Low toxicity of magnetite-based modified bionanocomposites with potential application for wastewater treatment: Evaluation in a zebrafish animal model.

In recent years, the escalating concerns surrounding environmental pollution and the need for sustainable wastewater treatment solutions have underscored the significance of developing technologies that can efficiently treat wastewater while also reducing negative ecological effects. In this context, our study aims to contribute to the advancement of sustainable technologies for wastewater treatment, by investigating the effects that bare magnetite nanoparticles and those functionalized with the enzyme laccase could have in an aquatic animal, zebrafish, at various life cycle stages. Exposure to magnetite nanoparticles shows some effects on embryo hatching, survival rates, or larval behavior at higher concentrations. For both treatments, the hatching percentages were close to 80% compared to 93% for the control group. At the end of the observations in larvae, survival in all the evaluated groups was higher than 90%. Additionally, we evaluated the accumulation of nanoparticles in various stages of zebrafish. We found that, although there was accumulation during embryonic stages, it did not affect normal development or subsequent hatching. Iron levels in different organs such as gills, muscles, gastrointestinal tract, and brain were also evaluated in adults. Animals treated with a mix of food and nanoparticles at 10 µg/mL (Food group) presented a higher concentration of iron accumulation in muscle, gastrointestinal tract, and gills compared to the untreated control group. Although iron levels increased depending on the dose and exposure method applied, they were not statistically significant from the control groups. Our findings suggest that bionanocomposites evaluated here can be considered safe for removal of contaminants in wastewater without toxic effects or detrimental accumulation fish's health.

Effects of environmental exposure to iron powder on healthy and elastase-exposed mice.

Prolonged exposure to iron powder and other mineral dusts can threaten the health of individuals, especially those with COPD. The goal of this study was to determine how environmental exposure to metal dust from two different mining centers in Brazil affects lung mechanics, inflammation, remodeling and oxidative stress responses in healthy and elastase-exposed mice. This study divided 72 male C57Bl/6 mice into two groups, the summer group and the winter group. These groups were further divided into six groups: control, nonexposed (SAL); nonexposed, given elastase (ELA); exposed to metal powder at a mining company (SAL-L1 and ELA-L1); and exposed to a location three miles away from the mining company (SAL-L2 and ELA-L2) for four weeks. On the 29th day of the protocol, the researchers assessed lung mechanics, bronchoalveolar lavage fluid (BALF), inflammation, remodeling, oxidative stress, macrophage iron and alveolar wall alterations (mean linear intercept-Lm). The Lm was increased in the ELA, ELA-L1 and ELA-L2 groups compared to the SAL group (p < 0.05). There was an increase in the total number of cells and macrophages in the ELA-L1 and ELA-L2 groups compared to the other groups (p < 0.05). Compared to the ELA and SAL groups, the exposed groups (ELA-L1, ELA-L2, SAL-L1, and SAL-L2) exhibited increased expression of IL-1ß, IL-6, IL-10, IL-17, TNF-α, neutrophil elastase, TIMP-1, MMP-9, MMP-12, TGF-ß, collagen fibers, MUC5AC, iNOS, Gp91phox, NFkB and iron positive macrophages (p < 0.05). Although we did not find differences in lung mechanics across all groups, there were low to moderate correlations between inflammation remodeling, oxidative stress and NFkB with elastance, resistance of lung tissue and iron positive macrophages (p < 0.05). Environmental exposure to iron, confirmed by evaluation of iron in alveolar macrophages and in air, exacerbated inflammation, initiated remodeling, and induced oxidative stress responses in exposed mice with and without emphysema. Activation of the iNOS, Gp91phox and NFkB pathways play a role in these changes.

Physiological and molecular mechanisms of plant-root responses to iron toxicity.

The chemical form and physiological activity of iron (Fe) in soil are dependent on soil pH and redox potential (Eh), and Fe levels in soils are frequently elevated to the point of causing Fe toxicity in plants, with inhibition of normal physiological activities and of growth and development. In this review, we describe how iron toxicity triggers important physiological changes, including nitric-oxide (NO)-mediated potassium (K+) efflux at the tips of roots and accumulation of reactive oxygen species (ROS) and reactive nitrogen (RNS) in roots, resulting in physiological stress. We focus on the root system, as the first point of contact with Fe in soil, and describe the key processes engaged in Fe transport, distribution, binding, and other mechanisms that are drawn upon to defend against high-Fe stress. We describe the root-system regulation of key physiological processes and of morphological development through signaling substances such as ethylene, auxin, reactive oxygen species, and nitric oxide, and discuss gene-expression responses under high Fe. We especially focus on studies on the physiological and molecular mechanisms in rice and Arabidopsis under high Fe, hoping to provide a valuable theoretical basis for improving the ability of crop roots to adapt to soil Fe toxicity.

Difference in the Mechanism of Iron Overload-Enhanced Acute Hepatotoxicity Induced by Thioacetamide and Carbon Tetrachloride in Rats.

Iron overload has been recognized as a risk factor for liver disease; however, little is known about its pathological role in the modification of liver injury. The purpose of this study is to investigate the influence of iron overload on liver injury induced by two hepatotoxicants with different pathogenesis in rats. Rats were fed a control (Cont), 0.8% high-iron (0.8% Fe), or 1% high-iron diet (1% Fe) for 4 weeks and were then administered with saline, thioacetamide (TAA), or carbon tetrachloride (CCl4). Hepatic and systemic iron overload were seen in the 0.8% and 1% Fe groups. Twenty-four hours after administration, hepatocellular necrosis induced by TAA and hepatocellular necrosis, degeneration, and vacuolation induced by CCl4, as well as serum transaminase values, were exacerbated in the 0.8% and 1% Fe groups compared to the Cont group. On the other hand, microvesicular vacuolation induced by CCl4 was decreased in 0.8% and 1% Fe groups. Hepatocellular DNA damage was increased by iron overload in both models, whereas a synergistic effect of oxidative stress by excess iron and hepatotoxicant was only present in the CCl4 model. The data showed that dietary iron overload exacerbates TAA- and CCl4-induced acute liver injury with different mechanisms.

C5b-9 promotes ferritinophagy leading to ferroptosis in renal tubular epithelial cells of trichloroethylene-sensitized mice.

Trichloroethylene (TCE) is a common environmental contaminant that can cause a severe allergic reaction called TCE hypersensitivity syndrome, which often implicates the patient's kidneys. Our previous study revealed that C5b-9-induced tubular ferroptosis is involved in TCE-caused kidney damage. However, the study did not explain how tubule-specific C5b-9 causes free iron overload, a key event in ferroptosis. Here, we aimed to explore the role of NCOA4-mediated ferritinophagy in C5b-9-induced iron overload and ferroptosis in TCE-sensitized mice. Our results showed that TCE sensitization does not affect iron import or export, but does affect iron storage, causing ferritin degradation and free iron overload. In addition, mitochondrial ROS was upregulated, and these changes were blocked by C5b-9 inhibition. Interestingly, TCE-induced ferritin degradation and ferroptosis were significantly antagonized by the application of the mitochondrial ROS inhibitor, Mito-TEMPO. Moreover, all of these modes of action were further verified in C5b-9-attack signalling HK-2 cells. Further investigation demonstrated that C5b-9-upregulated mitochondrial ROS induced a marked increase in nuclear receptor coactivator 4 (NCOA4), a master regulator of ferritinophagy. In addition, the application of NCOA4 small interfering RNA not only significantly reversed ferritinophagy caused by C5b-9 but also reduced C5b-9-induced ferroptosis in HK-2 cells. Taken together, these results suggest that tubule-specific C5b-9 deposition activates NCOA4 through the upregulation of mitochondrial ROS, causing ferritin degradation and elevated free iron, which ultimately leads to tubular epithelial cell ferroptosis and kidney injury in TCE-sensitized mice.

Surface reconstructed Fe@C1000 for enhanced Fenton-like catalysis: Sustainable ciprofloxacin degradation and toxicity reduction.

The Fe-based catalysts typically undergo severe problems such as deactivation and Fe sludge emission during the peroxymonosulfate (PMS) activation, which commonly leads to poor operation and secondary pollution. Herein, an S-doped Fe-based catalyst with a core-shell structure (Fe@CT, T = 1000°C) was synthesized, which can solve the above issues via the dynamic surface evolution during the reaction process. Specifically, the Fe0 on the surface of Fe@C1000 could be consumed rapidly, leaving numerous pores; the Fe3C from the core would subsequently migrate to the surface of Fe@C1000, replenishing the consumed active Fe species. The X-ray diffraction (XRD) and X-ray photoelectron spectroscopy (XPS) analyses demonstrated that the reaction surface reconstructed during the PMS activation, which involved the FeIII in-situ reduction by S species as well as the depletion/replenishment of effective Fe species. The reconstructed Fe@C1000 achieved near-zero Fe sludge emission (from 0.59 to 0.08-0.23 mg L-1) during 5 cycles and enabled the dynamic evolution of dominant reactive oxygen species (ROS) from SO4·- to FeIVO, sustainably improving the oxidation capacity (80.0-92.5% in following four cycles) to ciprofloxacin (CIP) and reducing the toxicity of its intermediates. Additionally, the reconstructed Fe@C1000/PMS system exhibited robust resistance to complex water matrix. This study provides a theoretical guideline for exploring surface reconstruction on catalytic activity and broadens the application of Fe-based catalysts in the contaminants elimination.

Physiological and transcriptomic analysis revealed the alleviating effect of 1,25(OH)2D3 on environmental iron overloading induced ferroptosis in zebrafish.

Iron overload in the aquatic environment can cause damage in fish bodies. Vitamin D3 (VD3) has been proven to have antioxidant and regulatory effects on iron transport. The current research investigated the effects of environmental iron overload on larval zebrafish and explored the effects of 1,25(OH)2D3 on ferroptosis in zebrafish larvae and zebrafish liver cells (ZFL) caused by iron overload in the environment and its possible regulatory mechanisms. The results showed that 1,25(OH)2D3 alleviated liver damage in zebrafish larvae and mitochondrial damage in ZFL after excessive ammonium ferric citrate (FAC) treatment, and improved the survival rate of ZFL. 1,25(OH)2D3 cleared and inhibited excessive FAC induced abnormal accumulation of ROS, lipid ROS, MDA, and Fe2+ in zebrafish larvae and ZFL, as well as enhanced the activity of antioxidant enzyme GPx4. Transcriptomic analysis showed that 1,25(OH)2D3 can regulate ferroptosis in ZFL by regulating signaling pathways related to oxidative stress, iron homeostasis, mitochondrial function, and ERS, mainly including ferroptosis, neoptosis, p53 signaling pathway, apoptosis, FoxO signaling pathway. Validation of transcriptome data showed that 1,25(OH)2D3 inhibits ferroptosis in zebrafish larvae and ZFL caused by excessive FAC via promoting the expression of slc40a1 and hmox1a genes and increasing SLC40A1 protein levels. In summary, 1,25(OH)2D3 can resist ferroptosis in zebrafish caused by iron overload in the environment mainly via regulating antioxidant capacity and iron ion transport.

Developmental iron exposure induces locomotor alterations in Drosophila: Exploring potential association with oxidative stress.

Prenatal iron (Fe) exposure has been associated with learning and cognitive impairments, which may be linked to oxidative stress resulting from elevated Fe levels and harm to the vulnerable brain. Drosophila melanogaster has contributed to our understanding of molecular mechanisms involved in neurological conditions. This study aims to explore Fe toxicity during D. melanogaster development, assessing oxidative stress and investigating behaviors in flies that are related to neurological conditions in humans. To achieve this goal, flies were exposed to Fe during the developmental period, and biochemical and behavioral analyses were conducted. The results indicated that 20 mM Fe decreased fly hatching by 50 %. At 15 mM, Fe exposure increased lipid peroxidation, and GSH levels decreased starting from 5 mM of Fe. Superoxide Dismutase activity was enhanced at 15 mM, while Glutathione S-Transferase activity was inhibited from 5 mM. Although chronic Fe exposure did not alter acetylcholinesterase (AChE) activity, flies exhibited reduced locomotion, increased grooming, and antisocial behavior from 5 mM of Fe. This research highlights potential Fe toxicity risks during development and underscores the utility of D. melanogaster in unraveling neurological disorders, emphasizing its relevance for future research.

Examining the effect of iron (ferric) on physiological processes: Invertebrate models.

Iron is a common and essential element for maintaining life in bacteria, plants and animals and is found in soil, fresh waters and marine waters; however, over exposure is toxic to organisms. Iron is used in electron transport complexes within mitochondria as well as a co-factor in many essential proteins. It is also established that iron accumulation in the central nervous system in mammals is associated with various neurological disorders. Ample studies have investigated the long-term effects of iron overload in the nervous system. However, its acute effects in nervous tissue and additional organ systems warrant further studies. This study investigates the effects of iron overload on development, behavior, survival, cardiac function, and glutamatergic synaptic transmission in the Drosophila melanogaster. Additionally, physiological responses in crayfish were examined following Fe3+ exposure. Fe3+ reduced neuronal excitability in proprioceptive neurons in a crayfish model. Thus, Fe3+ may block stretch activated channels (SACs) as well as voltage-gated Na+ channels. Exposure also rapidly reduces synaptic transmission but does not block ionotropic glutamatergic receptors, suggesting a blockage of pre-synaptic voltage-gated Ca2+ channels in both crustacean and Drosophila models. The effects are partly reversible with acute exposure, indicating the cells are not rapidly damaged. This study is relevant in demonstrating the effects of Fe3+ on various physiological functions in different organisms in order to further understand the acute and long-term consequences of overload.

Ferroptosis at the crossroads of manganese-induced neurotoxicity: A retrospective study.

Manganese is an essential trace element, but overexposure can cause neurotoxicity and subsequent neurodegenerative diseases. Ferroptosis is a form of cell death characterized by lipid peroxidation and iron overload inside cells, which is closely related to manganese neurotoxicity. Manganese can induce ferroptosis through multiple pathways: causing oxidative stress and increased cellular reactive oxygen species (ROS), resulting in lipid peroxidation; depleting glutathione (GSH) and weakening the antioxidant capacity of cells; disrupting iron metabolism and increasing iron-dependent lipid peroxidation; damaging mitochondrial function and disrupting the electron transport chain, leading to increased ROS production. Oxidative stress, iron metabolism disorders, lipid peroxidation, GSH depletion, and mitochondrial dysfunction, typical features of ferroptosis, have been observed in animal and cell models after manganese exposure. In summary, manganese can participate in the pathogenesis of neurodegenerative diseases by inducing events related to ferroptosis. This provides new insights into studying the mechanism of manganese neurotoxicity and developing therapeutic drugs.

Long-term pulmonary iron oxide nanoparticles exposure disrupts hepatic iron-lipid homeostasis and increases plaque vulnerability in ApoE-/- mice.

Iron oxide nanoparticles (Fe3O4 NPs) have attracted great attention due to their extensive applications, which warranted their environmental concerns. Although recent advances have proposed the relevance of Fe3O4 NPs to cardiovascular disease, the intrinsic mechanisms underlying the effects of NPs remain indistinct. ApoE-/- mice were chosen as a long-term exposure model to explore the immanent association between respiratory exposure to Fe3O4 NPs and the development of cardiovascular diseases. Pulmonary exposure to 20 nm and 200 nm Fe3O4 NPS resulted in significant lung injury, and pulmonary histopathological examination displayed inflammatory cell infiltration, septal thickening and alveolar congestion. Intriguingly, liver iron deposition and variations in the hepatic lipid homeostasis were found in Fe3O4 NPs-exposed mice, eventually leading to dyslipidemia, hinting the potential cardiovascular toxicity of Fe3O4 NPs. In addition, we not only found that Fe3O4 NPs exposure increased aortic plaque area, but also increased M1 macrophages in the plaque, which yielding plaque vulnerability in ApoE-/- mice Of note, 20 nm Fe3O4 NPs showed enhanced capability on the progression of atherosclerosis than 200 nm Fe3O4 NPs. This study may propose the potential mechanism for adverse cardiovascular disease induced by Fe3O4 NPs and provide convincing evidence for the safety evaluation of Fe3O4 NPs.

Neuroprotective responses of quercetin in regulation of biochemical, structural, and neurobehavioral effects in 28-day oral exposure of iron in rats.

BACKGROUND: Iron is one of the essential metals that functions as a cofactor in various biological cascades in the brain. However, excessive iron accumulation in the brain may lead to neurodegeneration and may show toxic effects. Quercetin, a pigment flavonoid compound, has been proven to be a potent antioxidant and anti-inflammatory that can inhibit lipid peroxidation during metal-induced neurotoxicity. Although iron-induced neuroinflammation and neurodegeneration have been reported in many studies, but the proof for its exact mechanisms needs to be explored. PURPOSE: The key target of the study was to explore the neuroprotective effect of quercetin after oral exposure of iron in rats and explore its underlying molecular mechanisms. RESULTS: The outcomes of the study have shown that oral exposure to ferrous sulfate may modulate behavioral paradigms such as locomotor activity, neuromuscular coordination, and increased anxiety level. The pro-inflammatory cytokines (TNF-α, IL-1ß and IL-6), apoptotic protein (caspase 3), beta-amyloid and phosphorylated tau were found to be increased on iron exposure. Also, the expressions of ferritin heavy and light chain, BACE-1 and GFAP expressions were altered. These behavioral, structural, and biochemical alterations in the brain were significantly and dose-dependently reversed by treatment with quercetin. CONCLUSION: The current study provides a fundamental understanding of molecular signaling pathways, and structural proteins implicated in iron-induced neurotoxicity along with the ameliorative effects of quercetin.

Manganese-induced miR-125b-2-3p promotes anxiety-like behavior via TFR1-mediated ferroptosis.

The toxic effects of excessive manganese (Mn) levels in the environment have led to a severe public health concern. Ferroptosis is a newly form of cell death relying on iron, inherent to pathophysiological processes of psychiatric disorders, such as anxiety and depression-like behaviors. Excessive Mn exposure causes various neurological effects, including neuronal death and mood disorders. Whether Mn exposure causes anxiety and depression-like behaviors, and the underlying mechanisms of Mn-induced ferroptosis have yet to be determined. Here, Mn-exposed mice showed anxiety-like behavior. We also confirmed the accumulation of ferrous ion (Fe2+), lipid peroxidation, and depletion of antioxidant defense system both in vitro and in vivo Mn-exposed models, suggesting that Mn exposure can induce ferroptosis. Furthermore, Mn exposure downregulated the expression of miR-125b-2-3p. In turn, overexpression of miR-125b-2-3p alleviated the Mn-induced ferroptosis by targeting Transferrin receptor protein 1 (TFR1). In summary, this novel study established the propensity of Mn to cause anxiety-like behavior, an effect that was regulated by miR-125b-2-3p and ensuing ferroptosis secondary to the targeting of TFR1. These results offer promising targets for the prevention and treatment of Mn-induced neurotoxicity.

Butyrate Protects and Synergizes with Nicotine against Iron- and Manganese-induced Toxicities in Cell Culture.

Toxic exposures to heavy metals, such as iron (Fe) and manganese (Mn), can result in long-range neurological diseases and are therefore of significant environmental and medical concerns. We have previously reported that damage to neuroblastoma-derived dopaminergic cells (SH-SY5Y) by both Fe and Mn could be prevented by pre-treatment with nicotine. Moreover, butyrate, a short chain fatty acid (SCFA) provided protection against salsolinol, a selective dopaminergic toxin, in the same cell line. Here, we broadened the investigation to determine whether butyrate might also protect against Fe and/or Mn, and whether, if combined with nicotine, an additive or synergistic effect might be observed. Both butyrate and nicotine concentration-dependently blocked Fe and Mn toxicities. Ineffective concentrations of nicotine and butyrate, when combined, provided full protection against both Fe and Mn. Moreover, the effects of nicotine but not butyrate could be blocked by mecamylamine, a non-selective nicotinic antagonist. On the other hand, the effects of butyrate, but not nicotine, could be blocked by beta-hydroxy butyrate, a fatty acid-3 receptor antagonist. These results not only provide further support for neuroprotective effects of both nicotine and butyrate but also indicate distinct mechanisms of action for each one. Furthermore, potential utility of butyrate and nicotine combination against heavy metal toxicities is suggested.

Sodium selenite (Na2SeO3) attenuates T-2 toxin-induced iron death in LMH cells through the ROS/PI3K/AKT/Nrf2 pathway.

T-2 toxin, is a monotrichous mycotoxin commonly found in animal feed and agricultural products that can damage tissues and organs through oxidative stress. Selenium is a trace element with favorable antioxidant effects. However, it is unclear whether T-2 toxin-induces ferroptosis in LMH cells and whether Na2SeO3 has a protective role in this process. To investigate the process of hepatic injury by T-2 toxin and its antagonistic effect by Na2SeO3, we used 20 ng/mL T-2 toxin as well as 160 nmol/L Na2SeO3 to treat the LMH cells. The results demonstrated that exposure to the T-2 toxin induced iron death by increasing the quantity of ROS, leading to oxidative damage, decreasing the quantities of SOD, GPx, and T-AOC, and increasing the accumulation of MDA and H2O2, which resulted in the accumulation of Fe2+ and the down-regulation of the manifestation of linked genes and proteins including FTH1, Gpx4, NQO-1, and HO-1. After the addition of Na2SeO3, the PI3K/AKT/Nrf2 pathway is activated by regulating the selenoproteins gene level, and the above abnormal changes are reversed. In summary, Na2SeO3 alleviated T-2 toxin-induced iron death via the PI3K/AKT/Nrf2 pathway. These study not only broaden the cytotoxic knowledge regarding T-2 toxin, but also serve as a foundation for the use of Na2SeO3 in daily life.

Co-exposure to Fe, Zn, and Cu induced neuronal ferroptosis with associated lipid metabolism disorder via the ERK/cPLA2/AA pathway.

Excessive amounts of iron (Fe), zinc (Zn), and copper (Cu) can be toxic to neuronal cells, even though these are essential trace elements for animals and humans. However, the precise mechanisms underlying the neurotoxicity of exposure to mixtures of Fe, Zn, and Cu are still mostly unclear. The research aimed to investigate the influence of co-exposure to iron, zinc and copper and the related mechanisms in HT22 murine hippocampal neuronal cells. Intracellular metal content, markers of oxidative damage, and biomarkers of ferroptosis were respectively detected. Afterward, metabolomic analyses were performed to obtain a comprehensive understanding of the metal mixtures on metabolism, and the functions of key enzymes on metabolic pathways were validated. The results showed that metal co-exposure resulted in cellular iron overload and increased lipid peroxidation, accompanied by significant pathological damage and mitochondrial abnormalities in HT22 cells. Meanwhile, it was found that GSH depletion, decreased GPX4, and increased expression of the lipid metabolism gene ACSL4 play important roles in ferroptosis induced by metal mixture. Further, metabolomic analysis revealed metal co-exposure induced significant alterations in metabolite levels, especially in the glycerophospholipid metabolism pathway and the arachidonic acid metabolism pathway. The levels of cPLA2 and its metabolite, arachidonic acid, were significantly increased after metal co-exposure. Then, inhibition of cPLA2 decreased the level of arachidonic acid and attenuated ferroptosis in neuronal cells. Collectively, our findings unveiled ferroptosis induced by metal co-exposure associated with crucial molecular changes in neuronal cells, providing a novel perspective on the comprehensive toxicity risk assessment of metal mixtures.

Genotoxic and mutagenic evaluation in Eisenia foetida annelids exposed to iron ore tailings from the region of Brumadinho, MG, Brazil.

Soils that have a disproportion of metallic elements due to anthropic activities endanger the terrestrial fauna. This study evaluated whether earthworms (Eisenia foetida) exposed to ore tailings from Brumadinho region presented a higher frequency of genotoxic and mutagenic damages than annelids from a reference area (control). The animals were exposed to substrates containing 0%, 25%, 50%, 75%, and 100% iron mining waste. The results indicated increased DNA damage (p < 0.05), detected by the comet assay at 25% and 50%. There was a three-fold increase in micronuclei in animals on the substrates with the highest concentrations (75% and 100%) [F = 3.095; p = 0.02]. The earthworms lost weight as the percentage of mining waste increased. We concluded that E. foetida presented DNA damage in the contaminated soils of Brumadinho. However, more research is fundamental, once the environmental disaster in Brumadinho was one of the biggest mining catastrophe in Brazil.

Adverse effects of iron-based nanoparticles on freshwater phytoplankton Scenedesmus armatus and Microcystis aeruginosa strains.

Zero-valent nano-iron particles (nZVI) are increasingly present in freshwater aquatic environments due to their numerous applications in environmental remediation. However, despite the broad benefits associated with the use and development of nZVI nanoparticles, the potential risks of introducing them into the aquatic environment need to be considered. Special attention should be focused on primary producer organisms, the basal trophic level, whose impact affects the rest of the food web. Although there are numerous acute studies on the acute effects of these nanoparticles on photosynthetic primary producers, few studies focus on long-term exposures. The present study aimed at assessing the effects of nZVI on growth rate, photosynthesis activity, and reactive oxygen activity (ROS) on the freshwater green algae Scenedesmus armatus and the cyanobacteria Microcystis aeruginosa. Moreover, microcystin production was also evaluated. These parameters were assessed on both organisms singly exposed to 72 h-effective nZVI concentration for 10% maximal response for 28 days. The results showed that the cell growth rate of S. armatus was initially significantly altered and progressively reached control-like values at 28 days post-exposure, while M. aeruginosa did not show any significant difference concerning control values at any time. In both strains dark respiration (R) increased, unlike net photosynthesis (Pn), while gross photosynthesis (Pg) only slightly increased at 7 days of exposure and then became equal to control values at 28 days of exposure. The nZVI nanoparticles generated ROS progressively during the 28 days of exposure in both strains, although their formation was significantly higher on green algae than on cyanobacteria. These data can provide additional information to further investigate the potential risks of nZVI and ultimately help decision-makers make better informed decisions regarding the use of nZVI for environmental remediation.

Metals linked with the most prevalent primary neurodegenerative dementias in the elderly: A narrative review.

The ageing population has been steadily increasing worldwide, leading to a higher risk of cognitive decline and dementia. Environmental toxicants, particularly metals, have been identified as modifiable risk factors for cognitive impairment. Continuous exposure to metals occurs mainly through dietary sources, with older adults being particularly vulnerable. However, imbalances in the gut microbiota, known as dysbiosis, have also been associated with dementia. A literature review was conducted to explore the potential role of metals in the development of cognitive decline and the most prevalent primary neurodegenerative dementias, as well as their interaction with the gut microbiota. High levels of iron (Fe) and copper (Cu) are associated with mild cognitive impairment (MCI) and Alzheimer's disease (AD), while low selenium (Se) levels are linked to poor cognitive status. Parkinson's disease dementia (PDD) is associated with elevated levels of iron (Fe), manganese (Mn), and zinc (Zn), but the role of copper (Cu) remains unclear. The relationship between metals and Lewy body dementia (LBD) requires further investigation. High aluminium (Al) exposure is associated with frontotemporal dementia (FTD), and elevated selenium (Se) levels may be linked to its onset. Challenges in comparing studies arise from the heterogeneity of metal analysis matrices and analytical techniques, as well as the limitations of small study cohorts. More research is needed to understand the influence of metals on cognition through the gut microbiota (GMB) and its potential relevance in the development of these diseases.