Manganese Toxicity Research Articles

Changes in the Microbiome of Sugarcane (Saccharum spp. Hybrids.) Rhizosphere in Response to Manganese Toxicity.

Manganese toxicity has limited sugarcane (Saccharum spp. hybrid.) growth and production in acidic soils in south China. The rhizosphere plays an irreplaceable role in plant adaptation to soil abiotic stress, but the responses of the sugarcane rhizosphere to manganese toxicity are still unknown. We designed pot experiments in Mn-rich acidic soil, collected the sugarcane rhizosphere and bulk soil samples, and then investigated the changes in Mn-related soil parameters and microbiome. The results indicated that the water-soluble and exchangeable manganese concentrations in the sugarcane rhizosphere were significantly lower than that in the bulk soil, which was not associated with soil pH changes. In contrast, the number of bacteria and the activity of peroxidase, sucrase, urease, and laccase in the rhizosphere were significantly higher. The 16S rDNA sequencing results showed that the bacterial diversity and quantity along with the abundance of Proteobacteria in the rhizosphere were significantly higher than in the bulk soil, while the abundance of Acidobacteria was lower than in the bulk soil. The soil laccase activity and the number of bacteria decreased significantly with the increase in the manganese toxicity stress. Finally, the relative abundance of proteins associated with manganese transportation and oxidation was significantly higher in the rhizosphere soil. In summary, the Mn-induced response of the rhizosphere is an important mechanism in sugarcane adaptation to manganese toxicity in acidic soil.

Assessment of Acidic Soil Nutrient Stoichiometry on Molybdenum Fertilization for Sustainable Crop Production

Background: Molybdenum (Mo), an essential micronutrient, is known to have a profound influence on various biochemical and physiological processes in plants. A variety of factors, including soil pH, organic matter content, and the abundance of particular minerals that interact with nutrient dynamics, affect the availability of essential nutrients in the soil. Acidic soil conditions frequently cause lower nutrient availability as a result of influencing factors like increased manganese and aluminium toxicity as well as lesser microbial activity. Soil acidification can impact agricultural productivity. For the creation of efficient and long-lasting soil management techniques that can ease nutrient constraints and boost agricultural productivity, it is essential to comprehend the impact of molybdenum on the dynamics of soil macronutrients and micronutrients in acid soils. Methods: A 60 days incubation experiment was carried out under laboratory conditions to study the effect of molybdenum fertilization on the release pattern of molybdenum and other nutrients from the soil. Soil samples were filled in jars, and treatments were imposed. Samples were collected at 15, 30, 45, and 60 days of incubation, dried, and processed for available nitrogen, phosphorus, and DTPA extractable micronutrients. Results: Molybdenum addition showed a significant influence on the release of various nutrients present in the soil. It was also observed that molybdenum has a synergistic effect on available nitrogen and phosphorus, while it exhibited antagonism towards DTPA extractable micronutrients, namely Zn, Fe, Mn, and Cu. Molybdenum fertilization holds great promise for enhancing the macronutrients' availability and reducing the toxicity of micronutrients in acid soils. It will be helpful for sustainable agricultural production under acidic soil.

The Role of Oxidative Stress in Manganese Neurotoxicity: A Literature Review Focused on Contributions Made by Professor Michael Aschner.

This literature review focuses on the evidence implicating oxidative stress in the pathogenesis of manganese neurotoxicity. This review is not intended to be a systematic review of the relevant toxicologic literature. Instead, in keeping with the spirit of this special journal issue, this review highlights contributions made by Professor Michael Aschner's laboratory in this field of study. Over the past two decades, his laboratory has made significant contributions to our scientific understanding of cellular responses that occur both in vitro and in vivo following manganese exposure. These studies have identified molecular targets of manganese toxicity and their respective roles in mitochondrial dysfunction, inflammation, and cytotoxicity. Other studies have focused on the critical role astrocytes play in manganese neurotoxicity. Recent studies from his laboratory have used C. elegans to discover new facets of manganese-induced neurotoxicity. Collectively, his body of work has dramatically advanced the field and presents broader implications beyond metal toxicology.

Effects of Manganese and Iron, Alone or in Combination, on Apoptosis in BV2 Cells.

The aim of study was to address the effects of manganese and iron, alone and in combination, on apoptosis of BV2 microglia cells, and to determine if combined exposure to these metals augments their individual toxicity. We used a murine microglial BV2 cell line. Cell cytotoxicity was analyzed by propidium iodide (PI) exclusion assay. Cell ROS production was analyzed by 2', 7'-dichlorofluorescin diacetate (DCFH-DA) probe staining. Pro-inflammatory cytokine production was monitored by ELISA. Cell apoptosis was analyzed by PE Annexin V/7-AAD staining. Mitochondrial membrane integrity was analyzed by flow cytometry. We used immunoblotting to analyze the effect of manganese, iron alone, or their combined exposure on the activation of caspase9, P53, Bax, and Bcl2 apoptosis signaling pathways. Caspase3 activity was determined using a Colorimetric. Manganese, iron, and their combined exposure for 24h induced the activation of BV2 microglia cells and increased ROS production and the expression of the inflammatory cytokines, IL-1β and TNF-α. And we also found that the apoptosis rate increased, mitochondrial membrane potential decreased, apoptosis-related proteins caspase9, P53, Bax, and Bcl2 expression increased, and caspase3 activity increased. Furthermore, we found that combined manganese-iron cytotoxicity was lower than that induced by manganese exposure alone. Manganese, iron alone, or their combination exposure can induce apoptosis in glial cells. Iron can reduce the toxicity of manganese, and there is an antagonistic effect between manganese and iron.

Acute and chronic toxicity of manganese to tropical adult coral (Acropora millepora) to support the derivation of marine manganese water quality guideline values

Adult corals are among the most sensitive marine organisms to dissolved manganese and experience tissue sloughing without bleaching (i.e., no loss of Symbiodinium spp.) but there are no chronic toxicity data for this sensitive endpoint. We exposed adult Acropora millepora to manganese in 2-d acute and 14-d chronic experiments using tissue sloughing as the toxicity endpoint. The acute tissue sloughing median effect concentration (EC50) was 2560 μg Mn/L. There was no chronic toxicity to A. millepora at concentrations up to and including the highest concentration of 1090 μg Mn/L i.e., the chronic no observed effect concentration (NOEC). A coral-specific acute-to-chronic ratio (ACR) (EC50/NOEC) of 2.3 was derived. These data were combined with chronic toxicity data for other marine organisms in a species sensitivity distribution (SSD). Marine manganese guidelines were 190, 300, 390 and 570 μg Mn/L to provide long-term protection of 99, 95, 90, and 80 % of marine species, respectively.

Manganese Exposure Induces Cellular Aggregates and the Accumulation of β-Catenin in Skin of Zebrafish Embryos.

The effects of manganese (Mn) toxicity in different organs and tissues in humans and other vertebrates have been studied since the beginning of the past century, but most of its cellular effects remain largely unknown. In this study, we studied the effects of Mn in zebrafish, at the cellular level, due to the transparent nature of zebrafish larvae that enables a powerful analysis under the light microscope. The collection of our results shows that environmental concentrations of 0.5 mg/L affect swim bladder inflation; at concentration of 50 and 100 mg/L Mn (1) induces alterations in viability, swim bladder, heart, and size of zebrafish larvae, (2) induces an increase in melanocyte area and the formation of cellular aggregates in the skin, and (3) induces an accumulation of β-Catenin in mesenchymal cells in the caudal fin of zebrafish larvae. Our data suggest that increased levels of Mn induce cell aggregate formation in the skin and the presence of more melanocytes in the zebrafish caudal fin. Interestingly, the adhesion protein β-Catenin was activated in mesenchymal cells near the cell aggregates. These results open important new questions on the role of Mn toxicity on cellular organization and β-Catenin responses in fishes.

Physiological Mechanisms in Which Manganese Toxicity Inhibits Root Growth in Soybean

Physiological Mechanisms in Which Manganese Toxicity Inhibits Root Growth in Soybean

CBL1/9-CIPK23-NRAMP1 axis regulates manganese toxicity.

Manganese (Mn) is an essential micronutrient in plants. However, excessive Mn absorption in acidic soils can cause Mn toxicity, which adversely affects plant growth and crop yields. At present, acidic soils cover c. 30% of the Earth's surface. However, the mechanism underpinning Mn uptake remains largely unknown. We identified cbl1/9 and cipk23 mutants exhibiting high-Mn-sensitive phenotype through the reverse genetics method. Furthermore, we identified the CIPK23 phosphorylated NRAMP1 through a variety of protein interaction techniques and protein kinase assays. Here, we demonstrated that two calcineurin B-like proteins, CBL1/9, and their interacting kinase CIPK23 positively regulated the tolerance of Mn toxicity in Arabidopsis. The cbl1 cbl9 double mutant and cipk23 mutants exhibited high-Mn-sensitive phenotypes, which manifested as decreased primary root length, biomass, and chlorophyll concentration, and higher accumulation of Mn. In addition, CIPK23 interacted with and phosphorylated the Mn transporter NRAMP1 primarily at Ser20/22 invitro and invivo, and thereby induced clathrin-mediated endocytosis of NRAMP1 to reduce its distribution on the plasma membrane and enhance plant tolerance to Mn toxicity. In summary, we found that the CBL1/9-CIPK23-NRAMP1 module regulates the tolerance to high-Mn toxicity and provide insight into a mechanism of the tolerance of plants to Mn toxicity.

Adult corals are uniquely more sensitive to manganese than coral early-life stages.

Manganese is an essential element and generally considered to be one of the least toxic metals to aquatic organisms, with chronic effects rarely seen at concentrations below 1000 µg/L. Anthropogenic activities lead to elevated concentrations of manganese in tropical marine waters. Limited data suggests that manganese is more acutely toxic to adult than to early life-stages of scleractinian corals in static renewal tests. However, to enable the inclusion of sufficient sensitive coral data in species sensitivity distributions to derive water quality guideline values (GVs) for manganese, we determined the acute toxicity of manganese to the adult scleractinian coral, Acropora muricata, in flow-through exposures. The 48-h EC50 was 824 µg Mn/L (based on time-weighted average, measured, dissolved manganese). The endpoint was tissue sloughing, a lethal process by which coral tissue detaches from the coral skeleton. Tissue sloughing was unrelated to superoxidase dismutase activity in coral tissue, and occurred in the absence of bleaching, i.e., toxic effects were observed for the coral host, but not for algal symbionts. We confirm that adult scleractinian corals are uniquely sensitive to manganese in acute exposures at concentrations 10 to 340 times lower than those reported to cause acute or chronic toxicity to coral early life stages, challenging the traditional notion that early life stages are more sensitive than mature organisms. This article is protected by copyright. All rights reserved. Environ Toxicol Chem 2023;00:0-0. © 2023 SETAC.

Parkinsonism in a Zambian Man with an unusual occupational exposure (P3-4.002)

<h3>Objective:</h3> Describe a case of Manganism encountered in Zambia. <h3>Background:</h3> Manganism is a neurodegenerative syndrome due to manganese toxicity and its excessive accumulation in the brain. <h3>Design/Methods:</h3> Case presentation <h3>Results:</h3> A 37-year-old man presented with a four-month history of mild, intermittent headache and three-month history of chest pain, dry cough and symmetrical distal-predominant paresthesias. He developed progressive cognitive decline associated with slowness in talking, low volume speech and difficulty completing activities of daily living two months prior to presentation. He reported fever and night sweats. Past medical history was unremarkable. Social history only notable for working as a manganese smelter for the past eight years. Neurological exam revealed memory and language deficits with psychomotor slowing, subtle left upper motor neuron facial weakness, hypomimia, bradykinesia and had a hyperkinetic tongue and upper limb tremor with normal tone and power in all limbs. Deep tendon reflexes were normal, but frontal release signs and an applause sign were present. Small and large fiber length-dependent sensory loss was noted with a cock-walk gait. MRI brain with gadolinium showed non-enhancing symmetric T1 hyperintensities in the globus pallidum and midbrain with corresponding T2 hypointensities in the same areas. <h3>Conclusions:</h3> A diagnosis of Manganism was made based on clinical history, strong occupational exposures, and neurological examination and imaging findings. Blood manganese levels and other heavy metals could not be obtained due to unavailability of tests in our setting, although blood manganese levels are often normal when obtained in cases of Manganism. The cough, headache, chest pain and fever were ascribed to metal fume fever and improved after a three-month withdrawal of manganese exposure, though neurologic symptoms did not improve during this period. This case demonstrates the importance of thorough history (including social history), examination, and correlation with limited investigations in diagnosing even rare diseases in resource-limited settings. <b>Disclosure:</b> Dr. Munkombwe has nothing to disclose. Dr. Asukile has nothing to disclose. Dr. Schwab has nothing to disclose. The institution of Dr. Saylor has received research support from National Institutes of Health. The institution of Dr. Saylor has received research support from National Multiple Sclerosis Society. The institution of Dr. Saylor has received research support from American Academy of Neurology. The institution of Dr. Saylor has received research support from United States Department of State. Dr. Saylor has a non-compensated relationship as a Member of multiple committees and task forces focused on improving access to MS medications to people across the world with Multiple Sclerosis International Federation that is relevant to AAN interests or activities. Dr. Saylor has a non-compensated relationship as a Member of the Neurology and COVID19 committee with World Health Organization that is relevant to AAN interests or activities. Dr. Saylor has a non-compensated relationship as a Member of the International Outreach Committee, Junior and Early Career Membership Committee, and Educational Innovation Commitees with American Neurological Association that is relevant to AAN interests or activities.

Fertirrigation with nanofiltration retentate from thermomechanical pulp mill effluents

The objective of the present study was to evaluate the potential for using the retentate from nanofiltration (NF) treatment of thermomechanical pulp (TMP) effluent for fertirrigation. Nanofiltration retentates from tertiary effluent treatment from a Brazilian TMP pulp mill were used. Electrical conductivity (EC) and the concentration of both metals (Mn2+, Mg2+, Fe2+, Ca2+, Na+, K+, Cu2+) and chlorides in the NF retentate were evaluated. The sodium (SAR) and potassium (PAR) adsorption ratios were calculated. The risks of increasing the salinity, effects on the infiltration rate, toxicity and excess nutrients were evaluated according to the American and European standards, and application according to crop and soil were analyzed according to the Brazilian standard. The NF retentate is classified as irrigation water Class I for the risks of reduced water infiltration into the soil, availability of nutrients and the concentration of copper and iron, Class II for the risks of toxicity, pH and concentration of manganese and Class III for the risks of salinity and concentrations of TS, TSS and turbidity, according to American and European standards. The salinity content and the physicochemical characteristics classify the effluent NF retentate, according to the Brazilian standard, as fresh water and Class III for irrigation. The NF retentate from thermomechanical pulp mill effluents, according to both the American and the European standards, cannot be used for fertirrigation, as it is classified as Class III. However, the Brazilian standard allows its use for the irrigation of any tree species, cereals and forages and as a source of nutrients to reduce fertilizer use. The retentate can be applied to highly salt-tolerant plant crops such as Eucalyptus globulus, Eucalyptus camaldulensis and sugarcane, and may be used in soil with a basic pH and high permeability.

Manganese toxicity and stress-induced tolerance responses in Psidium cattleianum and Eugenia involucrata

Manganese toxicity and stress-induced tolerance responses in Psidium cattleianum and Eugenia involucrata

African walnut (Tetracarpidium conophorum) extract upregulates glucocerebrosidase activity and circumvents Parkinsonian changes in the Hippocampus via the activation of heatshock proteins

BackgroundNeurodegenerative illnesses like Parkinson's and Alzheimer's are largely caused by the accumulation of aggregated proteins. Heat shock proteins (HSPs), which are molecular chaperons, have been linked with the modulation of β-glucocerebrosidase (GCase) function encoded by GBA1 and Synucleinopathies. Herein, the chaperonic properties of African walnut ethanolic extract (WNE) in manganese-induced Parkinsonian neuropathology in the hippocampus was examined. Methodology48 adult male rats weighing 185 g ± 10 g were randomly assigned into 6 (A – F) groups (n = 8) and treated orally as follows: A-PBS (1 ml daily for 28 days), B-WNE (200 mg/kg daily for 28 days), C- WNE (400 mg/kg daily for 28 days), D-Mn (100 mg/kg daily for 28 days), E-Mn plus WNE (100 mg/kg Mn + 200 mg/kg WNE daily concomitantly for 28 days), F-Mn plus WNE (100 mg/kg Mn + 400 mg/kg WNE daily concomitantly for 28 days). ResultsRats treated with WNE showed increased levels of HSP70 and HSP90 in comparison with the Mn-intoxicated group. GCase activity also increased significantly in animals treated with WNE. Our results further revealed the therapeutic tendencies of WNE against Mn toxicity by modulating oligomeric α-synuclein levels, redox activity, and glucose bioenergetics. Furthermore, immunohistochemical evaluation revealed reduced expression of neurofibrillary tangles, and reactive astrogliosis following WNE treatment. ConclusionThe ethanolic extract of African Walnut induced the activation of HSPs and increased the expression of GBA1 gene in the hippocampus. Activated heat shock proteins suppressed neurodegenerative changes due to Manganese toxicity. WNE was also shown to modulate neuroinflammatory, bioenergetics and neural redox balance in Parkinson-like neuropathology. This study was limited to the use of crude walnut extract and the evaluation of non-motor cascades of Parkinson’s disease.

Possible Involvement of Cellular Pathway and Cytokines in Manganese Induced Neurotoxicity in Neuroblastoma Cells via KH–Type Splicing Regulatory Protein

Pharmacognosy Research,2023,15,2,307-314.DOI:10.5530/pres.15.2.033Published:February 2023Type:Original Article Authors:Sharad Singh, Sunil More, G. S. Latha, Himanshu Agrawal, Veena S M, and Francois Niyonzima Author(s) affiliations:Sharad Singh1, Sunil More1,*, G. S. Latha2, Himanshu Agrawal3, Veena S M4, Francois Niyonzima5 1School of Basic and Applied Sciences, Dayananada Sagar University, Bangalore, Karnataka, INDIA. 2Department of Physiology, Rajarajeswari Medical College and Hospital, Bengaluru, Karnataka, A Constituent College under Dr. M.G.R. Educational and Research Institute, Chennai, Tamil Nadu, INDIA. 3Jubilant Biosys Limited, Bangalore, Karnataka, INDIA. 4Department of Biotechnology, Sapthagiri College of Engineering, Bengaluru, Karnataka, INDIA. 5Department of Mathematics, Sciences and Physical Education, University of Rwanda-College of Education (UR-CE), Kayonza Rukara Campus, RWANDA. Abstract:Background: Manganese is a toxic essential trace element and too high concentration instigates the neurodegenerative disease known as parkinsonism. Effects of manganese may lead to apoptosis. However, a detailed mechanism of manganese toxicity has not been fully elucidated. Previous published articles have highlighted the augmentation of KHSRP expression following Mn exposure. Objectives: In this work, the importance of KHSRP in Mn–induced toxicity was checked along with the impact of other known neurotoxicity inhibitors on KHSRP. Materials and Methods: KHSRP expression, pro and anti-inflammatory cytokines, chemokines, and pharmacological inhibitors (SAHA, Quercetin, and MCC950) were determined by exposing N2a cells to various MnCl2 concentrations. ANOVA and Dunnett’s test were used to decide on the significance. Results: MnCl2 treatment led to the augmentation of the KHSPR mRNA expression and protein increase in N2a cell line. The MnCl2 treatment of N2a cells also showed an elevated liberation of IL-6, TNF-α, MCP–1, and IL-1β. Pharmacological agents like quercetin inhibiting PI3K, MAPK, and WNT pathways, MCC950 blocking NLRP3 pathways, and SAHA showed a decrease in KHSRP expression post Mn treatment. With the inhibition of KHSRP, a decline in the release of IL-1β, IL-6, MCP–1, and TNF-α was also observed. Conclusion: These results suggested that MnCl2 treatment of N2a cells induce the expression of KHSRP via the PI3K–or NLRP3 pathway. Furthermore, this elevated expression of KHSRP is responsible for an increment in the liberation of pro-inflammatory markers in N2a cells. More exploration is needed to throw light on the pathway driving the KHSRP. Keywords:KH–type Splicing Regulatory Protein, Manganese Neurotoxicity, Neuroblastoma, Neurodegeneration, Neuroinflammation.View:PDF (1.26 MB)

Cellular Pathogenesis of Hepatic Encephalopathy: An Update.

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome derived from metabolic disorders due to various liver failures. Clinically, HE is characterized by hyperammonemia, EEG abnormalities, and different degrees of disturbance in sensory, motor, and cognitive functions. The molecular mechanism of HE has not been fully elucidated, although it is generally accepted that HE occurs under the influence of miscellaneous factors, especially the synergistic effect of toxin accumulation and severe metabolism disturbance. This review summarizes the recently discovered cellular mechanisms involved in the pathogenesis of HE. Among the existing hypotheses, ammonia poisoning and the subsequent oxidative/nitrosative stress remain the mainstream theories, and reducing blood ammonia is thus the main strategy for the treatment of HE. Other pathological mechanisms mainly include manganese toxicity, autophagy inhibition, mitochondrial damage, inflammation, and senescence, proposing new avenues for future therapeutic interventions.

Effect of exogenous taurine on pea (Pisum sativum L.) plants under salinity and iron deficiency stress

Soil salinity and Fe deficiency affect plant growth and survival by changing nutrient availability and disrupting water balance. Natural and human activities, such as evaporation and deforestation, can intensify these soil conditions. Taurine, a novel growth regulator, holds promise in mediating plant defense responses. Its effects on defense responses are still unclear. Previously, taurine showed potential in improving clover tolerance to alkaline stress and manganese toxicity. Taurine impact on plant growth under Fe deficiency and salinity stress remains uninvestigated. A pot experiment was conducted to evaluate the effects of taurine on pea plant growth, ion uptake, and defense strategies in response to salt stress and Fe deficiency. Iron deficiency was established by substituting 0.1 mM FeSO4 for 0.1 mM Fe-EDTA in the nutrient solution. Salinity stress was induced by incorporating a mixture of NaCl, MgCl2, KCl, Na2SO4, Na2CO3, NaHCO3 and CaCl2 in a 1:1:1:1:1:1:1 ratio to produce a salinity concentration of 100 mM. The simultaneous imposition of salinity and Fe deficiency significantly exacerbated oxidative stress, as evidenced by elevated levels of relative membrane permeability, hydrogen peroxide (H2O2), superoxide radical (O2•−), methylglyoxal (MG), malondialdehyde (MDA), and increased activity of lipoxygenase (LOX). Salinity stress alone and the combination of salinity and Fe deficiency resulted in substantial accumulation of Na+ ions that impeded acquisition of essential nutrients. Taurine (100 and 200 mg L−1) notably improved osmotic adjustment and oxidative defense to diminish water imbalance and oxidative injury in plants under stress. These results suggest that exogenous taurine may serve as a promising means of mitigating the detrimental effects of salt stress and Fe deficiency in plants.

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.

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.

Interaction Mechanism of Fe, Mg and Mn in Karst Soil-Mango System

Manganese (Mn), an essential trace element for plants in which it is involved in redox reactions as a cofactor for many enzymes, represents an important factor in environmental contamination. Excess Mn can lead to toxicity conditions in natural and agricultural sites. Manganese toxicity is one of the most severe growth limiting factors in acid soil, which accounts for 21% of the total arable lands in China. The more significant part of Mn-toxicity is its interactions with other mineral elements, in particular with phosphorus (P), calcium (Ca) and iron (Fe). The application of P or Ca can be beneficial in the detoxification of manganese, whereas Mn seems to interfere with Fe metabolism. Manganese toxicity varies with plant species, nutrients, and the soil environment. Mango is the main economic fruit in the karst area of the subtropical region of China. The karst soil in the mango orchard is characterized by high Fe, Mn and Mg. In order to explore the interaction among Fe, Mg, and Mn in karst soil and mango systems under high Mn conditions, a typical mango orchard in the karst depression landform in Baise in southern China was selected to study the effects of Fe and Mg on the toxic expression of Mn in mango plants and the interaction mechanism of Fe-Mn-Mg in mango plants. The results show that: (1) the mango growth status is closely correlated with Fe2+ (active iron) and Mg under the same soil Mn concentration; (2) The black spots on mango leaves were mainly caused by Fe and Mn. There is a lot of Fe3+ and Mn3+ in the black spots, which accounts for more than 90% of the total; (3) In addition, the studies also showed that the Fe and Mg inhibited the expression of Mn toxicity in mango. Conclusively, the interaction effect of Fe, Mn, and Mg is an important factor that affects mango growth, which can indicate the status of the soil and plants.

Comparative Transcriptome Analysis Reveals Complex Physiological Response and Gene Regulation in Peanut Roots and Leaves under Manganese Toxicity Stress

Excess Manganese (Mn) is toxic to plants and reduces crop production. Although physiological and molecular pathways may drive plant responses to Mn toxicity, few studies have evaluated Mn tolerance capacity in roots and leaves. As a result, the processes behind Mn tolerance in various plant tissue or organ are unclear. The reactivity of peanut (Arachis hypogaea) to Mn toxicity stress was examined in this study. Mn oxidation spots developed on peanut leaves, and the root growth was inhibited under Mn toxicity stress. The physiological results revealed that under Mn toxicity stress, the activities of antioxidases and the content of proline in roots and leaves were greatly elevated, whereas the content of soluble protein decreased. In addition, manganese and iron ion content in roots and leaves increased significantly, but magnesium ion content decreased drastically. The differentially expressed genes (DEGs) in peanut roots and leaves in response to Mn toxicity were subsequently identified using genome-wide transcriptome analysis. Transcriptomic profiling results showed that 731 and 4589 DEGs were discovered individually in roots and leaves, respectively. Furthermore, only 310 DEGs were frequently adjusted and controlled in peanut roots and leaves, indicating peanut roots and leaves exhibited various toxicity responses to Mn. The results of qRT-PCR suggested that the gene expression of many DEGs in roots and leaves was inconsistent, indicating a more complex regulation of DEGs. Therefore, different regulatory mechanisms are present in peanut roots and leaves in response to Mn toxicity stress. The findings of this study can serve as a starting point for further research into the molecular mechanism of important functional genes in peanut roots and leaves that regulate peanut tolerance to Mn poisoning.