μM Mn Research Articles

Remediation of Aquatic Environments Contaminated with As(III) and Mn2+(aq) Using Hematite Photocatalyst

Arsenic (As) and manganese (Mn) commonly coexist in nature and are well known to have high carcinogenic and neurotoxicity effects. Therefore, many regulatory agencies impose a maximum contamination level for As and Mn in water at 10 and 400 μg L-1, respectively. Additionally, since As and Mn often occur together, there is a need for a method that can simultaneously remove As and Mn. However, currently, As is removed using iron oxide, and Mn is removed using Mn oxide. These methods suffer from decreased removal efficiency over time and have limitations in effectively removing As(III), which is more toxic, mobile, and difficult to eliminate. Therefore, a method is needed that can effectively and simultaneously remove As(III) and Mn. In this study, we investigated the simultaneous oxidation and removal of As(III) and Mn2+(aq) using a photocatalytic reaction with hematite. The reason we used hematite is that it is one of the most abundant iron oxides in the crust and has a favorable band gap of 2.1 eV, making it suitable for photocatalytic oxidation using sunlight. We found that 0.1 g/L hematite can simultaneously and rapidly oxidize 89 μM As(III) and 44 μM Mn2+(aq) through photocatalytic process under natural sunlight. Additionally, we confirmed that a positive hole is the primary pathway for the oxidation of As(III) and Mn2+(aq). Our finding provides that As(III) and Mn2+(aq) can be effectively removed using hematite from aquatic systems contaminated with As(III) and Mn2+(aq). Moreover, our finding provides insights to understand the redox processes among As(III/V), Mn2+(aq), and hematite in natural environments.

Manganese Exposure Enhances the Release of Misfolded α-Synuclein via Exosomes by Impairing Endosomal Trafficking and Protein Degradation Mechanisms.

Excessive exposure to manganese (Mn) increases the risk of chronic neurological diseases, including Parkinson's disease (PD) and other related Parkinsonisms. Aggregated α-synuclein (αSyn), a hallmark of PD, can spread to neighboring cells by exosomal release from neurons. We previously discovered that Mn enhances its spread, triggering neuroinflammatory and neurodegenerative processes. To better understand the Mn-induced release of exosomal αSyn, we examined the effect of Mn on endosomal trafficking and misfolded protein degradation. Exposing MN9D dopaminergic neuronal cells stably expressing human wild-type (WT) αSyn to 300 μM Mn for 24 h significantly suppressed protein and mRNA expression of Rab11a, thereby downregulating endosomal recycling, forcing late endosomes to mature into multivesicular bodies (MVBs). Ectopic expression of WT Rab11a significantly mitigated exosome release, whereas ectopic mutant Rab11a (S25N) increased it. Our in vitro and in vivo studies reveal that Mn exposure upregulated (1) mRNA and protein levels of endosomal Rab27a, which mediates the fusion of MVBs with the plasma membrane; and (2) expression of the autophagosomal markers Beclin-1 and p62, but downregulated the lysosomal marker LAMP2, thereby impairing autophagolysosome formation as confirmed by LysoTracker, cathepsin, and acridine orange assays. Our novel findings demonstrate that Mn promotes the exosomal release of misfolded αSyn by impairing endosomal trafficking and protein degradation.

Hyperaccumulation of metal in the apoplast contributes to the tolerance of the phytoremediator Pistia stratiotes L. to manganese-contaminated water

Phytoremediation of manganese (Mn)-contaminated water requires the selection of Mn-tolerant species. This study reports on physiological changes and Mn bioaccumulation in the aquatic macrophyte Pistia stratiotes cultivated under various MnCl2 concentrations: control, 80, 340, 600, 1000, 2000, and 4000 µM. Few visual symptoms of Mn toxicity, such as chlorosis, were observed after 10 days, especially in plants treated with 2000 and 4000 µM MnCl2. High Mn accumulation was recorded, with maximum values of 23,700 and 24,600 µg g−1 DW in the shoots and roots, respectively, at 4000 µM Mn, contrasting with 825.01 and 1587.53 µg g−1 DW in control plants. Cellular fractioning showed that Mn in shoots and roots was mainly associated with the cell wall, with approximately 90% of the Mn in roots detected in the apoplast. There were no significant changes in net CO2 assimilation or respiratory rates after 5 and 10 days of Mn exposure. These results demonstrate that P. stratiotes is a Mn hyperaccumulator species with excellent phytoremediation potential, as shown by its high bioaccumulation capacity and its ability to maintain photosynthetic efficiency under Mn stress.

Ca2+-controlled Mn(II) removal process in Aurantimonas sp. HBX-1: Microbially-induced carbonate precipitation (MICP) versus Mn(II) oxidation

The application of manganese-oxidizing bacteria (MnOB) to produce manganese oxides (MnOx) has been widely studied, but often overlooking the concurrent formation of MnCO3. In this study, we found Ca2+ plays a crucial role in controlling Mn(II) removal in the bacterium Aurantimonas sp. HBX-1. Under conditions with 6.8 mM Ca2+ and without adding Ca2+, 100 μM Mn(II) was removed by 96.96 % and 38.28 % within 8 days, respectively. X-ray photoelectron spectroscopy (XPS) showed that adding Ca2+ increased the average oxidation state (AOS) of the solid products from 2.05 to 2.37. X-ray absorption fine structure (XAFS) analysis revealed the product proportions as follows: under Ca2+-supplemented condition, the ratio of MnOx (1 < x ≤ 2) to MnCO₃ was 52 % to 28.1 %, while under Ca2+-free condition, the ratio shifted to 4.6 % for MnOx (1 < x ≤ 2) and 55.2 % for MnCO₃. Urease activity assay and proteomic analysis confirmed the expression of urease and carbonic anhydrase, leading to the formation of MnCO3. Additionally, animal heme peroxidase (AHP) in strain HBX-1 was found to be responsible for Mn(II) oxidation through superoxide production, with Ca2+ addition promoting its expression level. Given the widespread presence of Ca2+ in wastewater, its potential impact on the biogeochemical Mn(II) cycle driven by bacteria should be reconsidered.

Effect of Mn on Cd2+ uptake by protoplasts of the Cd/Mn hyperaccumulator Celosia argentea Linn. differs by treatment method

The effect mechanism of Mn on Cd uptake by Celosia argentea was investigated via a series of hydroponics experiments. The results showed that different manganese treatments had different effects on Cd uptake by C. argentea. Mn pretreatment increased Cd uptake by root protoplasts at Cd concentrations (4 and 6 μM). Protoplasts reached peak Cd uptake rate at 6 μM Cd and 25 °C, with 67.71 ± 0.13 μM h−1 mL−1 in the control, and 77.99 ± 0.49 μM h−1 mL−1 in the 50 μM Mn pretreatment group. However, simultaneous treatment with Cd and Mn reduced the Cd2+ uptake by root protoplasts. This discrepancy may be attributed to the fact that cadmium and manganese share some transporters in root cells. The transcriptome analysis in roots revealed that ten genes (including ABCC, ABCA, ABCG, ABCB, ABC1, BZIP19, and ZIP5) were significantly upregulated in response to Mn stress (p < 0.05). These genes regulate the expression of transporters belonging to the ABC, and ZIP families, which may be involved in Cd uptake by root cells of C. argentea. Mn pretreatment upregulates the expression of Mn/Cd transporters, enhancing Cd uptake by root protoplasts. For the simultaneous treatment of Cd and Mn, inhibition of Cd uptake was due to the competition of the same transporters. These findings provide helpful insights for understanding the mechanism of Mn and Cd uptake in hyperaccumulators and give implications to improve the phytoremediation of Cd-contaminated soil by C. argentea.

Synergistic catalysis of tungsten disulfide and manganese ions for the degradation of dimethyl disulfide using chlorine dioxide

Dimethyl disulfide (DMDS) is a typical odorant in chemical and pesticide-contaminated sites, characterized by low odor threshold and high volatility. In this study, a ClO2/Mn2+/WS2 catalytic system was constructed for the degradation of DMDS. Under the reaction conditions of 400 μm ClO2, 20 μm Mn2+, 80 μM WS2, and pH = 7.0, the residual rate of DMDS decreased to 10.58 % within 80 min. Analyses using XPS, FRSEM, XRD, and EDX confirmed the synergistic catalytic effect of WS2 and Mn2+. The cyclic valence states of Mn2+/Mn4+ and W4+/W6+ were identified as the primary factors enhancing ClO2 activation for DMDS degradation. WS2 maintained good catalytic activity even after four cycles, demonstrating excellent reusability. Furthermore, EPR testing and quenching experiments elucidated the main reactive oxygen species (ROS) during the reaction, including 1O2, OH, and ClO2. In the initial 10 min, the oxidation process was dominated by 1O2 (44.48 % rate contribution) and ClO2 (55.52 % rate contribution), while in the subsequent 70 min, OH (49.16 % rate contribution) and ClO2 (50.84 % rate contribution) played the primary role. DFT calculations combined with GC–MS detection were utilized to propose possible degradation pathways of DMDS. Various anions (HCO3−, Cl−, SO2 − 4, NO3−) and humic acid (HA) exhibited different degrees of inhibition on DMDS degradation in the ClO2/Mn2+/WS2 system. This study provides a feasible approach for efficiently removing DMDS in pesticide plants and chemical industrial parks.

Regulatory Mechanism through Which Old Soybean Leaves Respond to Mn Toxicity Stress.

Manganese (Mn) is a heavy metal that can cause excessive Mn poisoning in plants, disrupting microstructural homeostasis and impairing growth and development. However, the specific response mechanisms of leaves to Mn poisoning have not been fully elucidated. This study revealed that Mn poisoning of soybean plants resulted in yellowing of old leaves. Physiological assessments of these old leaves revealed significant increases in the antioxidant enzymes activities (peroxidase (POD), superoxide dismutase (SOD), ascorbate peroxidase (APX), and catalase (CAT)) and elevated levels of malondialdehyde (MDA), proline, indoleacetic acid (IAA), and salicylic acid (SA), under 100 μM Mn toxicity. Conversely, the levels of abscisic acid (ABA), gibberellin 3 (GA3), and jasmonic acid (JA) significantly decreased. The Mn content in the affected leaves significantly increased, while the levels of Ca, Na, K, and Cu decreased. Transcriptome analysis revealed 2258 differentially expressed genes in the Mn-stressed leaves, 744 of which were upregulated and 1514 were downregulated; these genes included genes associated with ion transporters, hormone synthesis, and various enzymes. Quantitative RT-PCR (qRT-PCR) verification of fifteen genes confirmed altered gene expression in the Mn-stressed leaves. These findings suggest a complex gene regulatory mechanism under Mn toxicity and stress, providing a foundation for further exploration of Mn tolerance-related gene regulatory mechanisms in soybean leaves. Using the methods described above, this study will investigate the molecular mechanism of old soybean leaves' response to Mn poisoning, identify key genes that play regulatory roles in Mn toxicity stress, and lay the groundwork for cultivating high-quality soybean varieties with Mn toxicity tolerance traits.

Effect and Cytotoxic Influence of High Concentrations of Manganese on the Phenotypic Variation of different Chickpea (Cicer arietinum L.) Seedlings

This study explores the phenotypic responses of diverse chickpea (Cicer arietinum L.) germplasms to heavy metal (Mn) stress, emphasizing seedling traits vital for plant establishment and growth. Chickpea seeds obtained from Acharya Narendra Deva University of Agriculture and Technology underwent meticulous examination and were stressed with manganese (Mn) supplementation at 200 µM Mn. Germination assays were meticulously conducted under controlled conditions, with data recorded over a 14-day span. Statistical analysis uncovered significant variations among germplasms concerning traits such as seed volume, germination percentage, 100-seed weight, speed of germination, field emergence, shoot and root lengths, seedling length, and vigour index-I. Correlation analysis delineated intricate interrelationships between these traits under heavy metal (Mn) stress. Notably, ICCV 92944 emerged as a superior variety, showcasing rapid germination, vigorous seedling growth, and remarkable stress tolerance. Other promising genotypes include HC 3, BG 267, and SBD 377. These findings offer valuable insights for breeding programs aimed at cultivating stress-tolerant chickpea varieties, thereby contributing to sustainable crop production in contaminated environments.

Can xenobiotics support the growth of Mn(II)-oxidizing bacteria (MnOB)? A case of phenol-utilizing bacteria Pseudomonas sp. AN-1

Biogenic manganese oxides (BioMnOx) produced by Mn(II)-oxidizing bacteria (MnOB) have garnered considerable attention for their exceptional adsorption and oxidation capabilities. However, previous studies have predominantly focused on the role of BioMnOx, neglecting substantial investigation into MnOB themselves. Meanwhile, whether the xenobiotics could support the growth of MnOB as the sole carbon source remains uncertain. In this study, we isolated a strain termed Pseudomonas sp. AN-1, capable of utilizing phenol as the sole carbon source. The degradation of phenol took precedence over the accumulation of BioMnOx. In the presence of 100 mg L−1 phenol and 100 µM Mn(II), phenol was entirely degraded within 20 h, while Mn(II) was completely oxidized within 30 h. However, at the higher phenol concentration (500 mg L−1), phenol degradation reduced to 32% and Mn(II) oxidation did not appear to occur. TOC determination confirmed the ability of strain AN-1 to mineralize phenol. Based on the genomic and proteomics studies, the Mn(II) oxidation and phenol mineralization mechanism of strain AN-1 was further confirmed. Proteome analysis revealed down-regulation of proteins associated with Mn(II) oxidation, including MnxG and McoA, with increasing phenol concentration. Notably, this study observed for the first time that the expression of Mn(II) oxidation proteins is modulated by the concentration of carbon sources. This work provides new insight into the interaction between xenobiotics and MnOB, thus revealing the complexity of biogeochemical cycles of Mn and C.

Zinc priming enhances Capsicum annuum immunity against infection by Botrytis cinerea– From the whole plant to the molecular level

Micronutrient manipulation can enhance crop resilience against pathogens, but the mechanisms are mostly unknown. We tested whether priming Capsicum annuum plants with zinc (5 μM Zn) or manganese (3 μM Mn) for six weeks increases their immunity against the generalist necrotroph Botrytis cinerea compared to deficient (0.1 μM Zn, 0.02 μM Mn) and control conditions (1 μM Zn, 0.6 μM Mn). Zinc priming reduced the pathogen biomass and lesion area and preserved CO2 assimilation and stomatal conductance. Zinc mobilization at the infection site, visualized by micro-X-ray fluorescence, was accompanied by increased Zn protein binding obtained by size exclusion HPLC-ICP/MS. A common metabolic response to fungal infection in Zn- and Mn-primed plants was an accumulation of corchorifatty acid F, a signaling compound, and the antifungal compound acetophenone. In vitro tests showed that the binding of Zn2+ increased, while Mn2+ binding decreased acetophenone toxicity against B. cinerea at concentrations far below the toxicity thresholds of both metals in unbound (aquo complex) form. The metal-specific response to fungal infection included the accumulation of phenolics and amino acids (Mn), and the ligand isocitrate (Zn). The results highlight the importance of Zn for pepper immunity through direct involvement in immunity-related proteins and low molecular weight Zn-complexes, while Mn priming was inefficient.

Transcriptome Sequencing Analysis of Root in Soybean Responding to Mn Poisoning.

Manganese (Mn) is among one of the essential trace elements for normal plant development; however, excessive Mn can cause plant growth and development to be hindered. Nevertheless, the regulatory mechanisms of plant root response to Mn poisoning remain unclear. In the present study, results revealed that the root growth was inhibited when exposed to Mn poisoning. Physiological results showed that the antioxidase enzyme activities (peroxidase, superoxide dismutase, ascorbate peroxidase, and catalase) and the proline, malondialdehyde, and soluble sugar contents increased significantly under Mn toxicity stress (100 μM Mn), whereas the soluble protein and four hormones' (indolebutyric acid, abscisic acid, indoleacetic acid, and gibberellic acid 3) contents decreased significantly. In addition, the Mn, Fe, Na, Al, and Se contents in the roots increased significantly, whereas those of Mg, Zn, and K decreased significantly. Furthermore, RNA sequencing (RNA-seq) analysis was used to test the differentially expressed genes (DEGs) of soybean root under Mn poisoning. The results found 45,274 genes in soybean root and 1430 DEGs under Mn concentrations of 5 (normal) and 100 (toxicity) μM. Among these DEGs, 572 were upregulated and 858 were downregulated, indicating that soybean roots may initiate complex molecular regulatory mechanisms on Mn poisoning stress. The results of quantitative RT-PCR indicated that many DEGs were upregulated or downregulated markedly in the roots, suggesting that the regulation of DEGs may be complex. Therefore, the regulatory mechanism of soybean root on Mn toxicity stress is complicated. Present results lay the foundation for further study on the molecular regulation mechanism of function genes involved in regulating Mn tolerance traits in soybean roots.

Phase-dependent reactivity of MnO2 catalysts for permanganate activation: Insight into the role of surface-adsorbed MnO4− species

The development of green and efficient heterogeneous catalysts for permanganate (Mn(VII)) activation remains unexplored. Given the different roles of crystal structures of MnO2 in many applications, it is of great significance to investigate the reactivity of MnO2 with different phases for Mn(VII) activation. In this study, it was found that the first-order rate constants for phenol degradation in the presence of 100 μM Mn(VII) follow an order of α-MnO2 (0.0884 min−1) > δ-MnO2 (0.0746 min−1) > β-MnO2 (0.0417 min−1) > γ-MnO2 (0.0396 min−1). The fact is in line with Mn(VII) adsorption, which can be related closely to the surface area, pore diameter, and isoelectric points of the catalysts. Other phenolic contaminants such as parachlorophenol and bisphenol A were also degraded efficiently by the Mn(VII)/α-MnO2 system. After coordination with surface Mn species in MnO2, the Mn–O bond of Mn(VII) is stretched with an increase in electron transfer reactivity and a decrease in oxygen atom transfer ability. A surface-promoted electron transfer process is then proposed for phenol degradation by the system. A good adaptability and reusability of the Mn(VII)/α-MnO2 system were observed. The influence of several parameters and comparisons with other catalysts were also studied. This work provides insights into the phase-dependent reactivity of MnO2 catalysts for Mn(VII) activation and pollutant degradation.

Quantitative Proteomics Reveals Manganese Alleviates Heat Stress of Broiler Myocardial Cells via Regulating Nucleic Acid Metabolism.

Heat stress threatens severely cardiac function by caused myocardial injury in poultry. Our previous study has showed that manganese (Mn) has a beneficial effect on heat-stress resistance of broiler. Therefore, we tried to confirm the alleviation mechanism through proteomic analysis after heat stress exposure to primary broiler myocardial cells pretreated with Mn. The experiment was divided into four groups: CON group (37 °C, cells without any treatment), HS group (43 °C, cells treatment with heat stress for 4 h), HS+MnCl2 group (cells treated with 20 μM MnCl2 before heat stress), and HS+Mn-AA group (cells treated with 20 μM Mn compound amino acid complex before heat stress). Proteome analysis using DIA identified 300 differentially expressed proteins (DEPs) between CON group and HS group; 93 and 121 DEPs were identified in inorganic manganese treatment group and organic manganese treatment group, respectively; in addition, there were 53 DEPs identified between inorganic and organic manganese group. Gene Ontology (GO) analysis showed that DEPs were mainly involved in binding, catalytic activity, response to stimulus, and metabolic process. DEPs of manganese pretreatment involved in a variety of biological regulatory pathways, and significantly influenced protein processing and repair in endoplasmic reticulum, apoptosis, and DNA replication and repair. These all seem to imply that manganese may help to resist cell damage induced by heat stress by regulating key node proteins. These findings contribute to a better understanding of the effects of manganese on overall protein changes during heat-stress and the possible mechanisms, as well as how to better use manganese to protect heart function in high temperature.

Microglia Signaling Pathway Reporters Unveiled Manganese Activation of the Interferon/STAT1 Pathway and Its Mitigation by Flavonoids

Neuroinflammatory responses to neurotoxic manganese (Mn) in CNS have been associated with the Mn-induced Parkinson-like syndromes. However, the framework of molecular mechanisms contributing to manganism is still unclear. Using an in vitro neuroinflammation model based on the insulated signaling pathway reporter transposon constructs stably transfected into a murine BV-2 microglia line, we tested effects of manganese (II) together with a set of 12 metal salts on the transcriptional activities of the NF-κB, activator protein-1 (AP-1), signal transducer and activator of transcription 1 (STAT1), STAT1/STAT2, STAT3, Nrf2, and metal-responsive transcription factor-1 (MTF-1) via luciferase assay, while concatenated destabilized green fluorescent protein expression provided for simultaneous evaluation of cellular viability. This experiment revealed specific and strong responses to manganese (II) in reporters of the type I and type II interferon-induced signaling pathways, while weaker activation of the NF-κB in the microglia was detected upon treatment of cells with Mn(II) and Ba(II). There was a similarity between Mn(II) and interferon-γ in the temporal STAT1 activation profile and in their antagonism to bacterial LPS. Sixty-four natural and synthetic flavonoids differentially affected both cytotoxicity and the pro-inflammatory activity of Mn (II) in the microglia. Whereas flavan-3-ols, flavanones, flavones, and flavonols were cytoprotective, isoflavones enhanced the cytotoxicity of Mn(II). Furthermore, about half of the tested flavonoids at 10–50 μM could attenuate both basal and 100–200 μM Mn(II)-induced activity at the gamma-interferon activated DNA sequence (GAS) in the cells, suggesting no critical roles for the metal chelation or antioxidant activity in the protective potential of flavonoids against manganese in microglia. In summary, results of the study identified Mn as a specific elicitor of the interferon-dependent pathways that can be mitigated by dietary polyphenols.

Biphasic Dose-Response of Mn-Induced Mitochondrial Damage, PINK1/Parkin Expression, and Mitophagy in SK-N-SH Cells.

Excessive manganese (Mn) exposure produces neurotoxicity with mitochondrial damage. Mitophagy is a protective mechanism to eliminate damaged mitochondria to protect cells. The aim of this study was to determine the dose-response of Mn-induced mitochondria damage, the expression of mitophagy-mediated protein PINK1/Parkin and mitophagy in dopamine-producing SK-N-SH cells. Cells were exposed to 0, 300, 900, and 1500μM Mn2+ for 24h, and ROS production, mitochondrial damage and mitophagy were examined. The levels of dopamine were detected by ELISA and neurotoxicity and mitophagy-related proteins (α-synuclein, PINK1, Parkin, Optineurin, and LC3II/I) were detected by western blot. Mn increased intracellular ROS and apoptosis and decreased mitochondrial membrane potential in a concentration-dependent manner. However, at the low dose of 300μM Mn, autophagosome was increased 11-fold, but at the high dose of 1500μM, autophagosome was attenuated to 4-fold, together with decreased mitophagy-mediated protein PINK1/Parkin and LC3II/I ratio and increased Optineurin expression, resulting in increased α-synuclein accumulation and decreased dopamine production. Thus, Mn-induced mitophagy exhibited a novel biphasic regulation: at the low dose, mitophagy is activated to eliminate damaged mitochondria, however, at the high dose, cells gradually loss the adaptive machinery, the PINK1/Parkin-mediated mitophagy weakened, resulting in neurotoxicity.

Integrated transcriptome and metabolome analysis reveals the mechanism of tolerance to manganese and cadmium toxicity in the Mn/Cd hyperaccumulator Celosia argentea Linn.

Understanding the molecular mechanism of tolerance to heavy metals in hyperaccumulators is important for improving the efficiency of phytoremediation and is interesting for evolutionary studies on plant adaption to abiotic stress. Celosia argentea Linn. was recently discovered to hyperaccumulate both manganese (Mn) and cadmium (Cd). However, the molecular mechanisms underlying Mn and Cd detoxification in C. argentea are poorly understood. Laboratory studies were conducted using C. argentea seedlings exposed to 360μM Mn and 8.9μMCd hydroponic solutions. Plant leaves were analyzed using transcriptional and metabolomic techniques. A total of 3960 differentially expressed genes (DEGs) in plants were identified under Cd stress, among which 17 were associated with metal transport, and 10 belonged to the ATP transporter families. Exposures to Mn or Cd led to the differential expression of three metal transport genes (HMA3, ABCC15, and ATPase 4). In addition, 33 and 77 differentially expressed metabolites (DEMs) were identified under Mn and Cd stresses, respectively. Metabolic pathway analysis showed that the ABC transporter pathway was the most affected in Mn/Cd exposed seedlings. Conjoint transcriptome and metabolome analysis showed that the glutathione (GSH) metabolic pathway was over-represented in the KEGG pathway of both DEGs and DEMs. Our results confirm that the ABC transporter and GSH metabolic pathways play important roles in Mn and Cd detoxification. These findings provide new insight into the molecular mechanisms of tolerance to Mn and Cd toxicity in plants.

Highly Efficient Utilization of Ferrate(VI) Oxidation Capacity Initiated by Mn(II) for Contaminant Oxidation: Role of Manganese Species.

Manganese ion [Mn(II)] is a background constituent existing in natural waters. Herein, it was found that only 59% of bisphenol A (BPA), 47% of bisphenol F (BPF), 65% of acetaminophen (AAP), and 49% of 4-tert-butylphenol (4-tBP) were oxidized by 20 μM of Fe(VI), while 97% of BPA, 95% of BPF, 96% of AAP, and 94% of 4-tBP could be oxidized by the Fe(VI)/Mn(II) system [20 μM Fe(VI)/20 μM Mn(II)] at pH 7.0. Further investigations showed that bisphenol S (BPS) was highly reactive with reactive iron species (RFeS) but was sluggish with reactive manganese species (RMnS). By using BPS and methyl phenyl sulfoxide (PMSO) as the probe compounds, it was found that reactive iron species contributed primarily for BPA oxidation at low Mn(II)/Fe(VI) molar ratios (below 0.1), while reactive manganese species [Mn(VII)/Mn(III)] contributed increasingly for BPA oxidation with the elevation of the Mn(II)/Fe(VI) molar ratio (from 0.1 to 3.0). In the interaction of Mn(II) and Fe(VI), the transfer of oxidation capacity from Fe(VI) to Mn(III), including the formation of Mn(VII) and the inhibition of Fe(VI) self-decay, improved the amount of electron equivalents per Fe(VI) for BPA oxidation. UV-vis spectra and dominant transformation product analysis further revealed the evolution of iron and manganese species at different Mn(II)/Fe(VI) molar ratios.

Sodium Nitroprusside Improves Bamboo Resistance under Mn and Cr Toxicity with Stimulation of Antioxidants Activity, Relative Water Content, and Metal Translocation and Accumulation.

Sodium nitroprusside (SNP), as a single minuscule signaling molecule, has been employed to alleviate plant stress in recent years. This approach has a beneficial effect on the biological and physiological processes of plants. As a result, an in vitro tissue culture experiment was carried out to investigate the effect of high and low levels of SNP on the amelioration of manganese (Mn) and chromium (Cr) toxicity in a one-year-old bamboo plant, namely Pleioblastus pygmaea L. Five different concentrations of SNP were utilized as a nitric oxide (NO) donor (0, 50, 80, 150, 250, and 400 µM) in four replications of 150 µM Mn and 150 µM Cr. The results revealed that while 150 µM Mn and 150 µM Cr induced an over-generation of reactive oxygen species (ROS) compounds, enhancing plant membrane injury, electrolyte leakage (EL), and oxidation in bamboo species, the varying levels of SNP significantly increased antioxidant and non-antioxidant activities, proline (Pro), glutathione (GSH), and glycine betaine (GB) content, photosynthesis, and plant growth parameters, while also reducing heavy metal accumulation and translocation in the shoot and stem. This resulted in an increase in the plant's tolerance to Mn and Cr toxicity. Hence, it is inferred that NO-induced mechanisms boosted plant resistance to toxicity by increasing antioxidant capacity, inhibiting heavy metal accumulation in the aerial part of the plant, restricting heavy metal translocation from root to leaves, and enhancing the relative water content of leaves.

Protective effect of manganese treatment on insulin resistance in HepG2 hepatocytes.

manganese (Mn) is closely related to type 2 diabetes mellitus and insulin resistance (IR), but the exact mechanism is unclear. This study aimed to explore the regulatory effects and mechanism of Mn on IR using hepatocyte IR model induced by high palmitate (PA), high glucose (HG) or insulin. HepG2 cells were exposed to PA (200 μM), HG (25 mM) or insulin (100 nM) respectively, alone or with 5 μM Mn for 24 hours. The expression of key proteins in insulin signaling pathway, intracellular glycogen content and glucose accumulation, reactive oxygen species (ROS) level and Mn superoxide dismutase (MnSOD) activity were detected. compared with control group, the expression of phosphorylated protein kinase B (Akt), glycogen synthase kinase-3β (GSK-3β) and forkhead box O1 (FOXO1) in the three IR groups was declined, and this decrease was reversed by Mn. The reduction of intracellular glycogen content and increase in glucose accumulation in IR groups were also inhibited by Mn. Additionally, the production of ROS was increased in IR models, compared with normal control group, while Mn reduced the excessive production of ROS induced by PA, HG or insulin. However, Mn did not alter the activity of MnSOD in the three IR models. this study demonstrated that Mn treatment can improve IR in hepatocytes. The mechanism is probably by reducing the level of intracellular oxidative stress, enhancing the activity of Akt/GSK-3β/FOXO1 signal pathway, promoting glycogen synthesis, and inhibiting gluconeogenesis.

Manganese-induced PINK1 S-nitrosylation exacerbates nerve cell damage by promoting ZNF746 repression of mitochondrial biogenesis

Occupational exposure and non-occupational exposure to excessive levels of manganese (Mn) result in neuronal cell damage through mitochondrial dysfunction. The functional integrity of mitochondria is maintained by mitophagy and mitochondrial biogenesis. Although Mn-induced S-nitrosylation of PTEN-induced putative kinase 1 (PINK1) can interfere with mitophagy, its effect on mitochondrial biogenesis remains unclear. In this study, we established a rat model of Mn poisoning or “manganism” to examine the relationship between PINK1 S-nitrosylation and impairment of mitochondrial biogenesis, and found that treatment with 60 mg/kg Mn induced marked neurobehavioral abnormalities in rats and significantly increased the S-nitrosylation level of PINK1. We also found that the nuclear-encoded peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PPARGC1A)-mediated mitochondrial biogenesis was significantly upregulated in rats treated with 15 and 30 mg/kg Mn, and downregulated in rats treated with 60 mg/kg Mn. We further investigated the role of S-nitrosylated PINK1 and its molecular mechanism in the high-dose Mn-mediated impairment of mitochondrial biogenesis in primary cultured neurons treated with the nitric oxide synthase 2 (NOS2) inhibitor 1400 W. Our results revealed that the PPARGC1A-mediated mitochondrial biogenesis was upregulated in neurons treated with 100 μM, but downregulated in neurons treated with 200 μM Mn, which was similar to the in vivo results. However, treatment with 1400W could effectively prevent the 200 μM Mn-mediated impairment of mitochondrial biogenesis by suppressing nitric oxide (NO)-mediated PINK1 S-nitrosylation and rescuing Parkin-interacting substrate (PARIS, ZNF746) degradation, thereby upregulating mitochondrial biogenesis via PPARGC1A. These findings demonstrated that S-nitrosylation of PINK1 and subsequent prevention of ZNF746 degradation were crucial signaling processes involved in the Mn-mediated impairment of mitochondrial biogenesis, which might serve as an underlying mechanism of Mn-induced neurotoxicity. Furthermore, this study provided a reliable target for the prevention and treatment of manganism.