 1700 h of stability tests, which compares well with the state-of-the-art stability of tin-based perovskite solar cells.

Effective removal of chromium,copper,and nickel heavy metal ions from industrial electroplating wastewater by in situ oxidative adsorption using sodium hypochlorite as oxidant and sodium trititanate nanorod as adsorbent

Sodium hypochlorite and synthesized sodium trititanate nanorods(Na_(2)Ti_(3)O_(7),186 nm×1270 nm)were used as the oxidant and adsorbents for in situ oxidative adsorption treatment of actual electroplating wastewater containing Cr(Ⅵ)(2.6-5.2 mg·L^(-1)),Cu^(2+)(2.7-5.4 mg·L^(-1)),and Ni^(2+)(0.2705-0.541 mg·L^(-1))ions at pH of 8.8-9.1 and 20-60℃.The as-synthesized sodium trititanate nanorods were characterized by XRD,HRTEM,N2 adsorption/desorption,SEM,EDX,and zeta potential techniques.The concentrations of heavy metal ions in wastewater were analyzed by ICP technique.After in situ oxidative adsorption treatment under the concentrations of 25 g·L^(-1) for sodium hypochlorite and 125 mg·L^(-1) for sodium trititanate nanorods at 60℃ for 5 h,the heavy metal ion concentrations could be reduced from initial value of 2.6 to final value of 1.92 mg·L^(-1) for Cr(Ⅵ),3.6 to 0.17 mg·L^(-1) for Cu^(2+),and from 0.2705 to 0.097 mg·L^(-1) for Ni^(2+),respectively.Cr(Ⅵ),Cu^(2+) and Ni^(2+) ions could be effectively removed by the in situ oxidative adsorption method.The in situ oxidative adsorption processes of Cr(Ⅵ),Cu^(2+) and Ni^(2+) ions are satisfactorily simulated by the pseudo-second order adsorption kinetics and Langmuir adsorption isotherm,respectively.Adsorption thermodynamics analyses reveal that the oxidative adsorption processes of Cr(Ⅵ),Cu^(2+) and Ni^(2+) ions are spontaneous and endothermic.The oxidation degree of metalcontained complexes influences the values of thermodynamics functions.

The effects of inner electrode shape on the performance of dielectric barrier discharge reactor for oxidative removal of NO and SO_(2)

Seagoing vessels are responsible for more than 90%of global freight traffic,but meanwhile,emission pollutants(NO_(x)and SO_(x))of seagoing vessels also cause serious air pollution.Nonthermal plasma(NTP)combined with wet scrubbing technology is considered to be a promising technology.In order to improve the oxidation efficiency and energy efficiency of the NTP reactor,the screw and rod inner electrodes of dielectric barrier discharge(DBD)reactor were investigated.To analyze the mechanism,the optical emission spectra(OES)of NTP were measured and numerical calculation was applied.The experiment results show that the NO oxidation removal efficiency of screw electrode is lower than that of rod electrode.However,the SO_(2)removal efficiency of screw electrode is higher.According to the OES experiment and numerical calculation,the electric field intensity of the screw electrode surface is much higher than that of the rod electrode surface,and it is easier to generate N radicals to form NO.For the same energy density condition,the OH radical generation efficiency of the screw electrode reactor is similar to that of the rod electrode,but the gas temperature in the discharge gap is higher.Therefore,the SO2 oxidation efficiency of the thread electrode is higher.This study provides guidance for the optimization of oxidation efficiency and energy consumption of DBD reactor.

Phlorizin alleviates deltamethrin-induced oxidative stress in brine shrimp Artemia

Deltamethrin(DEL),a commonly used pyrethroid pesticide,results in higher reactive oxygen species(ROS)levels in aquatic animals,which consequently unbalance the redox state.Phlorizin(PHL)is a flavonoid and a natural product promising to prevent or reduce pesticide-induced oxidative stress.Artemia is a micro-crustacean widely used in marine hatcheries and an experimental aquatic organism for environmental toxicology research.This research aimed to evaluate the toxicity of DEL on Artemia and the antioxidative effect of PHL against the toxicity.Results show that 0.08-mg/mL PHL exerted its antioxidative effects on hatching percentage of the cysts in 24-h incubation and on body length and survival rate of Artemia in 12-d culture.After 12-d culture,12-,24-,and 36-h DEL exposure showed significant drops in SOD,CAT,and GSH-Px enzyme activities,and significant increases in ROS and malondialdehyde(MDA)levels in Artemia(P<0.05).On the contrary,0.08-mg/mL PHL application improved the enzyme activities and decreased the ROS and MDA levels(P<0.05).Moreover,0.08-mg/mL PHL significantly increased mRNA expression levels of Cu/Zn SOD,CAT,GST,HO-1,NQO1,and Nrf2,and decreased mRNA expression level of Keap1 in the DEL-exposed Artemia(P<0.05).Therefore,DEL is toxic to Artemia,while PHL alleviates DEL-induced oxidative damage by possibly regulating the Nrf2signaling pathway.This study provided a theoretical basis for PHL to reduce pesticide-induced toxicity in aquatic animals.

Effects of Imazethapyr-Based Herbicide Formulation in the Zebrafish (Danio rerio) Hepatocyte Cell Line (ZF-L): Cytotoxicity and Oxidative Stress

Seizures of agrochemical formulations have increased in Brazil and Rio Grande do Sul is among the Brazilian states with the highest number of seizures of these products obtained illicitly. The use of illicit formulations can cause significant harm to agricultural production, the environment, and non-target species. This study evaluated the cytotoxicity and oxidative stress of a seized formulation containing the herbicide imazethapyr (IMZT). Characterization of the herbicide included gas chromatography-mass spectrometry (GC-MS) and thermal analyses (thermogravimetric analysis (TGA) and differential scanning calorimetry (DSC)). Hemolytic and cytotoxicity assays in ZF-L hepatic cells showed IC50 values of 12.75 µg/mL, 3.01 µg/mL, 2.67 µg/mL, and 1.61 µg/mL for erythrocytes, [3(4,5-dimethyl)-2 bromide-5 diphenyl tetrazolium] (MTT), neutral red (NR), and lactate dehydrogenase (LDH) assays, respectively. The median IC50 of 2.84 µg/mL was used in oxidative stress assays, revealing increased reactive oxygen species (ROS) production, reduced total sulfhydryl content, and decreased superoxide dismutase (SOD) and catalase (CAT) activity. This study is the first to report in vitro oxidative stress induced by IMZT in the ZF-L cell line, emphasizing the importance of in vitro assays for assessing the toxic effects of seized agrochemicals on human health and the environment.