Overproduction Of Reactive Oxygen Species Research Articles

Effects of sliver nanoparticles on nitrogen removal by the heterotrophic nitrification-aerobic denitrification bacteria Zobellella sp. B307 and their toxicity mechanisms

Due to the widespread use of sliver nanoparticles (AgNPs), a large amount of AgNPs has inevitably been released into the environment, and there is growing concern about the toxicity of AgNPs to nitrogen-functional bacteria. In addition to traditional anaerobic denitrifying bacteria, heterotrophic nitrification-aerobic denitrification (HNAD) bacteria are also important participants in the nitrogen cycle. However, the mechanisms by which AgNPs influence HNAD bacteria have yet to be explicitly demonstrated. In this study, the inhibitory effects of different concentrations of AgNPs on a HNAD bacteria Zobellella sp. B307 were investigated, and the underlying mechanism was explored by analyzing the antioxidant system and the activities of key denitrifying enzymes. Results showed that AgNPs could inhibit the growth and the HNAD ability of Zobellella sp. B307. AgNPs could accumulate on the surface of bacterial cells and significantly destroyed the cell membrane integrity. Further studies demonstrated that the presence of high concentration of AgNPs could result in the overproduction of reactive oxygen species (ROS) and related oxidative stress in the cells. Furthermore, the catalytic activities of key denitrifying enzymes (nitrate reductase (NAR), nitrite reductase (NIR), and nitrous oxide reductase (N2OR)) were significantly suppressed under exposure to a high concentration of AgNPs (20 mg·L−1), which might be responsible for the inhibited nitrogen removal performance of strain B307. This work could improve our understanding of the inhibitory effect and underlying mechanism of AgNPs on HNAD bacteria.

Gallic acid-loaded chitosan nanoparticles enhance the DNA damage and apoptotic features through inhibiting flap endonuclease-1 in triple-negative breast cancer cells.

This study investigated the fabrication of gallic acid-loaded chitosan nanoparticles (Gal-Chi-NPs) that enhanced the DNA damage and apoptotic features by inhibiting FEN-1 expressions in MDA-MB 231 cells. Gal-Chi-NPs were fabricated by the ionic gelation method, and it was characterized by several studies such as dynamic light spectroscopy, Fourier-transforms infrared spectroscopy, x-ray diffraction, scanning electron microscopy, energy-dispersive x-ray, atomic force microscopy, and thermogravimetric analysis. We have obtained that Gal-Chi-NPs displayed 182.2 nm with crystal, smooth surface, and heat stability in nature. Gal-Chi-NPs induce significant toxicity in MDA-MB-231 cells that compared with normal NIH-3T3 cells. A significant reactive oxygen species (ROS) overproduction was observed in Gal-Chi-NPs treated MDA-MB-231. Flap endonuclease-1 (FEN-1) is a crucial protein involved in long patch base excision repair that is involved in repairing the chemotherapeutic mediated DNA-damaged base. Therefore, inhibition of FEN-1 protein expression is a crucial target for enhancing chemotherapeutical efficacy. In this study, we have obtained that Gal-Chi-NPs treatment enhanced the DNA damage by observing increased p-H2AX, PARP1; and suppressed the expression of FEN-1 in MDA-MB-231 cells. Moreover, Gal-Chi-NPs inhibited the expression of tumor proliferating markers p-PI3K, AKT, cyclin-D1, PCNA, and BCL-2; induced proapoptotic proteins (Bax and caspase-3) in MDA-MB 231 cells. Thus, Gal-Chi-NPs induce DNA damage and apoptotic features and inhibit tumor proliferation by suppressing FEN-1 expression in triple-negative breast cancer cells.

Amino acid HPLC-FLD analysis of spirulina and its protective mechanism against the combination of obesity and colitis in wistar rats

ObjectiveThe cafeteria diet (CD), designed as an experimental diet mimicking the obesogenic diet, may contribute to the pathogenesis of inflammatory bowel diseases (IBD). This study delves into the influence of spirulina (SP) on obesity associated with colitis in Wistar rats. MethodsThe amino acids composition of SP was analyzed using HPLC-FLD. Animals were equally separated into eight groups, each containing seven animals and treated daily for eight weeks as follows: Control diet (SD), cafeteria diet (CD) group, CD + SP (500 mg/kg) and SD + SP. Ulcerative colitis was provoked by rectal injection of acetic acid (AA) (3 % v/v, 5 ml/kg b.w.) on the last day of treatment in the following groups: SD + AA, SD + AA + SP, CD + AA, and CD + AA + SP. ResultsFindings revealed that UC and/or CD increased the abdominal fat, weights gain, and colons. Moreover, severe colonic alteration, perturbations in the serum metabolic parameters associated with an oxidative stress state in the colonic mucosa, defined by overproduction of reactive oxygen species (ROS) and increased levels of plasma scavenging activity (PSA). Additionally, obesity exacerbated the severity of AA-induced UC promoting inflammation marked by the overexpression of pro-inflammatory cytokines. Significantly, treatment with SP provided notable protection against inflammation severity, reduced histopathological alterations, attenuated lipid peroxidation (MDA), and enhanced antioxidant enzyme activities (CAT, SOD, and GPX) along with non-enzymatic antioxidants (GSH and SH-G). ConclusionsThus, the antioxidant effects and anti-inflammatory proprieties of SP could be attributed to its richness in amino acids, which could potentially mitigate inflammation severity in obese subjects suffering from ulcerative colitis. These results imply that SP hold promise as a therapeutic agent for managing of UC, particularly in individuals with concomitant obesity. Understanding SP's mechanisms of action may lead novel treatment strategies for inflammatory bowel diseases and hyperlipidemia in medical research.

Heavy metal stress and mitogen activated kinase transcription factors in plants: Exploring heavy metal-ROS influences on plant signalling pathways.

Due to their stationary nature, plants are exposed to a diverse range of biotic and abiotic stresses, of which heavy metal (HM) stress poses one of the most detrimental abiotic stresses, targeting diverse plant processes. HMs instigate the overproduction of reactive oxygen species (ROS), and to mitigate the adverse effects of ROS, plants induce multiple defence mechanisms. Besides the negative implications of overproduction of ROS, these molecules play a multitude of signalling roles in plants, acting as a central player in the complex signalling network of cells. One of the ROS-associated signalling mechanisms is the mitogen-activated protein kinase (MAPK) cascade, a signalling pathway which transduces extracellular stimuli into intracellular responses. Plant MAPKs have been implicated in signalling involved in stress response, phytohormone regulation, and cell cycle cues. However, the influence of various HMs on MAPK activation has not been well documented. In this review, we address and summarise several aspects related to various HM-induced ROS signalling. Additionally, we touch on how these signals activate the MAPK cascade and the downstream transcription factors that influence plant responses to HMs. Moreover, we propose a workflow that could characterise genes associated with MAPKs and their roles during plant HM stress responses.

Methylglyoxal and Advanced Glycation End Products (AGEs): Targets for the Prevention and Treatment of Diabetes-Associated Bladder Dysfunction?

Methylglyoxal (MGO) is a highly reactive α-dicarbonyl compound formed endogenously from 3-carbon glycolytic intermediates. Methylglyoxal accumulated in plasma and urine of hyperglycemic and diabetic individuals acts as a potent peptide glycation molecule, giving rise to advanced glycation end products (AGEs) like arginine-derived hydroimidazolone (MG-H1) and carboxyethyl-lysine (CEL). Methylglyoxal-derived AGEs exert their effects mostly via activation of RAGE, a cell surface receptor that initiates multiple intracellular signaling pathways, favoring a pro-oxidant environment through NADPH oxidase activation and generation of high levels of reactive oxygen species (ROS). Diabetic bladder dysfunction is a bothersome urological complication in patients with poorly controlled diabetes mellitus and may comprise overactive bladder, urge incontinence, poor emptying, dribbling, incomplete emptying of the bladder, and urinary retention. Preclinical models of type 1 and type 2 diabetes have further confirmed the relationship between diabetes and voiding dysfunction. Interestingly, healthy mice supplemented with MGO for prolonged periods exhibit in vivo and in vitro bladder dysfunction, which is accompanied by increased AGE formation and RAGE expression, as well as by ROS overproduction in bladder tissues. Drugs reported to scavenge MGO and to inactivate AGEs like metformin, polyphenols, and alagebrium (ALT-711) have shown favorable outcomes on bladder dysfunction in diabetic obese leptin-deficient and MGO-exposed mice. Therefore, MGO, AGEs, and RAGE levels may be critically involved in the pathogenesis of bladder dysfunction in diabetic individuals. However, there are no clinical trials designed to test drugs that selectively inhibit the MGO–AGEs–RAGE signaling, aiming to reduce the manifestations of diabetes-associated bladder dysfunction. This review summarizes the current literature on the role of MGO–AGEs–RAGE–ROS axis in diabetes-associated bladder dysfunction. Drugs that directly inactivate MGO and ameliorate bladder dysfunction are also reviewed here.

Polydopamine contained hydrogel nanocomposites with combined antimicrobial and antioxidant properties for accelerated wound healing

Overproduction of reactive oxygen species (ROS) in infected wounds induces a tremendous inflammatory reaction to delay wound healing. To address this problem, we designed a multifunctional polyacrylamide/PVA-based hydrogel containing synthesized poly(1-glycidyl-3-butylimidazolium salicylate) (polyGBImSal) and fabricated polydopamine-coated polyphenolic nanosheet (PDA@PNS) for wound dressing. The PDA@PNS particles were designed to induce I) antioxidant and anti-inflammatory features through ROS-scavenging and II) cell adhesive properties by the existing polydopamine into the hydrogels. The poly(ionic liquid)-based polyGBImSal was designed to allocate effective hydrogel antimicrobial activity. The fabricated hydrogel nanocomposites showed excellent properties in the swelling ratio, cell adhesiveness, protein adsorption, and anti-inflammatory, proving their general performance for application in wound healing. Furthermore, these hydrogels showed high antimicrobial activity (over 95 %) against three common wound-infecting pathogenic microbes: Escherichia coli, Staphylococcus aureus, and Candida albicans. The healing process of full-thickness dermal wounds in rats was accelerated by applying hydrogel nanocomposites with 0.5 wt% of PDA@PNS and 28 wt% of polyGBImSal. The wound closure contraction attained full closure, reaching 100 %, after 14 days, contrasted with the control group employing commercial wound dressing (Tegaderm), which achieved a closure rate of 68 % within the equivalent timeframe. These results make these hydrogel nanocomposites promising candidates for multifunctional wound dressing applications.

Cinnamaldehyde /naringin co-loaded into lactoferrin/ casienate-coated zein nanoparticles as a gastric resistance oral carrier for mitigating doxorubicin-induced hepatotoxicity

Doxorubicin (DOX) is a potent anticancer drug with severe toxic side effects on vital organs. The main mechanism of DOX's toxicity includes overproduction of reactive oxygen species (ROS) causing extensive oxidative stress. In order to minimize DOX-induced hepatotoxicity, cinnamaldehyde (CNM) and naringin (NAR) were co-encapsulated into zein nanoparticles (NPs). Afterwards, the dual-loaded NPs were dual-coated with lactoferrin (LF) and sodium casieate (NaCAS) in order to resist the gastric acidity upon oral administration. CNM/NAR-loaded LF/NaCAS-coated zein NPs exhibited a double coated spherical shape with particle size of 268.5 ± 6.4 nm, zeta potential of −12 ± 1.1 mV, and EE% of 79.54 ± 4.3 for CNM and 73.61 ± 2.9 % for NAR. Moreover, dual drug-loaded LF/NaCAS-coated zein NPs demonstrated slow release of CNM and NAR in simulated gastric fluid (SGF) compared to NaCAS-coated NPs, free CNM and free NAR, resulting in enhanced bioavailability. In addition, the prepared formulation showed good physical stability and hemocompatibility. More importantly, when this formulation was orally administrated to DOX oxidative stress-induced mice, they showed improved liver architecture with reduced inflammation and better antioxidant potential with no signs of toxicity, suggesting a reduction in ROS-mediated damage. In conclusion, CNM/NAR-loaded LF/NaCAS-coated zein NPs might be administrated orally in patients receiving DOX as a natural supplement to reduce the detrimental effects of this potent cytotoxic drug.

Hormetic Nutrition and Redox Regulation in Gut-Brain Axis Disorders.

The antioxidant and anti-inflammatory effects of hormetic nutrition for enhancing stress resilience and overall human health have received much attention. Recently, the gut-brain axis has attracted prominent interest for preventing and therapeutically impacting neuropathologies and gastrointestinal diseases. Polyphenols and polyphenol-combined nanoparticles in synergy with probiotics have shown to improve gut bioavailability and blood-brain barrier (BBB) permeability, thus inhibiting the oxidative stress, metabolic dysfunction and inflammation linked to gut dysbiosis and ultimately the onset and progression of central nervous system (CNS) disorders. In accordance with hormesis, polyphenols display biphasic dose-response effects by activating at a low dose the Nrf2 pathway resulting in the upregulation of antioxidant vitagenes, as in the case of heme oxygenase-1 upregulated by hidrox® or curcumin and sirtuin-1 activated by resveratrol to inhibit reactive oxygen species (ROS) overproduction, microbiota dysfunction and neurotoxic damage. Importantly, modulation of the composition and function of the gut microbiota through polyphenols and/or probiotics enhances the abundance of beneficial bacteria and can prevent and treat Alzheimer's disease and other neurological disorders. Interestingly, dysregulation of the Nrf2 pathway in the gut and the brain can exacerbate selective susceptibility under neuroinflammatory conditions to CNS disorders due to the high vulnerability of vagal sensory neurons to oxidative stress. Herein, we aimed to discuss hormetic nutrients, including polyphenols and/or probiotics, targeting the Nrf2 pathway and vitagenes for the development of promising neuroprotective and therapeutic strategies to suppress oxidative stress, inflammation and microbiota deregulation, and consequently improve cognitive performance and brain health. In this review, we also explore interactions of the gut-brain axis based on sophisticated and cutting-edge technologies for novel anti-neuroinflammatory approaches and personalized nutritional therapies.

Short communication: The boring sponge (Pione vastifica, Hancock, 1849) induces oxidative stress in the Pacific oyster (Magallana gigas, Thunberg, 1793)

Boring sponge infection affects growth, development and reduces the soft tissue weight of oysters. In this study, we investigated the effects of boring sponge on the activity of three antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GP)) in the mantle, and the production of reactive oxygen species (ROS) and potential genotoxicity in hemocytes of the Pacific oyster Magallana gigas. Our results showed a significant increase in ROS production and DNA damage in hemocytes. Notably, the activity of SOD, CAT, and GP in the mantle was not significantly affected by boring sponge infection. Collectively, these results suggest that sponge invasion may cause oxidative stress in Pacific oyster hemocytes through ROS overproduction.

Quest for a stable Cu-ligand complex with a high catalytic activity to produce ROS.

Metal ion-catalysed overproduction of reactive oxygen species (ROS) are believed to contribute significantly to oxidative stress and be involved in several biological processes, from immune defence to development of diseases. Among the essential metal ions, copper is one of the most efficient catalysts in ROS production in the presence of O2 and a physiological reducing agent such as ascorbate. To control this chemistry, Cu ions are tightly coordinated to biomolecules. Free or loosely bound Cu ions are generally avoided to prevent their toxicity. In the present report, we aim to find stable Cu-ligand complexes (Cu-L) that can catalyse efficiently the production of ROS in presence of ascorbate under aerobic conditions. Thermodynamic stability would be needed to avoid dissociation in biological environment and high ROS catalysis is of interest for applications as in antimicrobial or anticancer agents. A series of Cu complexes with the well-known tripodal and tetradentate ligands containing a central amine linked to three pyridyl-alkyl arms of different lengths were investigated. The two of them with mixed armlength showed higher catalytic activity in oxidation of ascorbate and subsequent ROS production than Cu salts in buffer, which is an unprecedented result. Despite these high catalytic activities, no increased antimicrobial activity towards E. coli or cytotoxicity against eukaryotic AGS cells in culture related to Cu-L based ROS production could be observed. The potential reasons for discrepancy between in vitro and in cell data will be discussed.

Tebuconazole promotes spread of a multidrug-resistant plasmid into soil bacteria to form new resistant bacterial strains

The development of antibiotic resistance threatens human and environmental health. Non-antibiotic stressors, including fungicides, may contribute to the spread of antibiotic resistance genes (ARGs). We determined the promoting effects of tebuconazole on ARG dissemination using a donor, Escherichia coli MG1655, containing a multidrug-resistant fluorescent plasmid (RP4) and a recipient (E. coli HB101). The donor was then incorporated into the soil to test whether tebuconazole could accelerate the spread of RP4 into indigenous bacteria. Tebuconazole promoted the transfer of the RP4 plasmid from the donor into the recipient via overproduction of reactive oxygen species (ROS), enhancement of cell membrane permeability and regulation of related genes. The dissemination of the RP4 plasmid from the donor to soil bacteria was significantly enhanced by tebuconazole. RP4 plasmid could be propagated into more genera of bacteria in tebuconazole-contaminated soil as the exposure time increased. These findings demonstrate that the fungicide tebuconazole promotes the spread of the RP4 plasmid into indigenous soil bacteria, revealing the potential risk of tebuconazole residues enhancing the dissemination of ARGs in soil environments.

Progress in the Use of Hydrogels for Antioxidant Delivery in Skin Wounds.

The skin is the largest organ of the body, and it acts as a protective barrier against external factors. Chronic wounds affect millions of people worldwide and are associated with significant morbidity and reduced quality of life. One of the main factors involved in delayed wound healing is oxidative injury, which is triggered by the overproduction of reactive oxygen species. Oxidative stress has been implicated in the pathogenesis of chronic wounds, where it is known to impair wound healing by causing damage to cellular components, delaying the inflammatory phase of healing, and inhibiting the formation of new blood vessels. Thereby, the treatment of chronic wounds requires a multidisciplinary approach that addresses the underlying causes of the wound, provides optimal wound care, and promotes wound healing. Among the promising approaches to taking care of chronic wounds, antioxidants are gaining interest since they offer multiple benefits related to skin health. Therefore, in this review, we will highlight the latest advances in the use of natural polymers with antioxidants to generate tissue regeneration microenvironments for skin wound healing.

Antifungal activity of a trypsin inhibitor from Salvia hispanica L. (chia) seeds against fluconazole-resistant strains of Candida spp. and evaluation of its toxicity in vitro.

The incidence of Candida species resistant to traditional antifungal drugs is increasing globally. This issue significantly impacts patients' lives and increases healthcare expenses, confirming the need to develop novel therapeutic strategies. Recently, a thermostable trypsin inhibitor named ShTI (11.558kDa), which has antibacterial effects on Staphylococcus aureus, was isolated from Salvia hispanica L. (chia) seeds. This study aimed to assess the antifungal effect of ShTI against Candida species and its synergism with fluconazole and to evaluate its mode of action. Preliminary toxicological studies on mouse fibroblasts were also performed. ShTI exhibited antifungal effects against C. parapsilosis (ATCC® 22,019), C. krusei (ATCC® 6258), and six clinical fluconazole-resistant strains of C. albicans (2), C. parapsilosis (2), and C. tropicalis (2). The minimum inhibitory concentration (MIC) values were 4.1µM (inhibiting 50% of the isolates) and 8.2µM (inhibiting 100% of the isolates). Additionally, when combined with fluconazole, ShTI had a synergistic effect on C. albicans, altering the morphological structure of the yeast. The mode of action of ShTI against C. krusei (ATCC® 6258) and C. albicans involves cell membrane permeabilization, the overproduction of reactive oxygen species, the formation of pseudohyphae, pore formation, and consequently, cell death. In addition, ShTI (8.65 and 17.3µM) had noncytotoxic and nongenotoxic effects on L929 mouse fibroblasts. These findings suggest that ShTI could be a promising antimicrobial candidate, but further research is necessary to advance its application as a novel antifungal agent.

Ferroptosis in liver cancer: a key role of post-translational modifications.

Ferroptosis is an emerging form of regulated cell death in an oxidative stress- and iron-dependent manner, primarily induced by the over-production of reactive oxygen species (ROS). Manipulation of ferroptosis has been considered a promising therapeutic approach to inhibit liver tumor growth. Nevertheless, the development of resistance to ferroptosis in liver cancer poses a significant challenge in cancer treatment. Post-translational modifications (PTMs) are crucial enzymatic catalytic reactions that covalently regulate protein conformation, stability and cellular activities. Additionally, PTMs play pivotal roles in various biological processes and divergent programmed cell death, including ferroptosis. Importantly, key PTMs regulators involved in ferroptosis have been identified as potential targets for cancer therapy. PTMs function of two proteins, SLC7A11, GPX4 involved in ferroptosis resistance have been extensively investigated in recent years. This review will summarize the roles of PTMs in ferroptosis-related proteins in hepatocellular carcinoma (HCC) treatment.

Optimizing the d-band center of Pd/CoPcS-Ti3C2Tx to enhance SOD/CAT-mimicking activities in the treatment of osteoarthritis

The development and pathogenesis of osteoarthritis (OA) are closely related to the redox imbalance caused by the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the inflammatory microenvironment. Herein, we developed Pd/CoPcS-Ti3C2Tx nanozymes combining cobalt sulfonated phthalocyanine (CoPcS) and titanium carbide (Ti3C2Tx) nanosheets by noncovalent π-π conjugation for loading of ultrafine Pd nanoclusters, as the superoxide dismutase (SOD) and catalase (CAT) mimics for OA therapy. The electron donor CoPcS-Ti3C2Tx facilitated electron transfer to Pd, effectively modulating the d-band center of Pd close to the Fermi energy level, which enhanced the adsorption energy of free radicals and decreased reaction energy barriers. As expected, Pd/CoPcS-Ti3C2Tx nanozymes had a lower electron escape work function than Ti3C2Tx, with improved photothermal conversion efficiency (49.1%) and enzyme catalytic activity. Experiments in vitro demonstrated that the SOD/CAT-mimicking Pd/CoPcS-Ti3C2Tx antioxidant system effectively eliminated ROS and RNS, inhibited inflammatory factors, restored mitochondrial function, and prevented energy deficiency, leading to a reduction in chondrocyte apoptosis. Particularly, near-infrared (NIR) radiation further enhanced the effects. In vivo studies proved the potent preventative effect of Pd/CoPcS-Ti3C2Tx on OA progression as well as its biosafety. This study is expected to provide a promising strategy for designing highly active nanozymes for the treatment of inflammatory diseases.

Redox priming could be an appropriate technique to minimize drought-induced adversities in quinoa.

The exogenous use of the redox compound (H2O2) plays a significant role in abiotic stress tolerance. The present study investigated various H2O2 application methods (seed priming, foliar spray, and surface irrigation) with varying concentration levels (0 mM, 5 mM, 10 mM, 15 mM, 40 mM, 80 mM, and 160 mM) to evaluate the efficiency of supplying exogenous H2O2 to quinoa under water-deficit conditions. Drought stress reduced quinoa growth and yield by perturbing morphological traits, leading to the overproduction of reactive oxygen species and increased electrolyte leakage. Although all studied modes of H2O2 application improved quinoa performance, surface irrigation was found to be sensitive, causing oxidative damage in the present study. Seed priming showed a prominent increase in plant height due to profound emergence indexes compared to other modes under drought conditions. Strikingly, seed priming followed by foliar spray improved drought tolerance in quinoa and showed higher grain yield compared to surface irrigations. This increase in the yield performance of quinoa was attributed to improvements in total chlorophyll (37%), leaf relative water content (RWC; 20%), superoxide dismutase (SOD; 35%), peroxidase (97%), polyphenol oxidase (60%), and phenylalanine ammonia-lyase (58%) activities, and the accumulation of glycine betaine (96%), total soluble protein (TSP; 17%), proline contents (35%), and the highest reduction in leaf malondialdehyde contents (MDA; 36%) under drought stress. PCA analysis indicated that physio-biochemical traits (proline, SOD, TSP, total chlorophyll, MSI, and RWC) were strongly positively correlated with grain yield, and their contribution was much higher in redox priming than other application methods. In conclusion, exogenous H2O2 application, preferably redox priming, could be chosen to decrease drought-induced performance and yield losses in quinoa.

Unveiling the hidden effects of hypoxia: Pituitary damage and hormonal imbalance in fat greenling (Hexagrammos otakii)

BackgroundIn fisheries, hypoxia stress is one of the most common environmental stresses that often lead to the death of large numbers of fish and cause significant economic losses. The pituitary, an important endocrine gland, lies below the hypothalamus region of the brain. It plays a crucial part in controlling vital physiological functions in fish, such as growth, reproduction, and responses to stress. However, the detailed mechanisms of how hypoxia affects these physiological processes via the pituitary remain largely unknown. MethodsFat greenlings (Hexagrammous otakii) were exposed to different dissolved oxygen (DO = 7. 6 mg/L and DO = 2 mg/L) for 24 h. miRNA-mRNA association analysis of H. otakii pituitary after hypoxia stress. Detecting apoptosis in H. otakii pituitary using Tunel and qPCR. Subsequent detection of hormones in H. otakii liver, gonads and serum by ELISA. ResultsIn this study, hypoxia causes immune system disorders and inflammatory responses through the combined analysis of miRNAs and mRNAs. Subsequent verification indicated a significant accumulation of reactive oxygen species (ROS) subsequent to hypoxia treatment. The overproduction of ROS cause oxidative stress and apoptosis in the pituitary, ultimately causing pituitary damage and reduced growth hormone and luteinising hormone release. ConclusionsAccording to the association study of miRNA-mRNA, apoptosis problems caused by hypoxia stress result in H. otakii pituitary damage. In the meantime, this work clarifies the possible impact of hypoxia-stress on the pituitary cells, as well as on the gonadal development and growth of H. otakii.

Chlorite and bromate alter the conjugative transfer of antibiotic resistance genes: Co-regulation of oxidative stress and energy supply

The widespread use of disinfectants during the global response to the 2019 coronavirus pandemic has increased the co-occurrence of disinfection byproducts (DBPs) and antibiotic resistance genes (ARGs). Although DBPs pose major threats to public health globally, there is limited knowledge regarding their biological effects on ARGs. This study aimed to investigate the effects of two inorganic DBPs (chlorite and bromate) on the conjugative transfer of RP4 plasmid among Escherichia coli strains at environmentally relevant concentrations. Interestingly, the frequency of conjugative transfer was initially inhibited when the exposure time to chlorite or bromate was less than 24h. However, this inhibition transformed into promotion when the exposure time was extended to 36h. Short exposures to chlorite or bromate were shown to impede the electron transport chain, resulting in an ATP shortage and subsequently inhibiting conjugative transfer. Consequently, this stimulates the overproduction of reactive oxygen species (ROS) and activation of the SOS response. Upon prolonged exposure, the resurgent energy supply promoted conjugative transfer. These findings offer novel and valuable insights into the effects of environmentally relevant concentrations of inorganic DBPs on the conjugative transfer of ARGs, thereby providing a theoretical basis for the management of DBPs. Environmental ImplicationDisinfection by-products (DBPs) and antibiotic resistance genes (ARGs) are harmful contaminants with widespread distribution in water environments. Our study demonstrated that the conjugative transfer of ARGs is initially suppressed and subsequently enhanced by environmental concentrations of chlorite and bromate exposure. Our results highlighted the potential risks of low-concentration inorganic DBPs on the spread of antibiotic resistance. Further, our findings contributed to advancing our understanding of the effective management and control of DBPs in water environments, especially considering the selection of chlorine dioxide and ozone to mitigate the formation of chorine-derived DBPs.

Redox Biomarkers - An Effective Tool for Diagnosing COVID-19 Patients and Convalescents.

COVID-19 triggers the overproduction of reactive oxygen species (ROS) which, in combination with a weakened antioxidant barrier, can lead to protein oxidation and lipid peroxidation. The aim of this study was to evaluate enzymatic and non-enzymatic antioxidants, the overall redox potential, and protein and lipid peroxidation products in COVID-19 patients, convalescents, and healthy subjects, and to the determine the diagnostic applicability of these parameters in COVID-19 patients. The study involved 218 patients with COVID-19, 69 convalescents, and 48 healthy subjects who were selected for the research based on age and sex. The study was conducted between 20 February 2021 and 20 November 2021 in Białystok, Poland. The antioxidant barrier, redox status, and oxidative damage products were assessed in serum/plasma samples with the use of colorimetric and spectrophotometric assays. Glutathione reductase (GR) activity was higher, whereas total antioxidant capacity (TAC) was lower in COVID-19 patients than in convalescents (p<0.0001) and the control group (p<0.0001). The concentrations of advanced glycation end products (AGEs), advanced oxidation protein products (AOPP), 4-hydroxynonenal (4-HNE), and malondialdehyde (MDA) were higher in COVID-19 patients (p<0.0001) and convalescents (p<0.0001) than in the control group. AGEs were the most effective diagnostic biomarker for differentiating COVID-19 patients from the control group (AUC=0.9971) and convalescents from the control group (AUC=1.000). An infection with the SARS-CoV-2 disrupts the redox balance and increases protein oxidation and lipid peroxidation. AGEs fulfill the criteria for a potential diagnostic biomarker in COVID-19 patients and convalescents.

Oroxyloside protects against dextran sulfate sodium-induced colitis by inhibiting ER stress via PPARγ activation

Ulcerative colitis (UC), a prevalent form of inflammatory bowel disease (IBD), may result from immune system dysfunction, leading to the sustained overproduction of reactive oxygen species (ROS) and subsequent cellular oxidative stress damage. Recent studies have identified both peroxisome proliferator-activated receptor-γ (PPARγ) and endoplasmic reticulum (ER) stress as critical targets for the treatment of IBD. Oroxyloside (C22H20O11), derived from the root of Scutellariabaicalensis Georgi, has traditionally been used in treating inflammatory diseases. In this study, we investigated the molecular mechanisms by which oroxyloside mitigates dextran sulfate sodium (DSS)-induced colitis. We examined the effects of oroxyloside on ROS-mediated ER stress in colitis, including the protein expressions of GRP78, p-PERK, p-eIF2α, ATF4, and CHOP, which are associated with ER stress. The beneficial impact of oroxyloside was reversed by the PPARγ antagonist GW9662 (1 mg·kg-1, i.v.) in vivo. Furthermore, oroxyloside decreased pro-inflammatory cytokines and ROS production in both bone marrow-derived macrophages (BMDM) and the mouse macrophage cell line RAW 264.7. However, PPARγ siRNA transfection blocked the anti-inflammatory effect of oroxyloside and even abolished ROS generation and ER stress activation inhibited by oroxyloside in vitro. In conclusion, our study demonstrates that oroxyloside ameliorates DSS-induced colitis by inhibiting ER stress via PPARγ activation, suggesting that oroxyloside might be a promising effective agent for IBD.