Ferric Research Articles

Plin4 exacerbates cadmium-decreased testosterone level via inducing ferroptosis in testicular Leydig cells

Strong evidence indicates that environmental stressors are the risk factors for male testosterone deficiency (TD). However, the mechanisms of environmental stress-induced TD remain unclear. Based on our all-cause male reproductive cohort, we found that serum ferrous iron (Fe2⁺) levels were elevated in TD donors. Then, we explored the role and mechanism of ferroptosis in environmental stress-reduced testosterone levels through in vivo and in vitro models. Data demonstrated that ferroptosis and lipid droplet deposition were observed in environmental stress-exposed testicular Leydig cells. Pretreatment with ferrostatin-1 (Fer-1), a specific ferroptosis inhibitor, markedly mitigated environmental stress-reduced testosterone levels. Through screening of core genes involved in lipid droplets formation, it was found that environmental stress significantly increased the levels of perilipins 4 (PLIN4) protein and mRNA in testicular Leydig cells. Further experiments showed that Plin4 siRNA reversed environmental stress-induced lipid droplet deposition and ferroptosis in Leydig cells. Additionally, environmental stress increased the levels of METTL3, METTL14, and total RNA m6A in testicular Leydig cells. Mechanistically, S-adenosylhomocysteine, an inhibitor of METTL3 and METTL14 heterodimer activity, restored the abnormal levels of Plin4, Fe2⁺ and testosterone in environmental stress-treated Leydig cells. Collectively, these results suggest that Plin4 exacerbates environmental stress-decreased testosterone level via inducing ferroptosis in testicular Leydig cells.

Heme metabolism in Strigomonas culicis: Implications of H2O2 resistance induction and symbiont elimination

Monoxenous trypanosomatid Strigomonas culicis harbors an endosymbiotic bacterium, which enables the protozoa to survive without heme supplementation. The impact of H2O2 resistance and symbiont elimination on intracellular heme and Fe2+ availability was analyzed through a comparison of WT strain with both WT H2O2-resistant (WTR) and aposymbiotic (Apo) protozoa. The relative quantification of the heme biosynthetic pathway through label-free parallel reaction monitoring targeted mass spectrometry revealed that H2O2 resistance does not influence the abundance of tryptic peptides. However, the Apo strain showed increased coproporphyrinogen III oxidase and ferrochelatase levels. A putative ferrous iron transporter, homologous to LIT1 and TcIT from Leishmania major and Trypanosoma cruzi, was identified for the first time. Label-free parallel reaction monitoring targeted mass spectrometry also showed that S.culicis Iron Transporter (ScIT) increased 1.6- and 16.4-fold in WTR and Apo strains compared to WT. Accordingly, antibody-mediated blockage of ScIT decreased by 28.0% and 40.0% intracellular Fe2+concentration in both WTR and Apo strains, whereas no effect was detected in WT. In a heme-depleted medium, adding 10μM hemin decreased ScIT transcript levels in Apo, whereas 10μM PPIX, the substrate of ferrochelatase, increased intracellular Fe2+ concentration and ferric iron reduction. Overall, the data suggest mechanisms dependent on de novo heme synthesis (and its substrates) in the Apo strain to overcome reduced heme availability. Given the importance of heme and Fe2+ as cofactors in metabolic pathways, including oxidative phosphorylation and antioxidant systems, this study provides novel mechanistic insights associated with H2O2 resistance in S.culicis.

Sulfiredoxin-1 accelerates erastin-induced ferroptosis in HT-22 hippocampal neurons by driving heme Oxygenase-1 activation

Ferroptosis, a recently identified non-apoptotic form of cell death, is strongly associated with neurological diseases and has emerged as a potential therapeutic target. Nevertheless, the fundamental mechanisms are still predominantly unidentified. In the current investigation, sulfiredoxin-1 (SRXN1) has been identified as a crucial regulator that enhances the susceptibility to ferroptosis in HT-22 mouse hippocampal cells treated with erastin. Utilizing TMT-based proteomics, a significant increase in SRXN1 expression was observed in erastin-exposed HT-22 cells. Efficient amelioration of erastin-induced ferroptosis was achieved via the knockdown of SRXN1, which resulted in the reduction of intracellular Fe2+ levels and reactive oxygen species (ROS) in HT-22 cells. Notably, the activation of Heme Oxygenase-1 (HO-1) was found to be crucial for inducing SRXN1 expression in HT-22 cells upon treatment with erastin. SRXN1 increased intracellular ROS and Fe2+ levels by activating HO-1 expression, which promoted erastin-induced ferroptosis in HT-22 cells. Inhibiting SRXN1 or HO-1 alleviated erastin-induced autophagy in HT-22 cells. Additionally, upregulation of SRXN1 or HO-1 increased the susceptibility of HT-22 cells to ferroptosis, a process that was counteracted by the autophagy inhibitor 3-Methyladenine (3-MA). These results indicate that SRXN1 is a key regulator of ferroptosis, activating the HO-1 protein through cellular redox regulation, ferrous iron accumulation, and autophagy in HT-22 cells. These findings elucidate a novel molecular mechanism of erastin-induced ferroptosis sensitivity and suggest that SRXN1-HO-1-autophagy-dependent ferroptosis serves as a promising treatment approach for neurodegenerative diseases.

NRF2 inhibits RSL3 induced ferroptosis in gastric cancer through regulation of AKR1B1

Gastric cancer is a malignant tumor associated with a high mortality rate. Recently, emerging evidence has shown that ferroptosis, a regulated form of cell death induced by iron (Fe)-dependent lipid peroxidation. Nuclear factor E2 related factor 2 (NRF2) is a key regulator of intracellular oxidation homeostasis that plays a pivotal role in controlling lipid peroxidation, which is closely related to the process of ferroptosis. However, the molecular mechanism of NRF2 on ferroptosis remains to be investigated in gastric cancer. In our study, NRF 2 was found to transcriptionally activate Aldo-keto reductase 1 member B1 (AKR1B1) expression in gastric cancer. AKR1B1 is involved in the regulation of lipid metabolism by removing the aldehyde group of glutathione. We found that AKR1B1 is highly expressed in gastric cancer and is associated with a poor prognosis of the patients. In vitro experiments found that AKR1B1 has the ability to promote the proliferation and invasion of gastric cancer cells. AKR1B1 inhibited RSL3-induced ferroptosis in gastric cancer by reducing reactive oxygen species accumulation and lipid peroxidation, as well as decreasing intracellular ferrous ion and malondialdehyde expression and increasing glutathione expression. Our study demonstrated that AKR1B1 resisted RSL3-induced ferroptosis by regulating GPX4, PTGS2 and ACSL4, which was further demonstrated in a xenograft nude mouse model. Our work reveals a critical role for the AKR1B1 in the resistance to RSL3-induced ferroptosis in gastric cancer.

Design, synthesis and biological evaluation of artesunate-Se derivatives as anticancer agents by inducing GPX4-mediated ferroptosis

A series of organoselenium compounds based on the hybridization of artesunate (ART) scaffolds and Se functionalities (–SeCN and –SeCF3) were synthesized. The redox properties of artesunate-SeCN and artesunate-SeCF3 derivatives were conducted by 2, 2-didiphenyl-1-picrylhydrazyl (DPPH), and the results showed that compounds 2c, 2f and 3e have a good free radical scavenging activity. Their cytotoxicity was evaluated against four types of cancer cell lines, SW480 (human colon adenocarcinoma cells), HCT116 (human colorectal adenocarcinoma cells), HepG2 (human hepatocellular carcinoma cells), MCF-7 (human breast cancer cells). The MTT results showed that compared with ART and 5-FU, compound 2c exhibited potent in vitro antiproliferative activity in SW480, HCT116, and MCF-7 cancer cell lines, and was thus chose for further antitumor mechanism investigation. The antitumor mechanism study revealed that compound 2c induced ferroptosis in HCT116 cells by inhibiting the expression of GPX4 protein, accompanying by the up-regulation of intracellular ROS levels. Mitochondria in HCT116 cells exhibit depolarization of mitochondrial membrane potential (MMP) and ultrastructural changes in morphology, which indicated that 2c resulted in mitochondrial dysfunction and ferroptosis. Moreover, 2c could increase the levels of lipid peroxidation and ferrous ion, which further confirm that compound 2c may exert its antitumor effect through ferroptosis. Overall, these results suggest that the artesunate-Se candidates could provide promising new lead derivatives for further potential anticancer drug development.

Modeling copper leaching from non-pulverized printed circuit boards at high concentrations of bioregenerated ferric sulfate

This work studies the leaching of copper contained in waste printed circuit boards (PCB) with ferric sulfate, with the aim of improving the results found in the literature for an industrial application of the process. For this purpose, temperatures and concentrations of ferric ion higher than those of previous works (up to 60 °C and 40 g/L) are used. Furthermore, ferric sulfate can be continuously regenerated by ferro-oxidizing bacteria immobilized in a bioreactor, avoiding physical contact between waste and microorganisms to optimize independently operation conditions. A kinetic model was developed for the interpretation of the experimental results validated at different conditions. The model was based on a shrinking core model limited by mass transfer inside the PCB where the geometry and structure of the PCB has been considered and an excellent fit of the model to the experimental data was obtained. The connection with the bioreactor for biooxidation of the generated ferrous ion allows maintaining high concentrations of ferric when operating at high solid concentrations (5–10 %). In all the cases studied, more than 99 % of the copper contained in the non-pulverized PCB parts was dissolved in less than 24 h, with an average copper extraction rate of 0.6 g/L·h higher than those found in previous works.

Structural determinants of Vibrio cholerae FeoB nucleotide promiscuity

Ferrous iron (Fe2+) is required for the growth and virulence of many pathogenic bacteria, including Vibrio cholerae (Vc), the causative agent of the disease cholera. For this bacterium, Feo is the primary system that transports Fe2+ into the cytosol. FeoB, the main component of this system, is regulated by a soluble cytosolic domain termed NFeoB. Recent reanalysis has shown that NFeoBs can be classified as either GTP-specific or NTP-promiscuous, but the structural and mechanistic bases for these differences were not known. To explore this intriguing property of FeoB, we solved the X-ray crystal structures of VcNFeoB in both the apo and the GDP-bound forms. Surprisingly, this promiscuous NTPase displayed a canonical NFeoB G-protein fold like GTP-specific NFeoBs. Using structural bioinformatics, we hypothesized that residues surrounding the nucleobase could be important for both nucleotide affinity and specificity. We then solved the X-ray crystal structures of N150T VcNFeoB in the apo and GDP-bound forms to reveal H-bonding differences surrounding the guanine nucleobase. Interestingly, isothermal titration calorimetry revealed similar binding thermodynamics of the WT and N150T proteins to guanine nucleotides, while the behavior in the presence of adenine nucleotides was dramatically different. AlphaFold models of VcNFeoB in the presence of ADP and ATP showed important conformational changes that contribute to nucleotide specificity among FeoBs. Combined, these results provide a structural framework for understanding FeoB nucleotide promiscuity, which could be an adaptive measure utilized by pathogens to ensure adequate levels of intracellular iron across multiple metabolic landscapes.

A Two-Step Leaching Process Using Thiourea for the Recovery of Precious Metals from Waste Printed Circuit Boards

The development of efficient recovery methods for waste printed circuit boards (WPCBs) not only tackles the environmental risks of disposal but also promotes the conservation of resources within the electronics industry. This study proposes a two-step leaching approach for recovering metals from WPCBs. Initially, transition metals are leached using nitric acid, followed by the recovery of precious metals with thiourea in the second stage. In the first stage, dissolution rates exceeding 90 wt% were achieved for transition metals, including Cu, Fe, Ni, Pb, and Sn. In this stage, the dissolution of precious metals (i.e., Au and Pd) was insignificant. In the second stage, the effect of four parameters was investigated, including the impact of temperature, concentrations of ferric ions, sulfuric media, and thiourea on the recovery of Au and Pd. Precise control over sulfate concentration played a vital role in achieving maximum Au recovery. The optimal acid concentration was 0.2 M, resulting in a recovery rate of ~50 wt%. Ferric ion concentration positively affects Au recovery, whereas, in extracting Pd, optimal conditions imposed the absence of ferric ions. Thiourea concentration positively impacted Au and Pd recovery rates, peaking at 49 wt% for Au at 1 M and 44 wt% for Pd at 1.5 M. Prolonged leaching resulted in declining Au recovery rates, indicating a decrease in reagent concentration. Temperature variation yielded similar outcomes, with 50 °C resulting in peak recovery rates of 53 wt% for Au and 54 wt% for Pd. Metal dissolution kinetics during leaching were analyzed using pseudo-first-order and pseudo-second-order models. The second-order model proved suitable for transition metals in the first stage, while only for Au and Pd in the second stage (with R2 = 0.99).

Brucella rough RB51 infection activates P53-Slc7a11-Gpx4/GSH pathway to induce ferroptosis to attenuate the intracellular survival on macrophages

B. abortus is a facultative intracellular bacterium that replicates within macrophages. Intracellular survival is one of the important indexes to evaluate the virulence of Brucella. Ferroptosis is a type of programmed cell death induced by the accumulation of free iron, reactive oxygen species (ROS), and toxic lipid peroxides, play roles on cancers, cardiovascular diseases, and inflammatory diseases. In this study, we found that Brucella rough strain RB51 induced ferroptosis on macrophages with reduced levels of host glutathione and glutathione peroxidase 4 (Gpx4), together with increased ferrous iron, lipid peroxidation, and ROS. The inhibitor ferrostatin-1 significantly reduced the ferroptosis of RB51-infected macrophages, confirming that ferroptosis occurred during infection with Brucella RB51. Furthermore, we found that RB51 infection induced ferroptosis is regulated by P53-Slc7a11-Gpx4/GSH signal pathway. Inhibiting P53 decreased the levels of ROS and lipid peroxidation, while the levels of Slc7a11, Gpx4 and GSH were rescued. More importantly, inhibiting ferroptosis by different ferroptosis inhibitors increased the intracellular survival of Brucella RB51, indicating ferroptosis functions on the attenuation of Brucella intracellular survival. Collectively, our observations demonstrate that Brucella RB51 infection induces ferroptosis on macrophages, which is regulated by P53-Slc7a11-Gpx4/GSH signal pathway and functions on the attenuation of intracellular survival of Brucella.

Extra Virgin Olive Oil's Main Components' Antioxidant Activity and in Silico Effect on AKT1.

The study compared the chemical composition of various olive oils from the northern Algerian province of Bejaia. The research focused on the antioxidant activities of the oil's main constituents and their ability to inhibit the AKT1 protein, which is implicated in the development of colorectal cancer. The findings revealed that all of the examined oils fell within the extra virgin olive oil (EVOO) category and exhibited a high oleic acid content, particularly for samples from wild olives. These oils include high amount of ligstroside and oleocanthal, two important phenolic compounds. Wild olive oils stand out from cultivated ones due to their higher bitterness index. In addition, these oils have the highest concentrations of α-tocopherols and the best oxidative stability. Olive oil extracts demonstrated their antioxidant properties by neutralizing DPPH and ABTS radicals and converting ferric ions (Fe3+) to ferrous ions (Fe2+) for FRAP assay. Molecular docking was applied to assess the interaction between the main compounds identified in the analyzed olive oils and the human AKT1 protein, which is involved in the genesis of colorectal cancer. The findings revealed that lutein, oleuropein aglycone, and ligstroside aglycone had the highest binding affinity for the AKT1 protein. The present study could provide the theoretical foundation for further research on the interaction between AKT1 protein and EVOO compounds.

Ferroptosis promotes valproate-induced liver steatosis in vitro and in vivo

Valproic acid (VPA), a common antiepileptic drug, can cause liver steatosis after long-term therapy. However, an impact of ferroptosis on VPA-induced liver steatosis has not been investigated. In the study, treatment with VPA promoted ferroptosis in the livers of mice by elevating ferrous iron (Fe2+) levels derived from the increased absorption by transferrin receptor 1 (TFR1) and the decreased storage by ferritin (FTH1 and FTL), disrupting the redox balance via reduced levels of solute carrier family 7 member 11 (SLC7A11), glutathione (GSH), and glutathione peroxidase 4 (GPX4), and augmenting acyl-CoA synthetase long-chain family member 4 (ACSL4) -mediated lipid peroxide generation, accompanied by enhanced liver steatosis. All the changes were significantly reversed by co-treatment with an iron-chelating agent, deferoxamine mesylate (DFO) and a ferroptosis inhibitor, ferrostatin-1 (Fer-1). Similarly, the increases in Fe2+, TFR1, and ACSL4 levels, as well as the decreases in GSH, GPX4, and ferroportin (FPN) levels, were detected in VPA-treated HepG2 cells. These changes were also attenuated after co-treatment with Fer-1. It demonstrates that ferroptosis promotes VPA-induced liver steatosis through iron overload, inhibition of the GSH-GPX4 axis, and upregulation of ACSL4. It offers a potential therapy targeting ferroptosis for patients with liver steatosis following VPA treatment.

Insight into the influence mechanism of chloride ions towards in-situ electric-induced uranium incorporation into magnetite

The application of electrochemical methods for incorporating uranium into the magnetite lattice has demonstrated efficacy and durability in remediating radioactive contamination. However, the impact of different ions, particularly electrolyte ions, on this process remains unclear. Herein, we successfully achieved simultaneous magnetite crystallization and uranium incorporation within an electrochemical system using an iron anode. Chloride ions have been identified as having a pivotal role in the generation of ferrous ions via pitting corrosion, thereby establishing an advantageous reducing environment that promotes the transformation of γ-FeOOH to magnetite. Unlike the surface adsorption process of γ-FeOOH, magnetite predominantly eradicates uranium through an incorporation mechanism. Consequently, the existence of chloride ions markedly boosts the effectiveness of uranium elimination and the stability of the resultant substance. Specifically, under conditions of a pH of 5 and a chloride ions concentration of 18 mM, uranium removal reaches nearly 100%. Additionally, findings from uranium leaching experiments indicate that γ-FeOOH removed 25.4% stable, 63.57% metastable, and 11.03% unstable uranium, while magnetite removed 60.35% stable, 24.81% metastable, and 14.84% unstable uranium. This research offers insight into the potential role of electrolyte ions in facilitating in-situ electric-induced uranium incorporation.

Self-assembled metal-polyphenolic based multifunctional nanomedicine to improve therapy treatment of pancreatic cancer by inhibition of glutamine metabolism

Cancer poses a significant threat to human health and life. Chemotherapy, immunotherapy and chemodynamic therapy (CDT) are effective treatments for cancer. However, the presence of metabolic reprogramming via glutamine in tumor cells limits their therapeutic effectiveness. Herein, we propose an effective assembly strategy to synthesize a novel metal-polyphenolic based multifunctional nanomedicine (Fe-DBEF) containing Pluronic F127 stable ferric ion crosslinked epigallocatechin gallate (EGCG) nanoparticles loaded with GLS1 inhibitor bis-2-(5-phenylacetamino-1,3,4-thiadiazole-2-yl) ethyl sulfide (BPTES) and chemotherapy drug doxorubicin (DOX). Our study demonstrates that Fe-DBEF nanomedicine exhibits high efficiency anti-proliferation properties in pancreatic cancer through a combination of in vitro cell experiments, human organoid experiments and KPC animal experiments. Notably, Fe-DBEF nanomedicine can reduce the production of glutathione (GSH) in tumor cells, thereby reducing their resistance to ROS therapy. Additionally, excessive ROS production also aggravates DNA damage caused by DOX, synergistically sensitizing chemotherapy and promoting apoptosis for efficient treatment of pancreatic cancer. Overall, our findings suggest that inhibiting glutamine metabolism to increase the sensitivity of chemotherapy/CDT using metal-polyphenolic based multifunctional nanomedicine provides a promising combination of multiple therapeutic means for treating pancreatic cancer.

Desulfurization of coal pyrite tailings with ozone

Mining is an important sector of the economy, and in the southern region of Brazil, coal mining stands out. This activity generates waste with a high pyritic content, which causes environmental problems such as acid mine drainage (AMD). Therefore, studies that aim to beneficiate or treat this waste are of high relevance. In this study, an alternative for desulfurizing pyritic waste using ozone was investigated. Ozone treatment of mining tailings suspension was evaluated as a new strategy for sulfur removal. Particle size analysis, sulfate content, ferrous ion concentration (and total iron), pH, Eh, conductivity, and X-ray fluorescence were performed. Furthermore, a kinetic analysis of ozone consumption was established. The behavior of sulfate and hydrogen ion concentrations indicates that sulfuric acid is the main reaction product, and conductivity suggests that ion release is continuous over the ozonation time. A reaction kinetics with ??1.2 was found for ozone depletion, which aids in predicting the dosage to be applied on a larger scale. This study represents a contribution to the search for alternatives for treating pyritic waste and contributes to the understanding of the reaction rate of ozone consumption in this type of reaction.

Application of the sono-Fenton/UV process on the treatment of table olive processing wastewater

AbstractThe Mediterranean Basin economies of Spain, Italy, Greece, and Turkey depend on the table olive and olive oil industries. Table olive processing wastewater characteristics and quantity depend on olive varietal and processing methods. Olives and processing methods provide phenol, suspended particles, dissolved inorganic solids, and refractory organics. Due of its complexity, conventional methods struggle to tackle table olive processing wastewater. A novel approach to enhanced oxidation processes integrates many ways to boost hydroxyl radical formation and scale up efficiency. UV assisted sono-Fenton process as a modified Fenton process was applied to table olive washing wastewater to achieve high formation of hydroxyl radicals. When UV assisted sono-Fenton experiments executed to determine the optimum reaction conditions, the effects of hydrogen peroxide, ferrous ion concentrations and reaction time on the oxidation of table olive washing wastewater investigated by using a statistical experimental design. Chemical oxygen demand (COD), total organic carbon (TOC) and phenol removal efficiencies were examined by keeping the pH constant. The UV assisted sono-Fenton process achieved 53% phenol, 68% TOC, and 80% COD removal efficiencies. The results show that the UV assisted sono-Fenton process can treat effectively table olive processing wastewater. Optimum reaction conditions for the UV assisted sono-Fenton process were determined. UV assisted sono-Fenton process provides a significant reduction in reaction time and minimizes the costs of process associated with low chemical requirements. So, these optimum reaction conditions were resulted in low sludge production at the UV assisted sono-Fenton process while treating table olive processing wastewater.

Extraction of phenolic compounds from Moringa oleifera Lam. leaves with ultrasonic-assisted deep eutectic solvents.

In this study, deep eutectic solvents (DESs) combined with ultrasound-assisted extraction (UAE) were used to extract bioactive compounds from the leaves of Moringa oleifera Lam. The FT-IR method was used to analyze the structural characteristics of the DESs, and the extraction efficiencies of the DESs for total phenolic content (TPC) and total flavonoid content (TFC) were evaluated. The stability of the extracts under high temperature and UV radiation was assessed, and their antioxidant activity was investigated after undergoing in vitro simulated digestion. The results show that the seven DESs extracted more TPC and TFC than did the 70% ethanol (36.27 ± 1.58 mg GAE/g, 23.09 ± 1.47 mg RT/g), and the extraction process of UAE-DES was optimized by selecting choline chloride: citric acid as the DES solvent, which has the highest extraction of TPC (86.92 ± 1.34 mg GAE/g) and TFC (49.73 ± 0.85 mg RT/g). The stability results indicated that the DES phenolic extracts were less stable when exposed to high temperature and UV radiation, indicating that DES extracts have better bioactivity. Moreover, after in vitro simulated digestion, the DES extract shows a higher DPPH free radical scavenging capacity (12.79 ± 3.88 mmol Trolox/g of DES extracts, 6.99 ± 4.02 mmol Trolox/g of ethanol extracts) and ferric ion reducing antioxidant power (62.61 ± 1.71 mmol Trolox/g of DES extracts, 55.07 ± 1.66 mmol Trolox/g of ethanol extracts) than ethanol extracts. This study confirmed that DESs are a new and environmentally friendly solvent that can be used for the extraction of phenolic compounds.

Microbead-Based Colorimetric and Portable Sensors for Polyphenol Detection.

Natural polyphenols found in health supplements and drinks have antioxidant and anti-inflammatory properties. In particular, to determine the beneficial qualities of antioxidant drinks and beverages, consumers demand precise quantification of the total amount of polyphenols as on-site detection. Herein, we developed a new concept of portable beads suitable for the field detection available: colorimetric quantification of polyphenols equipped with color converting software applications in a smartphone or tablet PC. The yellowish beads contain ferric ions to react with polyphenol to produce blackish metal-phenolic complexes. It is simple to perform the detection procedure: dipping the beads in the analytical sample and out-taking a photo-converting into RGB color values and quantification of the existed polyphenol. The overall process was completed within 5 min. Compared with the Folin-Ciocalteu assay, which is a representative optical sensor kit for total phenolic content, the bead-based sensor showed a better limit of detection of 0.0415 mM for tannic acid and comparable sensing capability for a polyphenol-containing plant extract and brewed tea. The beads conserved the shape and sensitivity after months of storage or under environmental interference such as a change in the temperature.

Melanin-Like Nanomedicine Functions as a Novel RPE Ferroptosis Inhibitor to Ameliorate Retinal Degeneration and Visual Impairment in Dry Age-Related Macular Degeneration.

Ferrous ion accumulation and lethal oxidative stress mediate irreversible retinal pigment epithelial (RPE) cell ferroptosis and subsequent photoreceptor degeneration, a potential key pathogenic factor in the onset of dry age-related macular degeneration (dAMD), causing irreversible vision loss in the global elderly population. However, currently, no effective interventional treatment strategy exists in clinical practice. Herein, lesion site-targeted melanin-like nanoparticles, named ConA-MelNPs, are designed as a novel ferroptosis inhibitor for retinal degenerative diseases. ConA-MelNPs possessed chelating iron ion characteristics, alleviating severe mitochondrial damage caused by oxidative stress and protecting RPE cells from ferroptosis induced by sodium iodate (NaIO3). In a preclinical dAMD mouse model, a single intravitreal injection of ConA-MelNPs yielded significant responses in electroretinograms and visually-driven optomotor responses in visually impaired mice, resisting the challenge posed by secondary NaIO3-induced injuries, with the long-term sustainability of its therapeutic effect. Mechanistically, ConA-MelNPs achieve a therapeutic effect by interrupting the detrimental cascade involving "RPE cell ferroptosis, lethal oxidative stress, and microglial proinflammatory activation," affording the restoration of retinal homeostasis. The synthesized ConA-MelNPs demonstrated good biosafety, with no detected ophthalmic or systemic side effects. Collectively, ConA-MelNPs are proposed as a promising therapeutic option for atrophic retinal diseases such as dAMD.

Deciphering microbial metabolic interactions and their implications for community dynamics in acid mine drainage sediments

The microbially-mediated reduction processes have potential for the bioremediation of acid mine drainage (AMD), which represents a worldwide environment problem. However, we know little about the microbial interactions in anaerobic AMD sediments. Here we utilized genome-resolved metagenomics to uncover the nature of cooperative and competitive metabolic interactions in 90 AMD sediments across Southern China. Our analyses recovered well-represented prokaryotic communities through the reconstruction of 2625 population genomes. Functional analyses of these genomes revealed extensive metabolic handoffs which occurred more frequently in nitrogen metabolism than in sulfur metabolism, as well as stable functional redundancy across sediments resulting from populations with low genomic relatedness. Genome-scale metabolic modeling showed that metabolic competition promoted microbial co-occurrence relationships, suggesting that community assembly was dominated by habitat filtering in sediments. Notably, communities colonizing more extreme conditions tended to be highly competitive, which was typically accompanied with increased network complexity but decreased stability of the microbiome. Finally, our results demonstrated that heterotrophic Thermoplasmatota associated with ferric iron and sulfate reduction contributed most to the elevated levels of competition. Our study shed light on the cooperative and competitive metabolisms of microbiome in the hazardous AMD sediments, which may provide preliminary clues for the AMD bioremediation in the future.

Concentrated Chloride Electrolyte Enabling SEI for Fe Metal Anode

Iron is one of the most abundant metal elements in the Earth’s crust and has been widely used worldwide since ancient times. Due to this natural abundance and well-established mass production methods, iron is a promising candidate as a battery electrode for cost-effective large-scale energy storage systems. Edison’s Ni-Fe battery, invented in 1900, used an alkaline electrolyte without ferrous or ferric ions that eventually limited its anode design using iron oxide. More recent Fe redox flow batteries and the newly suggested Fe-ion batteries that use an acidic electrolyte containing ferrous ions (Fe2+) can utilize iron foil as an anode. Combining iron foil with Fe2+ electrolyte enables a simple design and faster kinetics on the anode side. However, introducing acidic electrolytes accelerates hydrogen evolution reaction (HER) on the iron surface. Severe HER affects cell performance in various ways, including lower Coulombic efficiency (CE), drying out of the electrolyte by water consumption, and precipitation of Fe2+ ions due to increased pH of the electrolyte. In this work, a concentrated chloride-based electrolyte was introduced to Fe-ion batteries to suppress HER and achieve a high-CE Fe2+/Fe electrode. With the help of nonpolar [ZnCl4]2- which enables low-polarity organic additives to be soluble in the aqueous solution, an organic solid electrolyte interface (SEI) can be formed on top of the electrode while plating iron. Fe anode protected by the SEI shows a noticeable decrease in HER during cycling, which leads to higher CE of more than 98% and twice longer cycle life.