Search

Statement of problem Whether the disinfection of polymethyl methacrylate (PMMA) dentures eliminates Candida albicans biofilm is unclear. Purpose The purpose of this in vitro study was to determine the antimicrobial effect of immersion in hydrogen peroxide (H2O2) and subsequent application of microwaves on the formation of C albicans biofilm on the surface of polished and unpolished PMMA disks. Material and methods Polished and unpolished PMMA disks (n=40) were mounted in a Center for Disease Control (CDC) biofilm reactor by adding yeast-dextrose-peptone (YPD) broth inoculated with C albicans in a cell suspension for 24 hours. After this period, the PMMA disks (n=8) were disinfected with 5 different solutions: saline solution, 1% sodium hypochlorite (NaOCl), H2O2, H2O2 microwaved at 650 W for 3 minutes (H2O2/μw), and distilled water microwaved at 650 W for 3 minutes (H2O/μw). On the polished and unpolished surface of each disk, arbitrary fluorescence units (AFU) were quantified with the live/dead bacterial viability kit (Invitrogen) by using confocal laser scanning microscopy (CLSM) to evaluate 10 different areas of each surface; these were counted as the colony-forming units (CFUs). The mean values were compared by using the Mann–Whitney U test (α=.05). Results Polished surfaces disinfected with H2O2/μw obtained the lowest viable cells (9.76 AFU) and nonviable cells (12.46 AFU) compared with H2O/μw and H2O2. In the unpolished surface the lowest mean values of viable cells (14.64 AFU) and nonviable cells (12.46 AFU) were obtained for the PMMA disks disinfected with H2O/μw compared with H2O2/μw and H2O2. Both polished and unpolished disks showed significant difference (P Conclusions H2O2 alone did not eliminate the formation of the biofilm of C albicans; however, in combination with the use of the microwave at 650 W for 3 minutes, the biofilm formation of C albicans on polished surfaces was reduced. The number of AFUs of viable-nonviable cells and CFUs depended on whether the surfaces are polished or unpolished.

Iron chalcogenides have attracted great interest as potential substitutes of nature enzymes in the colorimetric biological sensing due to their unique chemodynamic characteristics. Herein, we reported the preparation of ultrathin FeS nanosheets (NSs) by a simple one-pot hydrothermal method and the prepared FeS NSs exhibit strong Fenton-reaction activity to catalyze hydrogen peroxide (H2O2) for generation of hydroxyl radical (•OH). Based on the chromogenic reaction of resultant •OH with 3,3′,5,5′-tetramethylbenzidine (TMB), we develop colorimetric biosensors for highly sensitive detection of H2O2 and glutathione (GSH). The fabricated biosensors show wide linear ranges for the detection of H2O2 (5-150 μmol/L) and GSH (5-50 μmol/L). Their detection limits for H2O2 and GSH reach as low as 0.19 μmol/L and 0.14 μmol/L, respectively. The experimental results of sensing intracellular H2O2 and GSH demonstrate that this colorimetric method can realize the accurate detection of H2O2 and GSH in normal cells (LO2 and 3T3) and cancer cells (MCF-7 and HeLa). Our results have demonstrated that the synthesized FeS NSs is a promising material to construct colorimetric biosensors for the sensitive detection of H2O2 and GSH, holding great promising for medical diagnosis in cancer therapy.

In this study defense responses in three potato varieties with different levels of reaction to the late blight disease caused by Phytophthora infestans were analyzed after inoculation with the pathogen. In the resistant cv. Pastusa Suprema, increased intensity of H2O2 and callose deposit accumulation was observed beginning at 24 hours after inoculation, followed by a hypersensitive response at the inoculation points. In the moderately resistant cv. Diacol-Monserrate, the same responses were observed as in the resistant variety, but with less intensity over time. For the susceptible cv. Diacol-Capiro, the responses observed occurred later than in the other two varieties, subsequent to the advance of the pathogen over extensive necrotic areas. These results suggest that early, intense peroxide and callose accumulation and a hypersensitive response are associated with the observed resistance of the cv. Pastusa Suprema and cv. Diacol-Monserrate to P. infestans.

The intrinsic hypoxic tumor microenvironment and limited accumulation of photosensitizers (PSs) result in unsatisfied efficiency of photodynamic therapy (PDT). To enhance the PDT efficiency against solid tumors, a functional oxygen self-supplying and PS-delivering nanosystem is fabricated via the combination of catalase (CAT), chlorin e6 (Ce6) and metal-phenolic network (MPN) capsule. It is demonstrated that the CAT encapsulated in the capsules (named CCM capsules) could catalyze the degradation of hydrogen peroxide (H2O2) to produce molecular oxygen (O2), which could be converted into cytotoxicity reactive oxygen species (ROS) by surface-loaded Ce6 under 660 nm laser irradiation, leading to synergistic anticancer effects in vitro and in vivo. Therefore, the application of CCM capsule could be a promising strategy to improve PDT effectiveness.

Fungal laccases are industrially important inducible enzymes extensively used in the delignification of lignocellulosics, detoxification of environmental wastes and decolorization of textile dyes. The discovery of new inducers is crucial for laccase productivity by filamentous fungi. In this study, a novel laccase-producing strain S8 from a bambusicolous fungus Shiraia bambusicola was identified by using 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonate) as laccase secretion indicator and native polyacrylamide gel electrophoresis. The corresponding full-length cDNA of laccase was cloned and characterized. The effect of lanthanum (LaCl3) on extracellular laccase activity was tested at the concentration from 0.2 to 2.0 g/L and at different addition time (day 1–4) in the mycelium culture. In the presence of 1.0 g/L La3+ at the beginning of the mycelium cultures, the highest laccase activity (2.7 × 104 U/L) reached after 10 days of cultivation, about tenfold higher compared with non-induced cultures. La3+ was shown to be a very strong inducer for fungal laccase activity with no inhibitory effect on fungal growth at the optimized concentration. In vivo, La3+ added to the mycelium culture not only promoted a continuous and high expression of laccase gene (lcc1), but also induced a rapid generation of signaling molecules including reactive oxygen species (ROS) and nitric oxygen (NO). Both the NO donor sodium nitroprusside (SNP) and exogenous hydrogen peroxide (H2O2) potentiated La3+-induced laccase activity and increased membrane permeability of hyphal cells. Moreover, the scavenger such as 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) for NO and vitamin C for ROS suppressed the induction. These results suggest these signals could mediate La3+-induced laccase biosynthesis and its secretion. Our study provides a basis for understanding the induction mechanism of La3+ on laccase and a practical strategy for enhanced fungal laccase production.

Background Heart transplantation, a life-saving approach for patients with end-stage heart disease, is limited by shortage of donor organs. While prolonged storage provides more organs, it increases the extent of ischemia. Therefore, we seek to understand molecular mechanisms underlying pathophysiological changes of donor hearts during prolonged storage. Additionally, considering mesenchymal stromal cell (MSC)-derived paracrine protection, we aim to test if MSC secretome preserves myocardial transcriptome profile and whether MSC secretome from a certain source provides the optimal protection in donor hearts during cold storage. Methods and results Isolated mouse hearts were divided into: no cold storage (control), 6 h cold storage (6 h-I), 6 h-I + conditioned media from bone marrow MSCs (BM-MSC CM), and 6 h-I + adipose-MSC CM (Ad-MSC CM). Deep RNA sequencing analysis revealed that compared to control, 6 h-I led to 266 differentially expressed genes, many of which were implicated in modulating mitochondrial performance, oxidative stress response, myocardial function, and apoptosis. BM-MSC CM and Ad-MSC CM restored these gene expression towards control. They also improved 6 h-I-induced myocardial functional depression, reduced inflammatory cytokine production, decreased apoptosis, and reduced myocardial H2O2. However, neither MSC-exosomes nor exosome-depleted CM recapitulated MSC CM-ameliorated apoptosis and CM-improved mitochondrial preservation during cold ischemia. Knockdown of Per2 by specific siRNA abolished MSC CM-mediated these protective effects in cardiomyocytes following 6 h cold storage. Conclusions Our results demonstrated that using MSC secretome (BM-MSCs and Ad-MSCs) during prolonged cold storage confers preservation of the normal transcriptional "fingerprint", and reduces donor heart damage. MSC-released soluble factors and exosomes may synergistically act for donor heart protection.

The rational integration of chemotherapy and hydroxyl radical (·OH)-mediated chemodynamic therapy (CDT) via functional metal-organic frameworks (MOF) carriers has great potential in cancer therapy. In this work, aminotriazole (3-AT) doped polyhedral metal organic frameworks (denoted as MAF) were prepared by template ligand replacement, where CDT was initiated by Cu2+/Cu+ modulated Fenton reaction and enhanced by effectively regulating the catalase activity with 3-AT. However, a rod-like Cu-MOF with 3-AT served as a ligand was obtained by the hydrothermal method without using template. In contrast to Cu-MOF, pH-responsive MAF was chosen as the carrier for targeted drug delivery due to its higher drug load of 17.6% and relatively uniform size, where doxorubicin (DOX) as a model drug was loaded in its cavity and hyaluronic acid (HA) was coated on its surface via electrostatic interactions (denoted as HA-MAF@DOX). In vitro experiments demonstrated that HA-MAF@DOX had high transport efficiency of DOX, effective regulation of catalase (CAT) activity and enhanced cytotoxicity to HepG2 cells. This work is the first use of enzyme inhibitors as ligands to construct functional MOFs via template ligand replacement for effective regulating enzyme activity, mediating intracellular redox homeostasis and enhancing CDT efficacy, which provides a feasible strategy for the construction the functional MOFs in cancer therapy.

Insulin resistance is one of the earliest pathological features of a suite of diseases including type 2 diabetes collectively referred to as metabolic syndrome. There is a growing body of evidence from both pre-clinical studies and human cohorts indicating that reactive oxygen species, such as the superoxide radical anion and hydrogen peroxide are key players in the development of insulin resistance. Here we review the evidence linking mitochondrial reactive oxygen species generated within mitochondria with insulin resistance in adipose tissue and skeletal muscle, two major insulin sensitive tissues. We outline the relevant mitochondria-derived reactive species, how the mitochondrial redox state is regulated, and methodologies available to measure mitochondrial reactive oxygen species. Importantly, we highlight key experimental issues to be considered when studying the role of mitochondrial reactive oxygen species in insulin resistance. Evaluating the available literature on both mitochondrial reactive oxygen species/redox state and insulin resistance in a variety of biological systems, we conclude that the weight of evidence suggests a likely role for mitochondrial reactive oxygen species in the etiology of insulin resistance in adipose tissue and skeletal muscle. However, major limitations in the methods used to study reactive oxygen species in insulin resistance as well as the lack of data linking mitochondrial reactive oxygen species and cytosolic insulin signaling pathways are significant obstacles in proving the mechanistic link between these two processes. We provide a framework to guide future studies to provide stronger mechanistic information on the link between mitochondrial reactive oxygen species and insulin resistance as understanding the source, localization, nature, and quantity of mitochondrial reactive oxygen species, their targets and downstream signaling pathways may pave the way for important new therapeutic strategies.

Diseases caused by harmful microorganisms pose a serious threat to human health. Safe and environment-friendly disinfectants are, therefore, essential in preventing and controlling such pathogens. This study aimed to investigate the antimicrobial activity and mechanism of a novel hydrogen peroxide and silver (H 2 O 2 -Ag + ) complex (HSC) in combatting Staphylococcus aureus ATCC 29213, Escherichia coli O157:H7 NCTC 12900 and Salmonella typhimurium SL 1344. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values against S. aureus were found to be 0.014 % H 2 O 2 -3.125 mg/L Ag + , while 0.028 % H 2 O 2 -6.25 mg/L Ag + for both E. coli and S. typhimurium . Results of the growth curve assay and time-kill trial suggest that the HSC could inhibit the growth of the tested bacteria, as 99.9 % of viable cells were killed following treatment at the 1 MIC for 3 h. Compared with Oxytech D10 disinfectant (0.25 % H 2 O 2 -5 mg/L Ag + ), the HSC exhibited better antibacterial efficacy at a lower concentration (0.045 % H 2 O 2 -10 mg/L Ag + ). The mechanism of antibacterial action of HSC was found including the disruption of the bacterial cell membrane, followed by entry into the bacteria cell to reduce intracellular adenosine triphosphate (ATP) concentration, and inhibit the activity of antioxidases, superoxide dismutase (SOD) and catalase (CAT). The enhanced bactericidal effect of hydrogen peroxide combined with silver indicates a potential for its application in environmental disinfection, particularly in the food industry.

Penicillium expansum is the causal agent of blue mold in harvested fruits and vegetables during storage and distribution, causing serious economic loss. In this study we seek the action modes of bifonazole against this pathogen. Bifonazole exhibited strong antifungal activity against P. expansum by inhibiting ergosterol synthesis. The ergosterol depletion caused damage to the cell structure and especially cell membrane integrity as observed by SEM and TEM. With increased unsaturated fatty acids contents, the cell membrane viscosity decreases and can no longer effectively maintain the cytoplasm, which ultimately decreases extracellular conductivity, changes intracellular pH and ion homeostasis. Exposure of hyphal cells to bifonazole shows that mitochondrial respiration is inhibited and reactive oxygen species (ROS) levels–including H2O2 and malondialdehyde (MDA) – are significantly increased. The functional impairment of mitochondria and cell membrane eventually cause cell death through intrinsic apoptosis and necroptosis.

Made available in DSpace on 2022-05-01T09:47:28Z (GMT). No. of bitstreams: 0 Previous issue date: 2022-01-01 This study aimed to evaluate the immunomodulatory effect of vitamin D (VD) on the NLRP1 and NLRP3 inflammasomes in placental explants from preeclamptic (PE) and normotensive (NT) pregnant women. Placental explants from eight PE and eight NT pregnant women were cultured with or without hydrogen peroxide (H2O2), VD or H2O2 + VD. Gene and protein expression of NLRP1, NLRP3, HMGB1, caspase-1, IL-1β, TNF-α and IL-18 were determined by qPCR and Western blotting/ELISA. Compared to NT pregnant women, the endogenous gene expression of NLRP1, NLRP3, HMGB1, IL-1β, TNF-α and IL-18 was significantly higher in explants from PE and became decreased after VD treatment. Similarly, VD decreased the protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1β, TNF-α and IL-18 in PE. Placental explants from NT cultured with H2O2 showed increased gene and protein expression of NLRP1, NLRP3, caspase-1, IL-1β, TNF-α and HMGB1, while H2O2 was also able to increase TNF-α and caspase-1 gene expression in PE. Treatment with H2O2 + VD decreased gene/protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1β, TNF-α and IL-18 in PE and NT explants with H2O2. NLRP1 and NLRP3 are upregulated in the PE. VD may play an immunomodulatory role in the placental inflammation and downregulates oxidative stress induced in vitro by H2O2. Botucatu Medical School Sao Paulo State University (Unesp) Institute of Biosciences Sao Paulo State University (Unesp) Botucatu Medical School Sao Paulo State University (Unesp) Institute of Biosciences Sao Paulo State University (Unesp)

Enhanced postruminal supply of methionine (Met) during the peripartal period alters protein abundance of insulin, AA, and antioxidant signaling pathways in subcutaneous adipose tissue (SAT). Whether SAT is directly responsive to supply of Met and can induce molecular alterations is unknown. Our objective was to examine whether enhanced Met supply during an oxidative stress challenge in vitro alters insulin, AA, inflammation, and antioxidant signaling-related protein networks. Four late-lactation Holstein cows (average 27.0 kg of milk per day) were used for SAT collection. Tissue was incubated in duplicate for 4 h in a humidified incubator with 5% CO2 at 37°C according to the following experimental design: control medium with an “ideal” profile of essential AA (CTR; Lys:Met 2.9:1), CTR plus 100 μM H2O2 (HP), or CTR with greater Met supply plus 100 μM H2O2 (HPMET; Lys:Met 2.5:1). Molecular targets associated with insulin signaling, lipolysis, antioxidant nuclear factor, erythroid 2 like 2 (NFE2L2), inflammation, and AA metabolism were determined through reverse-transcription quantitative PCR and western blotting. Data were analyzed using the MIXED procedure of SAS 9.4 (SAS Institute Inc.). Among proteins associated with insulin signaling, compared with CTR, HP led to lower abundance of phosphorylated AKT serine/threonine kinase (p-AKT) and solute carrier family 2 member 4 (SLC2A4; insulin-induced glucose transporter). Although incubation with HPMET restored abundance of SLC2A4 to levels in the CTR and upregulated abundance of fatty acid synthase (FASN) and phosphorylated 5′-prime-AMP-activated protein kinase (p-AMPK), it did not alter p-AKT, which remained similar to HP. Among proteins associated with AA signaling, compared with CTR, challenge with HP led to lower abundance of phosphorylated mechanistic target of rapamycin (p-MTOR), and HPMET did not restore abundance to CTR levels. Among inflammation-related targets studied, incubation with HPMET led to greater protein abundance of nuclear factor kappa B subunit p65 (NFKB-RELA). The response in NFKB observed with HPMET was associated with a marked upregulation of the antioxidant transcription regulator NFE2L2 and the antioxidant enzyme glutathione peroxidase 1 (GPX1). No effects of treatment were detected for mRNA abundance of proinflammatory cytokines or antioxidant enzymes, underscoring the importance of post-transcriptional regulation. Overall, data indicated that short-term challenge with H2O2 was particularly effective in reducing insulin and AA signaling. Although a greater supply of Met had little effect on those pathways, it seemed to restore the protein abundance of the insulin-induced glucose transporter. Overall, the concomitant upregulation of key inflammation and antioxidant signaling proteins when a greater level of Met was supplemented to oxidant-challenged SAT highlighted the potential role of this AA in regulating the inflammatory response and oxidant status. Further studies should be conducted to assess the role of postruminal supply of Met and other AA in the regulation of immune, antioxidant, and metabolic systems in peripartal cow adipose tissue.

The comparison between salt stress protectants in terms of their ability to increase growth and yield under salinity is of great importance in crop production. Melatonin (MT) and cobalt (Co) have been suggested to promote the plant's salt tolerance by mediating physiological mechanisms. To explore the difference between these protectants in increasing salt tolerance, cucumber plants (Cucumis sativus L., cv. Barracuda F1) were submitted to different levels of salt stress (control = 0.25, 2, 3 and 4 dS m−1) with pretreatment of MT (100 and 200 μM) or Co (15 and 20 mg L−1). The results indicated that the increasing level of salt reduced the growth and productivity of cucumber plants, which may result from ions toxicity (Na+ and Cl− accumulation), oxidative stress (hydrogen peroxide, H2O2 and malondialdehyde, MDA accumulation), and the reduction of essential nutrients content. The concentration used, whether from MT or Co, was instrumental in determining the level of salt tolerance in the cucumber plants. Foliar application with 15 mg L−1 Co and 100 μM MT mitigated, at a similar level, the NaCl- induced inhibition of cucumber growth, fruit number and weight. At the physiological levels, both treatments increased protein content, essential nutrients (N, P, K+, and Ca2+) content, and catalase (CAT) activity of stressed plants. The mitigation was also observed in the reduced levels of H2O2 and MDA. However, Co (15 mg L−1) showed superiority compared to MT in reducing the content of toxic ions (Na+ and Cl−) and increasing the total yield, especially under the high salt stress (4 dS m−1). These results suggest that Co and MT can improve the salt tolerance of the cucumber plants, but the level of improvement may differ in some aspects, and this may be due to the difference in salt tolerance mechanisms among those protectants.

Nanozyme has been regarded as an efficient antibiotic to kill bacteria using the reactive oxygen species (ROS) generated by Fenton-like reaction. However, its activity is still unsatisfied and requires large amount of hydrogen peroxide with side effects toward normal tissues. Herein, spherical mesoporous Fe-N-C single-atom nanozyme (SAzyme) is designed for antibacterial therapy via photothermal treatment enhanced Fenton-like catalysis process. Due to the large pore size (4.0 nm), high specific surface area (413.9 m2 g−1) and uniform diameter (100 nm), the catalytic performance of Fe-N-C SAzyme is greatly improved. The Michaelis-Menten constant (Km) is 4.84 mmol L−1, which is similar with that of horseradish peroxidase (3.7 mmol L−1). Moreover, mesoporous Fe-N-C SAzyme shows high photothermal conversion efficiency (23.3 %) owing to the carbon framework. The catalytic activity can be enhanced under light irradiation due to the elevated reaction temperature. The bacteria can also be killed via physical heat effect. Due to the synergistic effect of nanozyme catalysis and photothermal treatment, the antibacterial performance is much higher than that using single antibacterial method. This work provides an alternative for combined antibacterial treatment via photothermal treatment assisted catalytic process using spherical mesoporous single-atom nanozyme as an antibiotic.

Semiconducting polymers usually with high photostability, reactive oxygen species (ROS) generation ability and photothermal conversion efficiency hold tremendous promise for phototherapy. In this study, a biodegradable tri-component semiconducting polymer (NDT) has been designed and synthesized for phototheranostics. NDT nanoparticles (NPs) obtained by nano-precipitation with an ultrahigh photothermal conversion efficiency (65.6%) could be degraded in the presence of hydrogen peroxide in the tumor microenvironment (TME). Such NPs show high phototoxicity towards human cervical cancer cells (HeLa) with laser irradiation as well as negligible dark toxicity. Furthermore, the in vivo study demonstrates that tumor growth was inhibited efficiently when mice were injected with NDT NPs, even with low power laser irradiation (0.2 W cm−2). In contrast, higher power density (0.5 W cm−2) led to complete tumor suppression. No side effects were observed towards normal tissues, which was confirmed by the H&E stained pictures of the normal tissues, including heart, liver, spleen, lung and kidney. Further, hematological, liver and renal function parameters indicate the biosafety of NDT NPs.

Iron-containing zeolite possesses an active site capable of low-temperature partial oxidation of methane using hydrogen peroxide as an environmentally benign oxidant. However, only a trace number of active sites has been found in zeolite so far. The high turnover frequency was limited to low loading samples, resulting in an upper limit of ~50 mmol‧gcat-1‧h-1 yield of C1 oxygenase. In this study, we synthesized a ZSM-5 catalyst containing a high concentration single Fe site with a high turnover frequency, and achieved the conversion of methane to C1 oxygenase at ~200 mmol‧gcat-1‧h-1 yield. It was important to use ZSM-5 as a carrier, which can be synthesized by hydrothermal treatment of aluminosilicate gel containing only tetra-propyl ammonium cation as the structure-directing agent (SDA). This ZSM-5 carrier has a large fraction of the local environments possessing the nearest framework AlO4 tetrahedra required for fixation of the Fe cation in a mononuclear state while suppressing the co-generation of oligomeric Fe sites, making it possible to design a reaction field for the highly efficient partial oxidation of methane. The findings in the present study clearly showed that the fraction of the single Fe cation, as well as the Al distribution in the zeolite matrix, are the powerful activity descriptor for this class of materials. Furthermore, the Al-distribution modifications based on the previously-established protocols, i.e., rational choice of SDA used in the zeolite synthesis, are a meaningful way to tune not only the fabrication efficiency for the single Fe cation but also the catalytic performance of the Fe/ZSM-5 catalyst.

Allium cepa L. is a commonly consumed vegetable that belongs to the Amaryllidaceae family and contains nutrients and antioxidants in ample amounts. In spite of the valuable food applications of onion bulb, its peel and outer fleshy layers are generally regarded as waste and exploration of their nutritional and therapeutic potential is still in progress with a very slow progression rate. The present study was designed with the purpose of doing a comparative analysis of the antioxidant potential of two parts of Allium cepa, i.g., bulb (edible part) and outer fleshy layers and dry peels (inedible part). Moreover, the inhibitory effect of the onion bulb and peel extracts on rat intestinal α-glucosidase and pancreatic α-amylase of porcine was also evaluated. The antioxidant potential of onion peel and bulb extracts were evaluated using 2,2-diphenyl- 1-picryl hydrazyl (DPPH), ferric-reducing antioxidant power assay (FRAP), 2,2’-azino-bis- 3-ethylbenzothiazoline-6-sulfonic acid (ABTS) radical scavenging assay, H2O2 radical scavenging activity and Fe2+ chelating activity. Total flavonoids and phenolic content of ethanolic extract of onion peel were significantly greater as compared to that of onion bulb. Ethanolic extract of onion peel also presented better antioxidant and free-radical scavenging activity as compared to the ethanolic extract of bulb, while the aqueous extract of bulb presented weakest antioxidative potential. Onion peel extract’s α-glucosidase inhibition potential was also correlated with their phenolic and flavonoid contents. The current findings presented onion peel as a possible source of antioxidative agents and phenolic compounds that might be beneficial against development of various common chronic diseases that might have an association with oxidative stress. Besides, outer dry layers and fleshy peels of onion exhibited higher phenolic content and antioxidant activities, compared to the inner bulb. The information obtained by the present study can be useful in promoting the use of vegetable parts other than the edible mesocarp for several future food applications, rather than these being wasted. Resumo Allium cepa pertence à família Liliaceae e é rica em nutrientes e antioxidantes. Apesar das expressivas aplicações alimentares do bulbo da cebola, sua casca e outras camadas externas são geralmente consideradas resíduos, e seu potencial nutricional e terapêutico ainda é pouco explorado. O presente estudo foi delineado com o objetivo de investigar comparativamente o potencial antioxidante de duas partes de Allium cepa, por exemplo o bulbo (parte comestível) e camadas externas e cascas secas (parte não comestível). Além disso, o efeito inibitório dos extratos do bulbo de cebola e casca sobre a α-glucosidase intestinal de ratos e α-amilase pancreática suína também foi avaliado. O potencial antioxidante dos extratos da casca de cebola e bulbo foi avaliado utilizando-se 2,2-difenil-1-picrilhidrazil (DPPH), método de poder antioxidante de redução do ferro (FRAP), método 2,2'-azino-bis-3-etilbenzotiazolina-6-ácido sulfônico (ABTS) de eliminação de radicais, atividade de eliminação de radicais H2O2 e atividade quelante do Fe2+. Os flavonoides totais e os teores fenólicos do extrato de etanol da casca de cebola foram significativamente maiores quando comparados ao do bulbo. O extrato de etanol da casca de cebola também apresentou melhor atividade antioxidante e eliminação de radicais livres quando comparado ao extrato de etanol do bulbo, enquanto o extrato aquoso de bulbo apresentou menor potencial antioxidante. O potencial de inibição da α-glicosidase dos extratos de casca de cebola correlacionou-se com seus teores fenólicos e de flavonoides. Os resultados encontrados identificaram que a casca de cebola é uma possível fonte de agentes antioxidantes e compostos fenólicos que podem ser benéficos contra o desenvolvimento de várias doenças crônicas que estão associadas ao estresse oxidativo. Além disso, as camadas externas secas e as cascas da cebola exibiram maior conteúdo fenólico e atividades antioxidantes, em comparação com o bulbo interno. As informações obtidas pelo presente estudo podem promover o uso de outras partes vegetais além do mesocarpo comestível para futuras aplicações em alimentos, ao invés de serem desperdiçadas.

The popular genetic model organism Caenorhabditis elegans (C. elegans) encodes 34 globins, whereby the few that are well-characterized show divergent properties besides the typical oxygen carrier function. Here, we present a biophysical characterization and expression analysis of C. elegans globin-3 (GLB-3). GLB-3 is predicted to exist in two isoforms and is expressed in the reproductive and nervous system. Knockout of this globin causes a 99% reduction in fertility and reduced motility. Spectroscopic analysis reveals that GLB-3 exists as a bis-histidyl-ligated low-spin form in both the ferrous and ferric heme form. A function in binding of diatomic gases is excluded on the basis of the slow CO-binding kinetics. Unlike other globins, GLB-3 is also not capable of reacting with H2O2, H2S, and nitrite. Intriguingly, not only does GLB-3 contain a high number of cysteine residues, it is also highly stable under harsh conditions (pH = 2 and high concentrations of H2O2). The resilience diminishes when the N-and C-terminal extensions are removed. Redox potentiometric measurements reveal a slightly positive redox potential (+8 +/- 19 mV vs. SHE), suggesting that the heme iron may be able to oxidize cysteines. Electron paramagnetic resonance shows that formation of an intramolecular disulphide bridge, involving Cys70, affects the heme-pocket region. The results suggest an involvement of the globin in (cysteine) redox chemistry.

A huge amount of rice cultivation and consumption occur in Asia particularly in Pakistan and China. However, multiple abiotic stresses especially high and low-temperature proved to be a substantial threat for rice production ultimately risks for food security. To overcome various types of abiotic stress; seed priming is among the effective approaches to improve the rice seed germination and growth vigor. Therefore, the present study was planned to evaluate physiological and biochemical modifications in Chinese and Pakistani rice varieties by Qiangdi 863 biological assistant growth apparatus nano treated water (NTW), Osmopriming Calcium chloride (CaCl2), redox priming hydrogen peroxide (H2O2) and hormonal priming by Salicylic acid (SA) under temperature stress conditions. The experiment was performed with completely randomize design conditions. Five rice varieties, nomenclature as Zhongzoa 39, (Chinese rice variety) KSK 133, KS 282, Super basmati and PK 1121 aromatic (Pakistani rice variety) were sown under low temperature (LT) (17ºC), optimal temperature (OT) 27ºC and high temperature (HT) 37ºC conditions. The present study indicated that nanopriming were the most effective treatments increased Germination Energy Percentage (GEP) (96.1, 100, 100%), Speed of Germination (SG) (27.2, 35.45, 37.1), Final Germination Percentage (FGP) (98.2, 99.1, 99.4%), Seedling Dry Weight Biomass (DWB) (0.1, 0.137, 0.14g), Total Chlorophyll Content (0.502, 13.74, 15.21), antioxidant enzymes Superoxide Dismutase (SOD)(3145, 2559, 3345 µg-1FWh-1), Catalase (CAT) (300, 366, 3243 µg-1FWh-1) and decreased Malondialdehyde (MDA) (6.5, 12.2, 6.5 µmol g-1 FW) for Zhongzao 39 and KSK 133 rice varieties under low (LT+NTW), optimal temperature (OP+NTW) and high temperature (HT+NTW) stress., Therefore, nano-priming is recommended to cope with the high and low-temperature stress conditions along with improved productivity of rice.

A new homocysteine thiolactone derivative, thiolactomide (1), was isolated along with a known compound, N-acetyl homocysteine thiolactone (2), from a culture extract of soil-derived Streptomyces sp. RK88-1441. The structures of these compounds were elucidated by detailed NMR and MS spectroscopic analyses with literature study. Biological evaluation studies revealed that both 1 and 2 exhibit neuroprotective activity against 6-hydroxydopamine (6-OHDA) mediated neurotoxicity by blocking generation of hydrogen peroxide in neuroblastoma SH-SY5Y cells.

BACKGROUND Cooking oil is an indispensable component of the human diet. However, oils usually undergo thermal oxidation. Oxidized soybean oil (OSO) has been shown to have detrimental effects on humans and has emerged as a root cause of many chronic diseases. The objective of this work was to evaluate the effects of puerpera exposure to OSO on kidney damage in the mother and offspring using lactating rats as an experimental model. RESULTS Pathological sections and ultrastructure showed that OSO exposure resulted in various levels of damage to lactating rats and their offspring. OSO induced oxidative stress in the kidneys of lactating rats, as evidenced by increased levels of hydrogen peroxide, interleukin (IL)-1β, and IL-8. OSO increased the activities of glutathione peroxidase and superoxide dismutase. OSO upregulated the expression of apoptosis-related genes, nuclear factor-erythroid 2-related factor 2 (Nrf2), and nuclear factor κB-related inflammatory factor genes. In the offspring of the OSO-exposed mothers, hydrogen peroxide, malondialdehyde, IL-6, and tumor necrosis factor-alpha contents were increased. Furthermore, OSO enhanced the levels of Nrf2, NAD(P)H quinone oxidoreductase 1, heme oxygenase 1, and p65 and decreased B-cell lymphoma 2. CONCLUSION These findings indicated that the kidneys of two generations of rats were compromised by oxidative damage when fed OSO during lactation. This study provides evidence for increasing the genes expression of the Nrf2/heme oxygenase 1 pathway to alleviate the kidney damage caused by OSO in the mother and offspring. © 2021 Society of Chemical Industry.

1,3,5-Tri-O-caffeoyl quinic acid is a caffeoylquinic acid derivative isolated from the roots of Arctium lappa L. Our previous studies have revealed that the ethyl acetate extract of the roots of A. lappa L. and the caffeoylquinic acids contained in it possess antioxidant properties, especially 1,3,5-tri-O-caffeoyl quinic acid. The present study aimed to investigate the protective effects of 1,3,5-tri-O-caffeoyl quinic acid against hydrogen peroxide-induced oxidative stress and explore the underlying mechanism. We found that 1,3,5-tri-O-caffeoyl quinic acid prevented the decline of cell viability and excessive release of lactate dehydrogenase induced by hydrogen peroxide. In addition, Hoechst 33 342 staining and Annexin V-PI double staining showed that 1,3,5-tri-O-caffeoyl quinic acid inhibited hydrogen peroxide-induced neuronal cell apoptosis. 1,3,5-Tri-O-caffeoyl quinic acid reduced the excessive production of intracellular reactive oxygen species, decreased the malondialdehyde content, and improved the activity of superoxide dismutase. Furthermore, 1,3,5-tri-O-caffeoyl quinic acid restored the loss of mitochondrial membrane potential in SH-SY5Y cells induced by hydrogen peroxide. 1,3,5-Tri-O-caffeoyl quinic acid downregulated the overexpression of proapoptotic proteins, including Bax, cytochrome c, cleaved caspase-9, and cleaved caspase-3 as well as promoted the expression of the antiapoptotic protein Bcl-2. Moreover, the phosphorylation of mitogen-activated protein kinases induced by hydrogen peroxide was inhibited by 1,3,5-tri-O-caffeoyl quinic acid. Pretreatment with 1,3,5-tri-O-caffeoyl quinic acid also promoted the activation of phosphorylated Akt. Taken together, these findings suggest that 1,3,5-tri-O-caffeoyl quinic acid exerts protective effects against hydrogen peroxide-induced neuronal apoptosis. In addition, inhibition of the mitogen-activated protein kinase signaling pathway and the activation of Akt are implicated in the antioxidant activity of 1,3,5-tri-O-caffeoyl quinic acid, giving new insight in searching for a compound with antioxidant activity for the treatment of oxidative stress-associated neurological diseases.

AIM Oxidative stress and the inflammatory response contribute to the progression of cardiovascular disease. The present study aimed to investigate whether the mitochondrial-derived peptide MOTS-c could alleviate H2O2-induced oxidative stress and inflammatory status in H9c2 cells through activation of nuclear factor erythroid 2-related Factor 2 (Nrf2)/antioxidative response element (ARE) and inhibition of the NF-κB pathway. METHODS Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H2O2. Then, the cell was treated with 100 μM H2O2 for 1 h to induce oxidative stress. An inhibition model of sh-Nrf2 was constructed via a lentivirus expression system, and an activation model of NF-κB was achieved using phorbol 12-myristate-13-acetate (PMA). Cell viability was determined using a Cell Counting kit-8 assay. Relative measurement of relative protein and mRNA expression used western blotting and qRT-PCR, respectively. Intracellular reactive oxygen species (ROS) levels were detected using dichlorodihydrofluorescein diacetate, and malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined via commercial kits. The protein expression and distribution in the cells were visualized by immunofluorescence analysis. Enzyme-linked immunosorbent assay was used to detect the levels of inflammatory cytokines, including TNF-α, IL-6 and IL-1β. RESULTS We found that H2O2 treatment significantly decreased cell viability and the level of SOD, increased the levels of ROS and MDA, and upregulated the expression of inflammatory cytokines, including TNF-α, IL-6 and IL-1β, in H9c2 cells. The expression levels of Nrf2, HO-1 and NQO-1 were significantly downregulated in the H2O2, while the phosphorylation of NF-κBp65 was promoted by H2O2. However, pretreatment with MOTS-c significantly reversed H2O2-induced damage in H9c2 cells. Moreover, both inhibition of the Nrf2/ARE pathway and activation of the NF-κB pathway significantly decreased the effects of MOTS-c, suggesting that MOTS-c might play a role in alleviating oxidative damage via the Nrf2/ARE and NF-κB pathways. CONCLUSIONS Our investigation indicated that MOTS-c could protect against H2O2-induced inflammation and oxidative stress in H9c2 cells by inhibiting NF-κB and activating the Nrf2/ARE pathways.

To prevent postoperative skin tumor recurrence and repair skin wound, a glucose oxidase (GOx)-loaded manganese silicate hollow nanospheres (MS HNSs)-incorporated alginate hydrogel (G/MS-SA) was constructed for starvation-photothermal therapy and skin tissue regeneration. The MS HNSs showed a photothermal conversion efficiency of 38.5%, and endowed composite hydrogels with satisfactory photothermal effect. Taking advantage of the catalytic activity of Mn ions, the composite hydrogels could decompose hydrogen peroxide (H2O2) into oxygen (O2), which can alleviate the problem of tumor hypoxia microenvironment and endow GOx with an ability to consume glucose in the presence of O2 for tumor starvation. Meanwhile, hyperthermia triggered by near infrared (NIR) irradiation could not only accelerate the reaction rate of H2O2 decomposition by MS HNSs and glucose consumption by GOx, but also ablate tumor cells. The anti-tumor results showed that synergistic effect of starvation-photothermal therapy led to the highest death rate of tumor cells among all groups, and its anti-tumor effect was obviously improved as compared with that of single photothermal treatment or starvation treatment. Interestingly, the introduction of MS HNSs into hydrogels could distinctly promote the epithelialization of the wound beds by releasing Mn ions as compared with the hydrogels without MS HNSs. It is expected that such a multifunctional platform with starvation-photothermal therapy will be promising for treating tumor-caused skin defects in combination of its regeneration bioactivity in the future., Graphical abstract Schematic diagram. Schematic illustrations of (a) the fabrication of GOx-loaded MS HNSs-incorporated hydrogels (G/MS-5SA) and (b) the application of G/MS-5SA hydrogels in starvation-photothermal therapy and skin tissue regeneration.Image 1, Highlights • Glucose oxidase-loaded manganese silicate hollow nanospheres-incorporated alginate hydrogels consumed glucose in the presence of O2 for tumor starvation. • Hyperthermia could accelerate the reaction rate of H2O2 decomposition. And starvation-photothermal synergetic anti-tumor therapy effect was better than that of single treatment. • The composite hydrogels promote the epithelialization of the wound beds by releasing Mn ions.

Hypertrophic cardiomyopathy (HCM) is a complex myocardial disorder with no well-established disease-modifying therapy so far. Our study aimed to investigate how autophagy, oxidative stress, inflammation, stress signalling pathways, and apoptosis are hallmark of HCM and their contribution to the cardiac dysfunction. Demembranated cardiomyocytes from patients with HCM display increased titin-based stiffness (Fpassive), which was corrected upon antioxidant treatment. Titin as a main determinant of Fpassive was S-glutathionylated and highly ubiquitinated in HCM patients. This was associated with a shift in the balance of reduced and oxidized forms of glutathione (GSH and GSSG, respectively). Both heat shock proteins (HSP27 and α-s crystalline) were upregulated and S-glutathionylated in HCM. Administration of HSPs in vitro significantly reduced HCM cardiomyocyte stiffness. High levels of the phosphorylated monomeric superoxide anion-generating endothelial nitric oxide synthase (eNOS), decreased nitric oxide (NO) bioavailability, decreased soluble guanylyl cyclase (sGC) activity, and high levels of 3-nitrotyrosine were observed in HCM. Many regulators of signal transduction pathways that are involved in autophagy, apoptosis, cardiac contractility, and growth including the mitogen-activated protein kinase (MAPK), protein kinase B (AKT), glycogen synthase kinase 3s (GSK-3s), mammalian target of rapamycin (mTOR), forkhead box O transcription factor (FOXO), c-Jun N-terminal protein kinase (JNK), and extracellular-signal-regulated kinase (ERK1/2) were modified in HCM. The apoptotic factors cathepsin, procaspase 3, procaspase 9 and caspase 12, but not caspase 9, were elevated in HCM hearts and associated with increased proinflammatory cytokines (Interleukin 6 (IL-6), interleukin 18 (IL-18), intercellular cell adhesion molecule-1 (ICAM1), vascular cell adhesion molecule-1 (VCAM1), the Toll-like receptors 2 (TLR2) and the Toll-like receptors 4 (TLR4)) and oxidative stress (3-nitrotyrosine and hydrogen peroxide (H2O2)). Here we reveal stress signalling and impaired PQS as potential mechanisms underlying the HCM phenotype. Our data suggest that reducing oxidative stress can be a viable therapeutic approach to attenuating the severity of cardiac dysfunction in heart failure and potentially in HCM and prevent its progression.

The demand for the amino acid l -cysteine is increasing in the food, cosmetic, and pharmaceutical industries. Conventionally, the commercial production of l -cysteine is achieved by its extraction from the acid hydrolysate of hair and feathers. However, this production method is associated with the release of environmentally hazardous wastewater. Additionally, l -cysteine produced from animal sources cannot be halal-certified, which limits the market size. Although recent studies have developed an alternative commercial l -cysteine production method based on microbial fermentation, the production yield was insufficient owing to the cytotoxicity of l -cysteine against the host cells. In a previous study, we had developed an in vitro l -cysteine production method with a combination of 11 thermophilic enzymes, which yielded 10.5 mM l -cysteine from 20 mM glucose. In this study, we performed re-screening for enzymes catalyzing the rate-limiting steps of the in vitro pathway. Subsequently, the genes encoding enzymes necessary for the in vitro synthesis of l -cysteine were assembled in an expression vector and co-expressed in a single strain. To prevent the synthesis of hydrogen peroxide (H2O2), which is a byproduct and inhibits the enzyme activity, the redox balance in this biosynthetic pathway was maintained by replacing the H2O2-forming NADH oxidase with another enzymatic reaction in which pyruvate was used as a sacrificial substrate. The re-designed in vitro synthetic pathway resulted in the production of 28.2 mM l -cysteine from 20 mM glucose with a molar yield of 70.5%.

Hydrogen peroxide (H2O2) is a well-known oxidizing agent often used as a remedy by consumers to treat algae and root decay from presumed root disease on interior plants, as well as to encourage root growth and health. To characterize the phytotoxic effects and define the safe concentration threshold for H2O2 use on ‘Vivaldi’ hybrid phalaenopsis orchid (hybrid Phalaenopsis), root systems were dipped for 3 minutes in 0%, 3%, 6%, or 12% H2O2 one time and observed in greenhouse conditions for the following 27 days. Root systems of each plant were assessed over time for percent visible root damage; ratings of root health on a scale of 1 to 5 points, with 5 points indicating “very healthy”; and final fresh and dry weights. To determine when symptoms manifested above the root zone, foliage and flower damage was evaluated over time by assessing percent visible foliage damage, ratings of foliage health, percent foliar wilt, flower/bud count, and final foliage and flower fresh and dry weights. Over the evaluation period, the root health rating of the ‘Vivaldi’ hybrid phalaenopsis orchids treated with 12% H2O2 decreased from 5 to 1.13, whereas those treated with 3% H2O2 only decreased from 5 to 4.13. H2O2 concentrations of 6% and 12% damaged root health permanently, whereas the 3% H2O2 concentration only caused minor damage to overall root health. However, algae were not killed at the 3% rate. Neither foliage nor flowers were seriously affected during the 3 weeks after application, but foliage wilt did result in the 6% and 12% treatments by week 4. As H2O2 concentration increased, fresh weights decreased in roots and leaves. Although a single 3% H2O2 root dip did not result in severe symptoms of phytotoxicity, the treatment’s long-term plant health effects are unknown. Because the 3% H2O2 root dip caused minor plant health setbacks and failed to subdue algae populations in the root zone, consumers should be wary of using H2O2 to improve orchid (Orchidaceae) root health and should instead focus on altering care and watering practices.

Disturbances in the gut microbiota are known to be associated with numerous human diseases. Mice have proven to be an invaluable tool for investigating the role of the gut microbiota in disease processes. Nonexperimental factors related to maintaining mice in the laboratory environment are increasingly being shown to have inadvertent effects on the gut microbiota and may function as confounding variables. Microisolation technique is a term used to describe the common biosecurity practice of spraying gloved hands with disinfectant before handling research mice. This practice prevents contamination with pathogenic microorganisms. To investigate if exposure to disinfectants can affect the mouse gut microbiota, C57BL/6 mice were exposed daily for 27 consecutive days to commonly used laboratory disinfectants through microisolation technique. The effects of 70% ethanol and disinfectant products containing chlorine dioxide, hydrogen peroxide, or potassium peroxymonosulfate were each evaluated. Fecal pellets were collected after 7, 14, 21, and 28 d of disinfectant exposure, and cecal contents were collected at day 28. DNA extractions were performed on all cecal and fecal samples, and microbial community structure was characterized using 16S ribosomal RNA amplicon sequencing. Alpha and β diversity metrics and taxon-level analyses were used to evaluate differences in microbial communities. Disinfectant had a small but significant effect on fecal microbial communities compared with sham-exposed controls, and effects varied by disinfectant type. In general, longer exposure times resulted in greater changes in the fecal microbiota. Effects on the cecal microbiota were less pronounced and only seen with the hydrogen peroxide and potassium peroxymonosulfate disinfectants. These results indicate that laboratory disinfectant use should be considered as a potential factor that can affect the mouse gut microbiota.

Oxidative stress inflicts mitochondrial dysfunction, which has been recognized as a key driver of intestinal diseases. Resveratrol (RSV) and its derivative pterostilbene (PTS) are natural antioxidants and exert a protective influence on intestinal health. However, the therapeutic effects and mechanisms of RSV and PTS on oxidative stress-induced mitochondrial dysfunction and intestinal injury remain unclear. The present study used porcine and cellular settings to compare the effects of RSV and PTS on mitochondrial redox homeostasis and function to alleviate oxidative stress-induced intestinal injury. Our results indicated that PTS was more potent than RSV in reducing oxidative stress, maintaining intestinal integrity, and preserving the mitochondrial function of diquat-challenged piglets. In the in vitro study, RSV and PTS protected against hydrogen peroxide (H2O2)-induced mitochondrial dysfunction in intestinal porcine enterocyte cell line (IPEC-J2) by facilitating mitochondrial biogenesis and increasing the activities of mitochondrial complexes. In addition, both RSV and PTS efficiently mitigated mitochondrial oxidative stress by increasing sirtuin 3 protein expression and the deacetylation of superoxide dismutase 2 and peroxiredoxin 3 in H2O2-exposed IPEC-J2 cells. Furthermore, RSV and PTS preserved mitochondrial membrane potential, which restrained the release of cytochrome C from mitochondria to the cytoplasm and caspase-3 activation and further reduced apoptotic rates in H2O2-exposed IPEC-J2 cells. Mechanistically, depletion of sirtuin 1 (SIRT1) abrogated RSV's and PTS's benefits against mitochondrial reactive oxygen species overproduction, mitochondrial dysfunction, and apoptosis in H2O2-exposed IPEC-J2 cells, suggesting that SIRT1 was required for RSV and PTS to protect against oxidative stress-induced intestinal injury. In conclusion, RSV and PTS improve oxidative stress-induced intestinal injury by regulating mitochondrial redox homeostasis and function via SIRT1 signaling pathway. In offering this protection, PTS is superior to RSV.

The removal of mixture of two azo dyes, Acid blue 29 and Ponceau xylidine, was studied by heterogeneous Fenton and Fenton-type processes using hydrogen peroxide and sodium persulphate as oxidants in the presence of and nano and micro-Fe2O3 particles as catalysts. The synthesised nano-Fe2O3 particles were characterised using analytical techniques viz. FT-IR, TEM, EDX, powder XRD and VSM. We have examined the effects of particle size on the COD removal efficiency and the reusability of the catalyst after optimising pH, and concentrations of catalyst and oxidant. Combination of nano-Fe2O3 and hydrogen peroxide possessed higher COD removal efficiency, which was accelerated in acidic pH and inhibited at pH > 6. Total consumption of hydrogen peroxide confirmed the efficiency of the optimised parameters. The mechanism of the formation of intermediate ions and products are proposed. COD removal and consumption of hydrogen peroxide follow pseudo-first-order kinetics. The toxicity of the solutions was assessed using Aliivibrio fischeri light loss and Escherichia coli growth inhibition assays. Both the assays showed different toxicity levels for the same solution.

Polycyclic aromatic hydrocarbon (PAH) contamination has a negative impact on ecosystems. PAHs are a large group of toxins with two or more benzene rings that are persistent in the environment. Some PAHs can be cytotoxic, teratogenic, and/or carcinogenic. In the bacterium Pseudomonas, PAHs can be modified by dioxygenases, which increase the reactivity of PAHs. We hypothesize that some plant dioxygenases are capable of PAH biodegradation. Herein, we investigate the involvement of Arabidopsis thaliana At1g14130 in the degradation of phenanthrene, our model PAH. The At1g14130 gene encodes Dioxygenase For Auxin Oxidation 1 (AtDAO1), an enzyme involved in the oxidative inactivation of the hormone auxin. Expression analysis using a β-glucuronidase (GUS) reporter revealed that At1g14130 is prominently expressed in new leaves of plants exposed to media with phenanthrene. Analysis of the oxidative state of gain-of-function mutants showed elevated levels of H2O2 after phenanthrene treatments, probably due to an increase in the oxidation of phenanthrene by AtDAO1. Biochemical assays with purified AtDAO1 and phenanthrene suggest an enzymatic activity towards the PAH. Thus, data presented in this study support the hypothesis that an auxin dioxygenase, AtDAO1, from Arabidopsis thaliana contributes to the degradation of phenanthrene and that there is possible toxic metabolite accumulation after PAH exposure.

Candida albicans is an opportunistic human fungal pathogen that exists in normal flora but can cause infection in immunocompromised individuals. The transition to pathogenic C. albicans requires a change of various gene expressions. Because histone-modifying enzymes can regulate gene expression, they are thought to control the virulence of C. albicans. Indeed, the absence of H3 lysine 4 (H3K4) methyltransferase Set1 has been shown to reduce the virulence of C. albicans; however, Set1-regulated genes responsible for this attenuated virulence phenotype remain unknown. Here, we demonstrated that Set1 positively regulates the expression of mitochondrial protein genes by methylating H3K4. In particular, levels of cellular mitochondrial reactive oxygen species (ROS) were higher in Δset1 than in the wild-type due to the defect of those genes’ expression. Set1 deletion also increases H2O2 sensitivity and prevents proper colony formation when interacting with macrophage in vitro, consistent with its attenuated virulence in vivo. Together, these findings suggest that Set1 is required to regulate proper cellular ROS production by positively regulating the expression of mitochondrial protein genes and subsequently sustaining mitochondrial membrane integrity. Consequently, C. albicans maintains proper ROS levels via Set1-mediated transcriptional regulation, thus establishing a rapid defense against external ROS generated by the host.

Hypoxia within the tumor microenvironment, which leads to excessive ROS and genomic instability, is one of the hallmarks of cancer, contributing to self-renewal capability, metastasis, and radio-chemotherapy resistance. PRL-3 is an oncoprotein involved in various pro-survival signaling pathways, such as Ras/Erk, PI3K/Akt, Src/STAT, mTORC1 and JAK/STAT. However, there is little evidence connecting PRL-3-mediated apoptosis resistance to tumor microenvironmental stress. In this study, by profiling the PRL-3 expression of multiple tumor types retrieved from public databases (TCGA and NCBI GEO), we confirmed the oncogenic function of PRL-3 and found an intriguing connection between PRL-3 expression and tumor hypoxia signature genes. Moreover, by using CoCl2, a hypoxia mimetic and ROS inducer, we discovered that cells stably expressing PRL-3, but not catalytically-inactive mutant PRL-3 C104S, showed significant resistance to CoCl2 -induced apoptosis. This resistance to apoptosis was found to depend on p38 MAPK signaling and was further confirmed in other conditions of microenvironmental stress, including UV, H2O2 and hypoxia. Mechanistically, we proved that PRL-3 is a direct phosphatase of p38 MAPK under stressed conditions. Additionally, in mouse models of tumor metastasis, higher lung metastatic burden and lower p38 MAPK phosphorylation were found in mice seeded with GFP-PRL-3 expressing cells compared with those seeded with GFP-Ctrl cells. Taken together, our study identified a critical role of RPL-3 in tumorigenesis by negatively regulating p38 MAPK activity in order to facilitate tumor cell adaptation to a hypoxic stressed tumor microenvironment and suggests that PRL-3 could serve as a promising novel therapeutic target for cancer patients.

Streptococcus suis (S. suis) is an important rising pathogen that causes serious diseases in humans and pigs. Although some putative virulence factors of S. suis have been identified, its pathogenic mechanisms are largely unclear. Here, we identified a putative virulence-associated factor MutT, which is unique to S. suis serotype 2 (SS2) virulent strains. To investigate the biological roles of MutT in the SS2 virulent strain ZY05719, the mutT knockout mutant (ΔmutT) was generated and used to explore the phenotypic and virulent variations between the parental and ΔmutT strains. We found that the mutT mutation significantly inhibited cell growth ability, shortened the chain length, and displayed a high susceptibility to H2O2-induced oxidative stress. Moreover, this study revealed that MutT induced the adhesion and invasion of SS2 to host cells. Deletion of mutT increased microbial clearance in host tissues of the infected mice. Sequence alignment results suggested that mutT was encoded in a strain-specific manner, in which the detection was strongly linked to bacterial pathogenicity. In both zebrafish and mice infection models, the virulence of ΔmutT was largely reduced compared with that of ZY05719. Overall, this study provides compelling evidence that MutT is indispensable for the virulence of SS2 and highlights the biological role of MutT in bacteria pathogenesis during infection.

Two–electron ( 2 e - ) oxygen reduction reaction (ORR) shows great promise for on–site electrochemical synthesis of hydrogen peroxide (H2O2). However, it is still a great challenge to design efficient electrocatalysts for H2O2 synthesis. To address this issue, the logical design of the active site by controlling the geometric and electronic structures is urgently desired. Therefore, using density functional theory (DFT) computations, two kinds of hybrid double–atom supported on C2N nanosheet (RuCu@C2N and PdCu@C2N) are screened out and their H2O2 performances are predicted. PdCu@C2N exhibits higher activity for H2O2 synthesis with a lower overpotential of 0.12 V than RuCu@C2N (0.59 V), Ru3Cu(110) facet (0.60 V), and PdCu(110) facet (0.54 V). In aqueous phase, the adsorbed O2 is further stabilized with bulk H2O and the thermodynamic rate–determining step of 2 e - ORR change. The activation barrier on PdCu@C2N is 0.43 eV lower than the one on RuCu@C2N with 0.68 eV. PdCu@C2N is near the top of 2 e - ORR volcano plot, and exhibits high selectivity of H2O2. This work provides guidelines for designing highly effective hybrid double–atom electrocatalysts (HDACs) for H2O2 synthesis.

In the past, the PHB gene function was mainly focused on anti-cell proliferation and antitumor effects. But the molecular mechanism of the PHB gene regarding saline and oxidative stresses is unclear. To study the role of AtPHB6 in salt and oxidative stress, AtPHB6 was cloned from A. thaliana. Bioinformatics analysis showed that AtPHB6 was closely related to AtPHB1 and AtPHB2, which are both type II PHB. RT–qPCR results indicated that the AtPHB6 in the leaves and roots of A. thaliana was obviously induced under different stress treatments. AtPHB6-overexpressing plants were larger and more lush than wild-type and mutant plants when placed under stress treatments during seed germination. The root length and fresh weight of AtPHB6 transgenic plants showed the best resistance compared to wild-type plants under different treatments, in contrast, the AtPHB6 mutants had the worst resistance during the seedling stage. AtSOT12 was an interacting protein of AtPHB6, which screened by yeast two-hybrid system. The interaction between the two proteins were further confirmed using in vitro pull-down experiments and in vivo BiFC experiments. Subcellular localization showed both AtPHB6 and AtSOT12 protein expressed in the nucleus and cytoplasm. The H2O2 content in both the transgenic AtPHB6 and AtSOT12 plants were lower than that in the wild type under stresses. Thus, AtPHB6 increased plant resistance to salt stress and interacted with the AtSOT12 protein.

Horseradish peroxidase (HRP) was immobilized in calcium alginate beads by extruding an alginate/HRP solution through a syringe onto calcium chloride. The aim of this study was to evaluate their use to remove the azo-dye Orange II (OII), under different experimental conditions, such as the number of beads, pH, reuse of the biocatalyst, hydrogen peroxide feeding strategy. A mathematical model that takes into account the diffusion of reactants, products, and HRP throughout the beads and the effect of the enzyme leakage on the observable oxidation rate was also developed. Results indicated that the immobilization efficiency decreased as a function of the incubation time in CaCl2. Although enzyme-containing beads had a low OII adsorption capacity, under the presence of hydrogen peroxide, the dye removal was highly increased due to the catalytic activity of HRP. Besides, the initial OII oxidation rate (RS0) using 3 beads at pH 9 was higher than at pH 7. Also, RS0 increased as a function of the number of tested beads. The developed model was fitted to experimental data obtained at different conditions. Then, the model was validated against a new data set that was not used for the calibration of the model, obtaining a satisfactory agreement between simulation results and these new data. Simulations demonstrate that 70–90% of the total OII removed was due to its oxidation by hydrogen peroxide catalyzed by HRP in the liquid phase.

Regulation of stress-responsive genes represent one of the best examples of gene induction, and the relevance and involvement of different regulators may change for a given gene depending on the challenging stimulus. The HSP12 gene is induced by very different stimuli; however, the molecular response to stress has been characterized in detail only for heat shock treatments. In this study, we aimed to verify whether the regulation of transcription induced by oxidative stress utilizes the same epigenetic solutions as those employed in the heat shock response. We also monitored HSP12 induction by employing spermidine, a known acetyltransferase inhibitor, and observed an oxidative stress that synergizes with spermidine treatment. Our data show that during transcriptional response to H2O2, histone acetylation and chromatin remodeling occur. However, when the relevance of Gcn5p to these processes was studied, we observed that induction of transcription is GCN5-dependent, and this does not rely on histone acetylation by Gcn5p despite its HAT activity. Chromatin remodeling accompanying gene activation is GCN5 dependent. Thus, GCN5 controls HSP12 transcription after H2O2 treatment by allowing chromatin remodeling, and it is only partially involved in HSP12 histone acetylation regardless of its HAT activity.

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder characterized by complex pathogenesis, of which oxidative stress has long been regarded as a major mechanism. Previously, the protective effects of estradiol on SH-SY5Y cells against Aβ42-induced injuries were demonstrated. In this study, the protection of SH-SY5Y cells by estradiol from H2O2-caused oxidative stress injury and Alzheimer's mice was further confirmed. H2O2 downregulated, whereas estradiol upregulated miR-223 expression. miR-223 overexpression promoted cell viability, inhibited cell apoptosis, reduced ROS levels, enhanced Superoxide Dismutase (SOD) activity, and decreased malondialdehyde (MDA) content. However, miR-223 inhibition exerted opposite effects. miR-223 directly targeted forkhead box O3 (FOXO3) and inhibited FOXO3 expression. H2O2 increased, whereas estradiol decreased thioredoxin interacting protein (TXNIP) levels; FOXO3 positively regulated TXNIP protein levels. In SH-SY5Y cells, FOXO3 overexpression increased, whereas FOXO3 knockdown reduced the cell apoptosis and ROS levels. FOXO3 bound to TXNIP promoter region and activated TXNIP transcription, whereas the activation could be partially inhibited by estradiol. Collectively, the FOXO3/TXNIP axis is downstream of miR-223. miR-223 enhances the neuroprotection of estradiol against oxidative stress injury through the FOXO3/TXNIP axis.

Methods to detect and quantify disease biomarkers with high specificity and sensitivity in biological fluids play a key role in enabling clinical diagnosis, including point-of-care testing. Myeloperoxidase (MPO) is an emerging biomarker for the detection of inflammation, neurodegenerative diseases, and cardiovascular disease, where excess MPO can lead to oxidative damage to biomolecules in homeostatic systems. While numerous methods have been developed for MPO analysis, most techniques are challenging in clinical applications due to the lack of amplification methods, high cost, or other practical drawbacks. Enzyme-linked immunosorbent assays are currently used for the quantification of MPO in clinical practice, which is often limited by the availability of antibodies with high affinity and specificity and the significant nonspecific binding of antibodies to the analytical surface. In contrast, nucleic acid-based biosensors are of interest because of their simplicity, fast response time, low cost, high sensitivity, and low background signal, but detection targets are limited to nucleic acids and non-nucleic acid biomarkers are rare. Recent studies reveal that the modification of a genome in the form of phosphorothioate is specifically sensitive to the oxidative effects of the MPO/H2O2/Cl- system. We developed an oxidative cleavage-based three-dimensional DNA biosensor for rapid, ratiometric detection of HOCl and MPO in a "one-pot" method, which is simple, stable, sensitive, specific, and time-saving and does not require a complex reaction process, such as PCR and enzyme involvement. The constructed biosensor has also been successfully used for MPO detection in complex samples. This strategy is therefore of great value in disease diagnosis and biomedical research.

In this study, the silver nanoparticles (AgNPs) were extracellularly synthesized using a bioluminescent bacterium, Vibrio campbellii, and characterized their functional properties and morphological nature by UV–Vis spectroscopy, X-ray diffraction (XRD), Fourier transformed infrared spectroscopy, scanning electron microscopy coupled with energy dispersive X-ray spectroscopy (SEM–EDS), and atomic force microscopy (AFM). Further, the synthesized AgNPs were analyzed for their antibacterial and antioxidant activity (2,2-diphenyl-1-picrylhydrazyl (DPPH), and hydrogen peroxide) in in vitro method. The antibacterial activity of AgNPs was tested against pathogenic bacteria such as Aeromonas hydrophila MTCC 1739, Klebsiella pneumoniae MTCC 4030, Klebsiella oxytoca MTCC 3030, and Pseudomonas aeruginosa MTCC 1934. Characterization studies revealed that the synthesized AgNPs were poly-dispersed, spherical shaped with various size ranges, and exhibited as crystalline in nature. The assay of antibacterial activity showed the synthesized AgNPs strongly inhibited the tested pathogenic bacterial growth. Also, the AgNPs showed good antioxidant activity by strong scavenging actions on DPPH (61.88%) and hydrogen peroxide (53.48%) free radicals. Overall results demonstrated that AgNPs could be used in the pharmaceutical field due to their good antibacterial and antioxidant activity.

The resistant phenotype of pear cultivars includes either complete resistance or tolerance to the attack by the causative agent of fire blight. The effect of ferritin and active iron (Fe2+) concentrations was compared in resistant (Dargazi), tolerant (Harrow Sweet), and susceptible (Bartlett) pear cultivars inoculated with a wild type strain of Erwinia amylovora (Ea273). The examination of necrosis revealed that resistance to the disease manifested itself as a delay in the appearance of symptoms and progression of the disease. Despite a rise in ferritin levels in all cultivars following disease agent inoculation, resistant and tolerant cultivars showed greater ferritin levels than susceptible cultivar. In addition, only resistant and tolerant cultivars displayed a drop in Fe2+ levels. The rate of decrease in Fe2+ content in Dargazi and Harrow sweet cultivars was 28 and 33%, respectively. Hydrogen peroxide (H2O2) and hydroxyl radical (OH•−) accumulation and intensities were considerably distinctive. Furthermore, tolerant and sensitive cultivars started producing OH•− radicals faster than resistant cultivar. According to these findings, different pathways are employed by pear cultivars to respond to the causative agent of fire blight.

Jatropha curcas received a lot of attention as a biodiesel feedstock in several countries around the world. The leaf area (LA) estimation is important for biological research due to its close relationship to soil fertility, plant physiological parameters, and photosynthetic efficiency. Allometric models for reliable and accurate models for estimating the leaf area of Jatropha curcas plants based on non-destructive measurements of leaf length (L), width (W), and/ or leaf margins length (P) were developed. Jatropha plant leaves were randomly selected for model construction to estimate the leaf area using L, W, and P leaf values. Simple and accurate equations were obtained, based on leaf width (AL = W1.795), R2 = 0.987, rib length (AL = L32.081), R2 = 0.989, width and rib length (AL = LW0.320), R2 = 0.997, rib length and leaf periphery segment (AL = LP1P120.274), R2 = 0.995, and half rib and width length (AL = LW/0.50.467), R2 = 0.994. The equations were accurate for estimating leaf area of small, medium, and large size of Jatropha leaves.

Fresh-cut peaches are susceptible to browning when exposed to air. Reducing the browning is important to maintain the quality of the fresh-cut peaches. Nitric oxide (NO) as the signal factor can improve the antioxidant capacity of organisms; sodium alginate (SA) is a natural polysaccharide with good antibacterial and film-forming properties. The study aimed to investigate the antioxidant and anti-browning activities of combined application of sodium alginate and nitric oxide on peaches slices preservation. The activities of some browning-related enzymes and antioxidant enzymes and the content of reactive oxygen species (ROS) and some browning-related components in fresh-cut peaches were determined. Results showed that combined treatment of 1% SA + 10 μmol/L NO slowed down the decrease in firmness, L*, and SSC, restrained the increase in browning degree and the activities of polyphenol oxidase, phenylalanine ammonia-lyase, peroxidase, and lipoxygenase. At the same time, it reduced the accumulation of O2•–, ·OH, H2O2, malondialdehyde, and total phenolic, and increased the activities of catalase and superoxide dismutase in peach slices. Overall, it was concluded that treatment with 1% SA + 10 μmol/L NO maintained quality and extended storage life of fresh-cut peaches.

Drought stress is one of the major constraints for soybean growth and productivity worldwide. The study was aimed to investigate drought-induced physiological and proteomic changes in soybeans, as well as drought relief using exogenous hydrogen peroxide (H2O2). In drought-stressed plants, H2O2 spray on the leaf surface improved relative water content (RWC), net photosynthetic rate (Pn), and stomatal conductance (Gs). Furthermore, exogenous H2O2 reduced drought stress-induced endogenous MDA and H2O2 levels, as well as increased the key antioxidant enzymes (SOD,CAT, APX and POD) activity and proline content in H2O2-treated soybean plants. These findings showed that H2O2 treatment significantly reduced drought stress by increasing the antioxidative defense system and osmotic adjustment. Furthermore, using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, a total of 27 differently expressed proteins was identified, wherein 23 were up-regulated and 4 were down-regulated under drought condition. These proteins were found to be involved in photosynthesis, energy and metabolism, plant defense and antioxidant, signaling and transport, and transcription regulation in response to H2O2 treatment in soybean under drought stress, according to in silico interactome analysis. These findings add to our understanding of H2O2-mediated drought stress alleviation, as well as the physiological and molecular responses of soybean to drought stress.

Hydrogen sulfide (H2S) can alleviate Cd-induced cell death, but the molecular mechanisms are not clear. To shed light on these mechanisms, cell death induced by 200 μM cadmium chloride in cucumber seedlings root tips was used as a model system. Here, we report that the negative effect of Cd stress in mitochondrial physiological functions include changes in cytochrome c/a, mitochondrial membrane permeability transition pores, and adenosine triphosphatase (ATPase). Moreover, Cd stress led to the release of mitochondrial Ca2+ into the cytosol. Exogenous application of sodium hydrosulfide (NaHS, a donor of H2S) inhibited cell death and maintains mitochondrial function by reducing mitochondrial hydrogen peroxide accumulation, increasing ATPase activity and down-regulating CsVDAC and CsANT expression. In summary, H2S suppressed Cd-induced cell death by improving mitochondrial physiological properties.