Oxidative Conditions Research Articles

MnSOD Mimetics in Therapy: Exploring Their Role in Combating Oxidative Stress-Related Diseases

Reactive oxygen species (ROS) are double-edged swords in biological systems—they are essential for normal cellular functions but can cause damage when accumulated due to oxidative stress. Manganese superoxide dismutase (MnSOD), located in the mitochondrial matrix, is a key enzyme that neutralizes superoxide radicals (O2•−), maintaining cellular redox balance and integrity. This review examines the development and therapeutic potential of MnSOD mimetics—synthetic compounds designed to replicate MnSOD’s antioxidant activity. We focus on five main types: Mn porphyrins, Mn salens, MitoQ10, nitroxides, and mangafodipir. These mimetics have shown promise in treating a range of oxidative stress-related conditions, including cardiovascular diseases, neurodegenerative disorders, cancer, and metabolic syndromes. By emulating natural antioxidant defenses, MnSOD mimetics offer innovative strategies to combat diseases linked to mitochondrial dysfunction and ROS accumulation. Future research should aim to optimize these compounds for better stability, bioavailability, and safety, paving the way for their translation into effective clinical therapies.

Hydrogen peroxide concentration as an indicator of cyanobacterial response to diurnal variation in light intensity

We measured diurnal variations in oxidative stress conditions of cyanobacteria utilizing field observations and laboratory experiments in order to evaluate photoinhibition effects. On clear summer days, transparent bottles filled with surface water were set up at several depths and were collected every three hours together with the measurement of the photosynthetically active radiation (PAR). In the laboratory experiment, two cyanobacterial species were exposed to gradually increasing and then decreasing light intensities. The samples were analyzed with the PAR-induced (H2O2), along with the total hydrogen peroxide concentrations (total H2O2), the catalase activities (CAT), OD730, protein (Protein), and chlorophyll a (Chl a) contents, and so on. Protein was significantly proportionate with OD730 and Chl a, and was used as an indicator of cell biomass. Increasing PAR, H2O2 concentration increased proportionately with the PAR intensity. Then, an oxidative stress indicator in a cell, H2O2/Protein is given by the PAR divided by cell volume, evaluated by Protein. CAT activity in a cell, far largest among antioxidant activities, solely followed total H2O2/Protein. The prediction model for H2O2/Protein was developed with the sufficient agreement with the experimental and field observation results. The model elucidated that the maximum H2O2/Protein in a day was larger with lower cell density even at the water surface, indicating that the higher photoinhibition was imposed at low density, in addition to the lower attenuation of PAR. These results indicate that H2O2/Protein is an effective biomarker to indicate the stress level of cyanobacteria; the observed levels of H2O2 to freshwater may prove useful in designing the criteria for cyanobacteria management.

Arginyltransferase1 drives a mitochondria-dependent program to induce cell death.

Cell death regulation is essential for stress adaptation and/or signal response. Past studies have shown that eukaryotic cell death is mediated by an evolutionarily conserved enzyme, arginyltransferase1 (Ate1). The downregulation of Ate1, as seen in many types of cancer, prominently increases cellular tolerance to a variety of stressing conditions. Conversely, in yeast and mammalian cells, Ate1 is elevated under acute oxidative stress conditions and this change appears to be essential for triggering cell death. However, studies of Ate1 were conventionally focused on its function in inducing protein degradation via the N-end rule pathway in the cytosol, leading to an incomplete understanding of the role of Ate1 in cell death. Our recent investigation shows that Ate1 dually exists in the cytosol and mitochondria, the latter of which has an established role in cell death initiation. Here, by using budding yeast as a model organism, we found that mitochondrial translocation of Ate1 is promoted by the presence of oxidative stressors and is essential for inducing cell death with characteristics of apoptosis. Also, we found that Ate1-induced cell death is dependent on the formation of the mitochondrial permeability pore and at least partly dependent on the action of mitochondria-contained factors including the apoptosis-inducing factor, but is not directly dependent on mitochondrial electron transport chain activity or its derived reactive oxygen species (ROS). Furthermore, our evidence suggests that, contrary to widespread assumptions, the cytosolic protein degradation pathways including ubiquitin-proteasome, autophagy, or endoplasmic reticulum (ER) stress response has little or negligible impacts on Ate1-induced cell death. We conclude that Ate1 controls the mitochondria-dependent cell death pathway.

Bench-Stable 2-Halopyridinium Ketene Hemiaminals as Reagents for the Synthesis of 2-Aminopyridine Derivatives.

2-Chloro-1-(1-ethoxyvinyl)pyridinium triflate and several other bench-stable N-(1-alkoxyvinyl) 2-halopyridinium triflates have been developed as reagents for the synthesis of valuable 2-aminopyridine scaffolds via unusually mild SNAr substitutions with amine nucleophiles. Advantages of this approach include an operationally simple mix-and-stir procedure at room temperature or mild heat and ambient atmosphere and without the need for transition metal catalysts, coupling reagents, or high-boiling solvents. The stable N-(1-ethoxyvinyl) moiety serves as a dual SNAr-activating group and pyridine N-protecting group that can be cleaved under thermal, acidic, or oxidative conditions. Preliminary results of other nucleophilic substitutions using oxygen-, sulfur-, and carbon-based nucleophiles are also demonstrated.

High-throughput screening-based design of multifunctional natural polyphenol nano-vesicles to accelerate diabetic wound healing

Oxidative stress is a major pathological factor that impedes the diabetic wound healing process. Procyanidins (PC) form nanoparticle-vesicles (PPNs) through hydrogen bonding and exhibit good drug delivery capability; however, their application in diabetic wounds is unsatisfactory. To meet the antioxidant needs for treating, high-throughput screening in the natural product library (NPL) under in vitro oxidative stress conditions was conducted to enhance the antioxidant activity of PPNs. HUVECs treated with tert-Butyl Hydroperoxide (TBHP) were established as screening model in vitro. Baicalein (BAI) was identified from over 600 products in the library as the most effective one to combat oxidative stress. Further study showed that PC and BAI may react in equal proportions to synthesize new vesicles, named BAI-PC Polyphenolic nanovesicles (BPPNs), which possess reactive oxygen species (ROS) responsive and antioxidant effects. Network pharmacology indicated that in diabetic wounds, the target genes of PC are mainly enriched in the vascular endothelial growth factor (VEGF)-related pathways, while BAI primarily regulates tyrosine phosphorylation. The complementarity between the two has been validated in both in vitro and in vivo experiments. In summary, the antioxidant drug BAI, identified through high-throughput screening of NPL, could optimize the biological function of PPNs; the newly-synthesized BPPNs may accelerate diabetic wound healing through dual mechanisms of promoting angiogenesis and combating oxidative stress.Graphical abstract

Characteristics and Functions of Rhizosphere Bacterial Communities of Camelli sinensis cv. Shifocui with Cold Resistance Characteristics in Anhui Province, China.

The rhizosphere bacterial community of plants has a crucial effect on healthy plant growth, and each rhizosphere has a specific microbial community. Camellia sinensis cv. Shifocui (C. sinensis cv. Shifocui) is a tea plant distributed in the Dabie Mountains of Anhui Province. It has the characteristics of high yield, good quality, strong cold resistance, and a high amino acid content. This study was the first to use 16S rRNA high-throughput sequencing technology and bioinformatics methods to explore the characteristics and functions of the rhizosphere bacterial community of the cold-tolerant tea tree C. sinensis cv. Shifocui, providing an important basis for the development and utilization of rhizosphere microbial resources. The dominant phylum in the rhizosphere microbes of the C. sinensis cv. Shifocui rhizosphere microorganisms were Proteobacteria, Chloroflexi, Acidobacteriota, and Actinobacteria. Network analysis showed significant positive and negative correlations among the rhizosphere bacterial groups of C. sinensis cv. Shifocui, among which Candidatus _ Xiphinematobacter, Acidobacteriale, Bradyrhizobium, Subgroup _ 2, Candidatus_Udaeobacter, Gemmataceae, and Gaiellales were notable nodes in theinteraction networks. Functional prediction of FAPROTAX indicated that C. sinensis cv. Shifocui was rich in chemoheterotrophic, cellulose hydrolysis, and oxidative heterotrophic conditions, indicating that the dominant bacterial flora was enriched in its rhizosphere microbes and played an important role in plant growth and development. These results lay a foundation for exploring the mechanism of interaction between C. sinensis cv. Shifocui and rhizosphere microorganisms and provide a research basis for the development and utilization of tea plant microbial resources.

Effect of Different Addition Amounts of Capsaicin on the Structure, Oxidation Sites, and Gel Properties of Myofibrillar Proteins under Oxidative Conditions.

This study aimed to explore the mechanism influencing different addition amounts of capsaicin on the gel characteristics and microstructure of myofibrillar protein (MP) gels under conditions induced by hydroxyl free radicals (•OH). Results indicate that adding capsaicin can improve the gelling characteristics of the MPs. With an increased amount of capsaicin added, the oxidation of MPs by •OH decreased, and the number of oxidation sites decreased. Peptides located around residues 651-851 in the head domain SH1 and S2 subunits of the myosin heavy chain were susceptible to oxidation. Capsaicin primarily interacted with amino acids in SH1 (residues 1-151 and 601-651), reducing the effect of •OH on MPs and consequently decreasing the occurrence of MP aggregation. Capsaicin protected the structure and oxidation sites of MPs under oxidative conditions, ensuring the formation of an MP gel with uniformly dense pores during heating, thereby improving the texture characteristics and water-holding capacity of the gel.

Enzymatic Oxidation of Aflatoxin M1 in Milk Using CotA Laccase.

Aflatoxin M1 (AFM1) in milk poses a significant threat to human health. This study examined the capacity of Bacillus licheniformis CotA laccase to oxidize AFM1. The optimal conditions for the CotA laccase-catalyzed AFM1 oxidation were observed at pH 8.0 and 70 °C, achieving an AFM1 oxidation rate of 86% in 30 min. The Km and Vmax values for CotA laccase with respect to AFM1 were 18.91 μg mL-1 and 9.968 μg min-1 mg-1, respectively. Computational analysis suggested that AFM1 interacted with CotA laccase via hydrogen bonding and van der Waals interactions. Moreover, the oxidation products of AFM1 mediated by CotA laccase were identified as the C3-hydroxy derivatives of AFM1 by HPLC-FLD and UPLC-TOF/MS. Toxicological assessment revealed that the hepatotoxicity of AFM1 was substantially reduced following oxidation by CotA laccase. The efficacy of CotA laccase in removing AFM1 in milk was further tested, and the result showed that the enzyme agent achieved an AFM1 removal rate of 83.5% in skim milk and 65.1% in whole milk. These findings suggested that CotA laccase was a novel AFM1 oxidase capable of eliminating AFM1 in milk. More effort is still needed to improve the AFM1 oxidase activity of CotA laccase in order to shorten the processing time when applying the enzyme in the milk industry.

Alterations in Adipose Tissue and Adipokines in Heterozygous APE1/Ref-1 Deficient Mice.

The role of apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) in adipose tissue remains poorly understood. This study investigates adipose tissue dysfunction in heterozygous APE1/Ref-1 deficiency (APE1/Ref-1+/-) mice, focusing on changes in adipocyte physiology, oxidative stress, adipokine regulation, and adipose tissue distribution. APE1/Ref-1 mRNA and protein levels in white adipose tissue (WAT) were measured in APE1/Ref-1+/- mice, compared to their wild-type (APE1/Ref-1+/+) controls. Oxidative stress was assessed by evaluating reactive oxygen species (ROS) levels. Histological and immunohistochemical analyses were conducted to observe adipocyte size and macrophage infiltration of WAT. Adipokine expression was measured, and micro-magnetic resonance imaging (MRI) was used to quantify abdominal fat volumes. APE1/Ref-1+/- mice exhibited significant reductions in APE1/Ref-1 mRNA and protein levels in WAT and liver tissue. These mice also showed elevated ROS levels, suggesting a regulatory role for APE1/Ref-1 in oxidative stress in WAT and liver. Histological and immunohistochemical analyses revealed hypertrophic adipocytes and macrophage infiltration in WAT, while Oil Red O staining demonstrated enhanced ectopic fat deposition in the liver of APE1/Ref-1+/- mice. These mice also displayed altered adipokine expression, with decreased adiponectin and increased leptin levels in the WAT, along with corresponding alterations in plasma levels. Despite no significant changes in overall body weight, microMRI assessments demonstrated a significant increase in visceral and subcutaneous abdominal fat volumes in APE1/Ref-1+/- mice. APE1/Ref-1 is crucial in adipokine regulation and mitigating oxidative stress. These findings suggest its involvement in adipose tissue dysfunction, highlighting its potential impact on abdominal fat distribution and its implications for obesity and oxidative stress-related conditions.

Role of Hog1-mediated stress tolerance in biofilm formation by the pathogenic fungus Trichosporon asahii

Trichosporon asahii, a dimorphic fungus, causes bloodstream infections in immunocompromised patients with neutropenia. Biofilms are formed on the surfaces of medical devices such as catheters as T. asahii transitions morphologically from yeast to hyphae in the host environment. Oxidative stress tolerance and morphological changes of T. asahii are regulated by Hog1, a mitogen-activated protein kinase. The role of Hog1 in the biofilm formation by T. asahii, however, has remained unknown. In the present study, we demonstrated that a hog1 gene-deficient T. asahii mutant formed excess biofilm under a rich medium in vitro, but did not form biofilm in an in vivo evaluation system using silkworms. The hog1 gene-deficient T. asahii mutant formed a greater amount of biofilm than the parent strain in vitro. Under an oxidative stress condition in vitro, however, lower amounts of biofilm were formed by the hog1 gene-deficient T. asahii mutant than by the parent strain. In an in vivo evaluation system using silkworms, lower amounts of biofilm were formed by the hog1 gene-deficient T. asahii mutant than by the parent strain. Our findings suggest that Hog1 regulates biofilm formation by T. asahii in response to host environmental conditions, including oxidative stress.

A Paper-Based Assay for the Determination of Total Antioxidant Capacity in Human Serum Samples.

Determining the total antioxidant capacity (TAC) of biological samples is a valuable approach to measuring health status under oxidative stress conditions, such as infertility and type 2 diabetes. The Trolox equivalent antioxidant capacity (TEAC) assay is the most common approach to evaluating TAC in biological matrices. This assay is typically performed in clinical settings on a microtiter plate using a plate reader. However, the instrumentation and expertise requirements, and the resulting delay in the reporting of assay outcomes, make solution-based TEAC assays impractical for point-of-care or at-home testing, where individuals may want to monitor their health status during treatment. This work introduces the first microfluidic paper-based analytical device (µPAD) that measures TAC in human serum using TEAC assay chemistry. TAC was determined through a colorimetric image analysis of the degree of decolorization of 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) radical cations (ABTS●+) by serum antioxidants. The µPAD showed a linear response to Trolox, ranging from 0.44 to 2.4 mM, (r = 0.999). The performance of paper-based TEAC assays was validated through direct comparison to solution-based TEAC assays. There was a 0.04 mM difference in TAC values between the two platforms, well within one standard deviation of a standard solution-based assay conducted on an aliquot of the same serum sample (±0.25 mM). The µPAD had a limit of detection (LOD) of 0.20 mM, well below the TAC of normal human serum. The results suggest that the proposed device can be used for biological TAC determination and expands the field of TAC analysis in point-of-care health monitoring.

Studies on the Oxidative Damage of the Wobble 5-Methylcarboxymethyl-2-Thiouridine in the tRNA of Eukaryotic Cells with Disturbed Homeostasis of the Antioxidant System.

We have previously shown that 2-thiouridine (S2U), either as a single nucleoside or as an element of RNA chain, is effectively desulfurized under applied in vitro oxidative conditions. The chemically induced desulfuration of S2U resulted in two products: 4-pyrimidinone nucleoside (H2U) and uridine (U). Recently, we investigated whether the desulfuration of S2U is a natural process that also occurs in the cells exposed to oxidative stress or whether it only occurs in the test tube during chemical reactions with oxidants at high concentrations. Using different types of eukaryotic cells, such as baker's yeast, human cancer cells, or modified HEK293 cells with an impaired antioxidant system, we confirmed that 5-substituted 2-thiouridines are oxidatively desulfurized in the wobble position of the anticodon of some tRNAs. The quantitative LC-MS/MS-MRMhr analysis of the nucleoside mixtures obtained from the hydrolyzed tRNA revealed the presence of the desulfuration products of mcm5S2U: mcm5H2U and mcm5U modifications. We also observed some amounts of immature cm5S2U, cm5H2U and cm5U products, which may have indicated a disruption of the enzymatic modification pathway at the C5 position of 2-thiouridine. The observed process, which was triggered by oxidative stress in the living cells, could impair the function of 2-thiouridine-containing tRNAs and alter the translation of genetic information.

An In Vitro Oxidative Stress Model of the Human Inner Ear Using Human-Induced Pluripotent Stem Cell-Derived Otic Progenitor Cells.

The inner ear organs responsible for hearing (cochlea) and balance (vestibular system) are susceptible to oxidative stress due to the high metabolic demands of their sensorineural cells. Oxidative stress-induced damage to these cells can cause hearing loss or vestibular dysfunction, yet the precise mechanisms remain unclear due to the limitations of animal models and challenges of obtaining living human inner ear tissue. Therefore, we developed an in vitro oxidative stress model of the pre-natal human inner ear using otic progenitor cells (OPCs) derived from human-induced pluripotent stem cells (hiPSCs). OPCs, hiPSCs, and HeLa cells were exposed to hydrogen peroxide or ototoxic drugs (gentamicin and cisplatin) that induce oxidative stress to evaluate subsequent cell viability, cell death, reactive oxygen species (ROS) production, mitochondrial activity, and apoptosis (caspase 3/7 activity). Dose-dependent reductions in OPC cell viability were observed post-exposure, demonstrating their vulnerability to oxidative stress. Notably, gentamicin exposure induced ROS production and cell death in OPCs, but not hiPSCs or HeLa cells. This OPC-based human model effectively simulates oxidative stress conditions in the human inner ear and may be useful for modeling the impact of ototoxicity during early pregnancy or evaluating therapies to prevent cytotoxicity.

The Salmonella enterica EnvE is an Outer Membrane Lipoprotein and Its Gene Expression Leads to Transcriptional Repression of the Virulence Gene msgA.

The envE gene of Salmonella enterica serovar Typhimurium is encoded within Salmonella Pathogenicity Island-11 (SPI-11) and is located immediately upstream of the virulence gene msgA (macrophage survival gene A) in the same transcriptional orientation. To date, the characteristics and roles of envE remain largely unexplored. In this study, we show that EnvE, a predicted lipoprotein, is localized on the outer membrane using sucrose gradient ultracentrifugation. Under oxidative stress conditions, envE transcription is suppressed, while msgA transcription is induced, indicating an inverse correlation between the mRNA levels of the two neighboring genes. Importantly, inactivation of envE leads to constitutive transcription of msgA regardless of the presence of oxidative stress. Moreover, trans-complementation of the envE mutant with a plasmid-borne envE fails to prevent the induction of msgA transcription, suggesting that envE functions as a cis-regulatory element rather than a trans-acting factor. We further show that both inactivation and complementation of envE confer wild-type levels of resistance to oxidative stress by ensuring the expression of msgA. Our data suggest that the S. enterica envE gene encodes an outer membrane lipoprotein, and its transcription represses msgA expression in a cis-acting manner, probably by transcriptional interference, although the exact molecular details are yet unclear.

Persulfidation of Human Cystathionine γ-Lyase Inhibits Its Activity: A Negative Feedback Regulation Mechanism for H2S Production.

Cystathionine γ-lyase (CSE) is the second enzyme in the trans-sulfuration pathway that converts cystathionine to cysteine. It is also one of three major enzymes responsible for the biosynthesis of hydrogen sulfide (H2S). CSE is believed to be the major source of endogenous H2S in the cardiovascular system, and the CSE/H2S system plays a crucial role in a variety of physiological and pathological processes. However, the regulatory mechanism of the CSE/H2S system is less well understood, especially at the post-translational level. Here, we demonstrated that the persulfidation of CSE inhibits its activity by ~2-fold in vitro. The loss of this post-translational modification in the presence of dithiothreitol (DTT) results in a reversal of basal activity. Cys137 was identified as the site for persulfidation by combining mass spectrometry, mutagenesis, activity analysis and streptavidin-biotin pull-down assays. To test the physiological relevance of the persulfidation regulation of CSE, human aortic vascular smooth muscle cells (HA-VSMCs) were incubated with vascular endothelial growth factor (VEGF), which is known to enhance endogenous H2S levels. Under these conditions, consistent with the change tendency of the cellular H2S level, the CSE persulfidation levels increased transiently and then gradually decreased to the basal level. Collectively, our study revealed a negative feedback regulation mechanism of the CSE/H2S system via the persulfidation of CSE and demonstrated the potential for maintaining cellular H2S homeostasis under oxidative stress conditions, particularly in tissues where CSE is a major source of H2S.

Formation of Ferrogabbro Through Fe-Ti Oxide Accumulation Under Moderate Oxidation Conditions: Insights from the Dashanshu Intrusion in the Emeishan Large Igneous Province, SW China

The mechanism of iron enrichment in ferrogabbro remains a controversial subject. This study provides valuable insights derived from the Dashanshu intrusion, located in the Emeishan Large Igneous Province in southwestern China, which features ferrogabbro with a notably high iron content (total Fe2O3 reaching up to 21.6 wt.%). The ferrogabbro samples exhibit distinctive petrographic features, including the early crystallization of plagioclase prior to pyroxenes, amphibole replacing pyroxenes, and magnetite–ilmenite intergrowth filling the interstices between plagioclase and pyroxenes. A quantitative mineral analysis based on micro-X-ray fluorescence element mapping reveals a positive correlation between Fe-Ti oxides and bulk-rock iron contents, suggesting that the formation of ferrogabbro is primarily attributed to the accumulation of Fe-Ti oxides. Petrographic characteristics combined with oxygen fugacity determinations indicate that the primitive magma had a low content of water and was moderately oxidized (ΔFMQ − 0.13 to ΔFMQ + 1.35). These conditions suppress the early crystallization of Fe-Ti oxides, thereby allowing for an enrichment of iron in the residual magma. Following the crystallization of plagioclase and pyroxenes, increased water content—evidenced by amphibole replacing pyroxenes—triggers extensive crystallization of Fe-Ti oxides. Due to their late-stage crystallization, these oxides do not settle within the magma, which possesses a high crystallinity (>50%) and consequently exhibits non-Newtonian fluid behavior. This results in the localized accumulation of Fe-Ti oxides and the formation of a ferrogabbro layer. However, the late-stage crystallization of Fe-Ti oxides also impedes the sinking and flow-sorting processes that are essential for the development of economically valuable Fe-Ti oxide layers. This may account for the lack of an economically valuable Fe-Ti oxide layer within the Dashanshu intrusion.

Anti-Inflammatory Effects of Cordyceps Cs-HK1 Fungus Exopolysaccharide on Lipopolysaccharide-Stimulated Macrophages via the TLR4/MyD88/NF-κB Pathway.

Chronic inflammation is a common factor in the pathological processes of multiple human diseases. EPS-LM, an exopolysaccharide (EPS) from the Cordyceps sinensis fungus Cs-HK1, has shown notable anti-inflammatory activities in previous studies. This study aimed to investigate the major signaling events mediating the anti-inflammatory effects of EPS-LM in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cell culture. EPS-LM treatment significantly reduced LPS-induced production of pro-inflammatory mediators, including nitric oxide (NO) and reactive oxygen species (ROS). It also suppressed the expression levels of Toll-like receptor 4 (TLR4) and myeloid differentiation primary response gene 88 (MyD88), subsequently delaying the translocation of nuclear factor-kappa B (NF-κB) to the nucleus. Additionally, co-immunoprecipitation (Co-IP) experiments demonstrated that EPS-LM inhibited the binding of TLR4 to MyD88. The ability of EPS-LM to inhibit the TLR4/MyD88/NF-κB pathway, coupled with its capacity to reduce oxidative stress, underscores its multifaceted anti-inflammatory effects. These effects render EPS-LM as a promising candidate for the comprehensive management of various inflammatory and oxidative stress-related conditions, protecting against cell damage.

Hot-Melt Extrusion Drug Delivery System-Formulated Haematococcus pluvialis Extracts Regulate Inflammation and Oxidative Stress in Lipopolysaccharide-Stimulated Macrophages.

Haematococcus pluvialis contains valuable bioactive compounds, including astaxanthin, proteins, and fatty acids. Astaxanthin is known for its various health benefits, such as preserving the redox balance and reducing inflammation. However, its low stability and poor water solubility present challenges for various applications. Hot-melt extrusion (HME) technology enhances the aqueous solubility of H. pluvialis extracts, increasing the usable astaxanthin content through nanoencapsulation (HME-DDS-applied extracts, ASX-60F and ASX-100F). This study compared the effects of HME-DDS-derived extracts (ASX-60F and ASX-100F) and the non-applied extract (ASX-C) under inflammatory and oxidative stress conditions. In animal models of sepsis, 60F and 100F treatment exhibited higher survival rates and a lower expression of pro-inflammatory biomarkers compared to those treated with C. In lipopolysaccharide-stimulated RAW 264.7 macrophages, nitric oxide (NO) production and the expression of pro-inflammatory mediators such as cyclooxygenase-2 and inducible NO synthase were reduced by 60F or 100F treatments via ERK/p-38 mitogen-activated protein kinase (MAPK) signaling. Moreover, 60F or 100F inhibited reactive oxygen species production regulated by nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. Collectively, these findings suggest that HME-DDS-derived H. pluvialis extracts exert anti-inflammatory and antioxidant effects by inhibiting MAPK phosphorylation and activating Nrf2/HO-1 expression.

Dual Responsive Emulsions Based on Amphiphilic Elastin-like Polypeptide Bioconjugates.

To achieve the desired therapeutic response, drug delivery systems must ensure the controlled release of the loaded content at the targeted site. One possible strategy relies on the improvement of conventional drug delivery systems. To do so, smart polymers, able to change their behavior upon chemical, physical, or biological stimuli, can be used. In this context, this study aims to evaluate the potential of natural amphiphilic smart elastin-like polypeptides grafted with alkyl chains (ELP-g-Bu) to stabilize conventional oil-in-water emulsions and trigger the release of loaded molecules upon dual stimuli. With butyl pendant chains and methionine residues, the macromolecular surfactant ELP-g-Bu demonstrated a modification of physicochemical properties, looking at critical aggregation concentration, upon both temperature and oxidation stimuli. The macromolecular surfactant was then able to stabilize a paraffin-oil-in-water emulsion. The ELP-g-Bu emulsion presented a droplet size of 9 ± 1 μm and stability for at least a month at 4 and 25 °C. After successful loading of a fluorescent lipophilic molecule used as a drug model, a complete destabilization of the ELP-g-Bu emulsion and burst release of the content was achieved with thermal triggering at 42 °C. In oxidative conditions, a partial release was measured, which can be improved by increasing the number of oxidable thioether groups. Overall, these dually responsive amphiphilic ELP-g-Bu demonstrated their potential for smart-polymer-based drug delivery systems that can be promising for inflammatory disease treatment as increased temperature and radical oxygen species are present in such cases.

Oxidation kinetics and electrical properties of oxide scales formed under exposure to air and Ar–H2-H2O atmospheres on the Crofer 22 H ferritic steel for high-temperature applications such as interconnects in solid oxide cell stacks

A 100 h isothermal oxidation kinetics study for Crofer 22H was conducted in air and the Ar–H2-H2O gas mixture (p(H2)/p(H2O) = 94/6) in the range of 973–1123 K. The parabolic rate constant was independent of oxygen partial pressure in the range from 6.2 × 10−24 to 0.21 atm at 1023 and 1073 K, while at 973 and 1123 K it was higher in air than in Ar–H2-H2O. The scales consisted of Cr2O3 and manganese chromium spinel with an Mn:Cr ratio dependent on the oxidation conditions. Cross-scale resistance was evaluated with regards to the application of the steel in solid oxide fuel cells using a number of methods, including X-ray diffraction, scanning electron microscopy, confocal Raman imaging and area-specific resistance measurements.