Iron Release Research Articles

Iron-dependent BMP6 Regulation in Liver Sinusoidal Endothelial Cells Is Instructed by Hepatocyte-derived Secretory Signals.

Iron-dependent BMP6 Regulation in Liver Sinusoidal Endothelial Cells Is Instructed by Hepatocyte-derived Secretory Signals.

In-situ electrochemical study of chalcopyrite pressure oxidation leaching from 110 °C to 150 °C under saturated vapor pressure

Pressure oxidation leaching behavior of chalcopyrite in sulfuric acid solution from 110 °C to 150 °C were investigated by in-situ electrochemical methods. Leaching experiments under saturated vapor pressure conditions were used to simulate the anoxic environment that may be encountered in industrial applications. Scanning electron microscope and X-ray photoelectron spectroscopy were used to characterize the morphology and the chemical status of chalcopyrite surface. Results show that the copper extraction was increased with the increase of leaching temperature. Under the optimal leaching conditions under saturated vapor pressure, the copper and iron extraction are 8.3% and 29.8%, respectively. When the temperature increased from 110 °C to 150 °C, the self-corrosion potential and electrochemical reaction resistance firstly increased and then decreased. In contrast, the resistance of the passive film was always increased with the increase of temperature. The electrochemical study results indicated that the increase in temperature affected the oxidation of chalcopyrite by altering the kinetics of the cathodic reaction and the anodic passivation. Both the self-corrosion current density ( i corr ) and rate constant were affected by the reduction of Fe(III). The XPS results show that elemental sulfur and H 3 O(Fe 3 (SO 4 ) 2 (OH) 6 ) were the main leaching solid products. The formation of H 3 O(Fe 3 (SO 4 ) 2 (OH) 6 ) not only caused a decrease in cathodic reaction kinetics, but also increased the resistance of mass transfer process. Due to the faster release of iron, copper-rich sulphides were formed, which mixed with the elemental sulfur and/or H 3 O(Fe 3 (SO 4 ) 2 (OH) 6 ) led to coverage of the chalcopyrite surface.

Hepcidin as a Potential Biomarker for the Diagnosis of Anemia.

There are several blood-based markers to assess iron stores, but they all have some limitations. Hepcidin, a low-molecular-weight peptide hormone, is produced mainly by the liver. It is the main regulator of iron homeostasis by preventing iron release into plasma from absorptive enterocytes and macrophages. This review aims to critically assess existing data on potential role of hepcidin in diagnosis, particularly the (pre) analytical implications of the hepcidin measurement. There is a well-known causative correlation between hepcidin and iron deficiency. Therefore, hepcidin is considered as a promising marker in the assessment of iron status, particularly in patients with a diagnostic dilemma, such as patients with chronic renal disease and infants. The clinical implications of this peptide hormone in diagnosis of other diseases have been expanded in the recent studies, including elevated hepcidin levels in neoplastic diseases, sepsis, and inflammation. The potential role of hepcidin in diagnosis is controversial in the various types of iron deficiency because data are conflicting (as in anaemia of chronic disease) or limited (as in infants), whereas in the case of hereditary haemochromatosis, it has been proposed that hepcidin may be used for stratification of molecular testing, or to improve the frequency of phlebotomy, however, this issue still needs to be investigated. Due to lack of a clinically approved test, the medical application of this peptide as a biomarker in diagnosis is restricted. Recently, assays have been developed to determine hepcidin levels in serum and urine, facilitating the future use of hepcidin in research and clinical practice.

Changes in Iron Availability with Roxadustat in Nondialysis- and Dialysis-Dependent Patients with Anemia of CKD.

Roxadustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor, increases hemoglobin by stimulating erythropoietin synthesis and improving iron availability through facilitation of iron uptake and/or release from stores. In this exploratory analysis, we assessed the effect of roxadustat treatment on laboratory parameters related to iron metabolism in patients with anemia of chronic kidney disease (CKD). Data were pooled from pivotal, randomized, phase 3 roxadustat trials: three placebo-controlled, double-blind trials in nondialysis-dependent (NDD) CKD and three open-label, active-comparator (epoetin alfa) trials in dialysis-dependent (DD) CKD. In this exploratory analysis, mean changes from baseline in hemoglobin, iron parameters, and hepcidin, and intravenous (iv) iron use were evaluated. Pooled results in NDD CKD and DD CKD patients are reported. Overall, 4277 patients with NDD CKD and 3890 patients with DD CKD were evaluated. Hemoglobin increases with roxadustat treatment were accompanied by increases in serum iron and total iron-binding capacity (TIBC) and decreases in serum ferritin and hepcidin from baseline through week 52. With epoetin alfa, the hemoglobin increase was accompanied by decreases in serum ferritin and hepcidin, but serum iron decreased, and there was no change in TIBC. With placebo, there were no changes in hemoglobin, iron parameters, or hepcidin. During treatment, iv iron use was reduced with roxadustat versus placebo and epoetin alfa. In patients with NDD CKD and DD CKD, roxadustat treatment is associated with increases in serum iron and TIBC, accompanied by reduced hepcidin and indicative of improved iron kinetics. Patients treated with roxadustat achieved target hemoglobin levels with less iv iron use versus comparators. Practitioners treating patients with anemia of CKD with roxadustat should consider its unique effects when interpreting iron parameters.

Bio-accessibility of iron and copper from seven Kenyan anti-anaemia medicinal plants

Anaemia is a blood disorder which is widespread among populations of the world. In this study, seven medicinal plants used by one hundred and sixty herbalists from Nyamira County to manage anaemia were evaluated for iron and copper bio-accessibility. The competence of four hundred herbalists was assessed, of which 160 participated in the study. Twenty-one different medicinal plants were reported to be used by various herbalists to manage a number of ailments afflicting their communities in three sub-counties in Kenya. A total of ten different medicinal plants were found to be used by the herbalists to manage anemia which is endemic in the country. Seven of the medicinal plants, Aloe Vera, Carissa edulis, Croton macrostachyus, Clerodendrum myricoides, Melia azedrach, Toddalia asiatica and Warburgia ugandensis, were studied by all herbalists. The seven medicinal plants were prepared according to the herbalists' procedure and analyzed for iron and copper through flame atomic absorption spectrophotometer. The mean iron level in Carissa edulis from Borabu was the highest (2635.48 ± 17.33 mg/kg), while that in Warburgia ugandensis from the Nyamira study area was the lowest (175.76 ± 5.03 mg/kg). The highest mean copper level (9.2 ± 1.24 mg/kg) was reported in Melia azedrach from Ekerenyo, while the lowest (2.12 ± 0.02 mg/kg) was reported in Carissa edulis from the Nyamira study area. Fractionation results indicated that the proportion of iron potentially released (bio-accessible) from all the medicinal plants was quite small. Clerodendrum myricoides had the highest mean iron release and solubility (16.4 mg/kg), while Warburgia ugandensis had the lowest (5.94 mg/kg) among the medicinal plants. More iron and copper were extracted enzymatically as compared to the aqueous extraction. The amount of iron extracted in the intestinal mimicked phase was more than that extracted in the gastric phase, while the reverse was observed for copper. The levels of bio-accessible iron and copper from the medicinal plants, especially those released in enzymatic extraction are quite high and the plants can be used in the management of anaemia.

NCOA4 Regulates Iron Recycling and Responds to Hepcidin Activity and Lipopolysaccharide in Macrophages.

Macrophages, via erythrophagocytosis, recycle iron from effete erythrocytes to newly developing red blood cells. Conversion of potentially cytotoxic levels of iron from its heme into nonheme form during iron recycling is safely accomplished via coordinated regulations of cellular iron transport and homeostasis. Herein, we demonstrate the roles and regulation of NCOA4 (nuclear receptor coactivator 4)-mediated ferritinophagy in macrophages after erythrophagocytosis using the mouse macrophage cell line J774 cells. Ferritin in J774 cells increased with the rise of nonheme iron by erythrocyte ingestion and declined when total cellular iron contents subsequently decreased. NCOA4, a selective autophagic cargo receptor for ferritin, was responsible for the control of cellular ferritin and total iron contents at the later stage of erythrophagocytosis. A hepcidin analog, which limits the flux of iron through iron-recycling by inhibiting iron export at the plasma membrane, repressed NCOA4 expression and led to accumulation of ferritin in the mouse macrophages. Transcriptome analyses revealed a functional association of immune response with NCOA4-dependent gene expressions, and we confirmed repression of Ncoa4 by lipopolysaccharide (LPS) in J774 cells and the spleen of mice. Collectively, our studies indicate that NCOA4 facilitates cellular ferritin turnover and the release of iron by macrophages after erythrophagocytosis and functions as a regulatory target for molecular signals of systemic iron overload and inflammation. These identify macrophage NCOA4 as a potential therapeutic target for disorders of systemic iron dysregulation, including anemia of inflammation and hemochromatosis.

Electrochemical sensor based on N-CQDs/AgNPs/β-CD nanomaterials: Application to simultaneous selective determination of Fe(Ⅱ) and Fe(Ⅲ) irons released from iron supplement in simulated gastric fluid

Simultaneous selective determination of Fe (Ⅱ) and Fe (Ⅲ) is of great significance to the study of iron ion tracking and release of iron supplement in gastric fluid. In this paper, a composite material (N-CQDs/AgNPs/β-CD) was prepared by a one-pot method. The various characterizations confirmed the silver nanoparticles (AgNPs) grew in situ on the surface of nitrogen-doped carbon quantum dots (N-CQDs), and the β-cyclodextrin (β-CD) and AgNPs linked together by Ag–O bonds finally presented gourd-like nanoparticles on the surface of N-CQDs. Then, N-CQDs/AgNPs/β-CD modified glassy carbon electrode (GCE) was applied to detect Fe(II) and Fe(III) simultaneously. The cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) results confirmed that N-CQDs/AgNPs/β-CD enhanced electrode performances because of the synergistic effect between N-CQDs, AgNPs and β-CD. The sensor was successfully applied for the determination by differential pulse voltammetry (DPV) of Fe(II) and Fe(III) released from four iron supplementations in simulated gastric fluid (SGF).

Impact of initial chlorine concentration on water quality change in old unlined iron pipes

Unlined iron pipe (UIP) is still widely in use in drinking water distribution systems (DWDS), discoloration easily happens after a long-time retention due to iron release, but the influence of initial chlorine on water quality under this condition is not clear. Here, we studied the water quality changes in UIP section reactors under different initial chlorine dosages. Results showed that chlorine could disappeared rapidly within 0.5 h in the UIP. The water with higher initial chlorine (5 mg/L) had higher turbidity in a short time (within 1.5 h), but for a longer retention time (2∼12 h), the highest turbidity was in the iron pipe without initial chlorine. Interestingly, a clear increase in adenosine triphosphate in the UIPs was observed with the increase of initial chlorine, which was in accordance with the results of heterotrophic plate count. Polysaccharide and protein increased with the increase of initial chlorine, which would benefit the formation of a protective layer to inhibit corrosion. This study reflects that during the overnight retention in UIP, raising chlorine would be effective to control discoloration, but chemical and microbiological risks may increase.

Iron Deposition and Ferroptosis in the Spleen in a Murine Model of Acute Radiation Syndrome.

Total body irradiation (TBI) can result in death associated with hematopoietic insufficiency. Although radiation causes apoptosis of white blood cells, red blood cells (RBC) undergo hemolysis due to hemoglobin denaturation. RBC lysis post-irradiation results in the release of iron into the plasma, producing a secondary toxic event. We investigated radiation-induced iron in the spleens of mice following TBI and the effects of the radiation mitigator captopril. RBC and hematocrit were reduced ~7 days (nadir ~14 days) post-TBI. Prussian blue staining revealed increased splenic Fe3+ and altered expression of iron binding and transport proteins, determined by qPCR, western blotting, and immunohistochemistry. Captopril did not affect iron deposition in the spleen or modulate iron-binding proteins. Caspase-3 was activated after ~7–14 days, indicating apoptosis had occurred. We also identified markers of iron-dependent apoptosis known as ferroptosis. The p21/Waf1 accelerated senescence marker was not upregulated. Macrophage inflammation is an effect of TBI. We investigated the effects of radiation and Fe3+ on the J774A.1 murine macrophage cell line. Radiation induced p21/Waf1 and ferritin, but not caspase-3, after ~24 h. Radiation ± iron upregulated several markers of pro-inflammatory M1 polarization; radiation with iron also upregulated a marker of anti-inflammatory M2 polarization. Our data indicate that following TBI, iron accumulates in the spleen where it regulates iron-binding proteins and triggers apoptosis and possible ferroptosis.

Mu opioid receptor-mediated release of endolysosome iron increases levels of mitochondrial iron, reactive oxygen species, and cell death.

Opioids including morphine and DAMGO activate mu-opioid receptors (MOR), increase intracellular reactive oxygen species (ROS) levels, and induce cell death. Ferrous iron (Fe2+) through Fenton-like chemistry increases ROS levels and endolysosomes are "master regulators of iron metabolism" and contain readily-releasable Fe2+ stores. However, mechanisms underlying opioid-induced changes in endolysosome iron homeostasis and downstream-signaling events remain unclear. We used SH-SY5Y neuroblastoma cells, flow cytometry, and confocal microscopy to measure Fe2+ and ROS levels and cell death. Morphine and DAMGO de-acidified endolysosomes, decreased endolysosome Fe2+ levels, increased cytosol and mitochondria Fe2+ and ROS levels, depolarized mitochondrial membrane potential, and induced cell death; effects blocked by the nonselective MOR antagonist naloxone and the selective MOR antagonist β-funaltrexamine (β-FNA). Deferoxamine, an endolysosome-iron chelator, inhibited opioid agonist-induced increases in cytosolic and mitochondrial Fe2+ and ROS. Opioid-induced efflux of endolysosome Fe2+ and subsequent Fe2+ accumulation in mitochondria were blocked by the endolysosome-resident two-pore channel inhibitor NED-19 and the mitochondrial permeability transition pore inhibitor TRO. Opioid agonist-induced increases in cytosolic and mitochondrial Fe2+ and ROS as well as cell death appear downstream of endolysosome de-acidification and Fe2+ efflux from the endolysosome iron pool that is sufficient to affect other organelles.

The critical role of ferritinophagy in human disease.

Ferritinophagy is a type of autophagy mediated by nuclear receptor activator 4 (NCOA4), which plays a role in inducing ferroptosis by regulating iron homeostasis and producing reactive oxygen species in cells. Under physiological conditions, ferritinophagy maintains the stability of intracellular iron by regulating the release of free iron. Studies have demonstrated that ferritinophagy is necessary to induce ferroptosis; however, under pathological conditions, excessive ferritinophagy results in the release of free iron in large quantities, which leads to lipid peroxidation and iron-dependent cell death, known as ferroptosis. Ferritinophagy has become an area of interest in recent years. We here in review the mechanism of ferritinophagy and its association with ferroptosis and various diseases to provide a reference for future clinical and scientific studies.

Transcriptional activation of hepcidin by the microphthalmia/transcription factor E family.

Hepcidin negatively regulates the circulating iron levels by inhibiting the intestinal absorption of iron as well as iron release from macrophages. Hepcidin activity is largely determined by its expression, which is regulated at the transcriptional level. Hepcidin transcription is induced not only by the iron status-related bone morphogenetic protein (BMP)-2/6, but also by inflammatory cytokines, such as interleukin (IL)-1β and IL-6. The present study reveals that the microphthalmia (MiT)/transcription factor E (TFE) family members are novel regulators of hepcidin transcription. Melanocyte-inducing transcription factor (MITF)-A, a member of the MiT/TFE family, was identified as a positive regulator of hepcidin transcription via stimulus screening for transcription regulators. An E-box (5'-CATGTG-3') spanning nt-645 to nt-640 of the murine hepcidin promoter was identified as an MITF-A-responsive element. Responsiveness to MITF-A on hepcidin transcription decreased when the cells were stimulated with BMP2 or IL-1β. These results suggest a functional interaction between the MITF pathway and BMP- or IL-1β-mediated signaling. TFEB and TFE3, members of the MiT/TFE family, also stimulated hepcidin transcription, but the main region responsible for hepcidin transcription was distinct from that induced by MITF-A. The region spanning nt-581 to nt-526 was involved in TFEB/TFE3-mediated hepcidin transcription. Considering that members of the MiT/TFE family act as regulators of starvation-induced lysosomal biogenesis, hepcidin expression may be controlled by additional pathways apart from those identified so far.

Evaluation of the antioxidant effect of a phytocomplex addition in clean label pork salami enriched in n-3 PUFA

Control and n-3 PUFA enriched raw material was used to manufacture clean label and conventional salami; the former were added with a phytocomplex having iron chelating, DPPH, and FRAP activity, obtained from olive vegetation water, oregano, green tea and blueberry leaves, and with acerola powder. Salami were dried at 3 ± 1 °C until an established decrease in the combined pH and aw values, while only the conventional ones underwent a standard process. In the cold dried salami pH changes, aw and weight decrease were delayed; the phytocomplex contributed to lower the pH, and to prevent lipid and protein oxidation, despite the n-3 PUFA enrichment and heme iron release due to nitrite removal. TBARS and protein carbonyls were the highest in the nitrite-added salami undergoing cold and standard drying, respectively. The oxidation marker MDA tended to increase in the simulated digests of salami n-3 PUFA enriched or subjected to cold drying.

Influence of Electrostatic Field on Mixed Aqueous Solution of Calcium and Ferrous Ions: Insights from Molecular Dynamics Simulations

In order to investigate the anti-scaling and anti-corrosion characteristics of an electrostatic anti-fouling system in the application process, the influence of an electrostatic field (EF) on the structure and dynamics of hydrated Ca2+ and hydrated Fe2+ in a mixed aqueous system was studied through the calculation and analysis of the radial distribution function (RDF), self-diffusion coefficients, viscosity, and hydrogen bond structure by using molecular dynamics simulation. The study results show that the EF can decrease the radius of the first water shell of hydrated Ca2+ but increase that of Fe2+, which will reduce the possibility of forming calcite. The EF can make water molecules and Fe2+ more active, which can hinder iron release and thus decrease iron corrosion products. In addition, the EF can enhance the hydrogen structure of water molecules in the aqueous solution.

Intracellular Biotransformation of Ultrasmall Iron Oxide Nanoparticles and Their Effect in Cultured Human Cells and in Drosophila Larvae In Vivo.

A systematic investigation on the cellular uptake, intracellular dissolution, and in vitro biological effects of ultra-small (<10 nm) iron hydroxide adipate/tartrate coated nanoparticles (FeAT-NPs) was carried out in intestinal Caco-2, hepatic HepG2 and ovarian A2780 cells, and the nucleotide excision repair (NER) deficient GM04312 fibroblasts. Quantitative evaluation of the nanoparticles uptake, as well as their transformation within the cell cytosol, was performed by inductively coupled plasma mass spectrometry (ICP-MS), alone or in combination with high performance liquid chromatography (HPLC). The obtained results revealed that FeAT-NPs are effectively taken up in a cell type-dependent manner with a minimum dissolution after 3 h. These results correlated with no effects on cell proliferation and minor effects on cell viability and reactive oxygen species (ROS) production for all the cell lines under study. Moreover, the comet assay results revealed significant DNA damage only in GM04312 cells. In vivo genotoxicity was further studied in larvae from Drosophila melanogaster, using the eye-SMART test. The obtained results showed that FeAT-NPs were genotoxic only with the two highest tested concentrations (2 and 5 mmol·L−1 of Fe) in surface treatments. These data altogether show that these nanoparticles represent a safe alternative for anemia management, with high uptake level and controlled iron release.

Effect of Cisplatin on Renal Iron Homeostasis Components: Implication in Nephropathy.

Cisplatin is an important chemotherapeutic drug for the treatment of solid tumors but often causes nephropathy as part of the off-target toxicity. Iron accumulation and related damage were implicated in cisplatin-induced kidney injury. However, the role of cisplatin in the renal iron sensing mechanism and its target genes responsible for iron uptake, storage, and release have not been investigated. Cellular iron homeostasis is controlled by the interaction of iron regulatory proteins (IRP1 and IRP2) and iron-responsive elements (IREs) present in the untranslated regions of iron transport and storage components. Here, we report that cisplatin does not influence the expressions of IRP targets such as transferrin receptor-1 (TfR1), divalent metal transporter-1 (DMT1), and ferroportin in renal cells despite the increased heme oxygenase-1 (HO-1) level. Ferritin subunits (Ft-H and Ft-L) are elevated in different magnitudes due to the increased mRNA expression. Intriguingly, a higher expression of Ft-L mRNA is detected than that of Ft-H mRNA. The inability of cisplatin in altering the IRE–IRP interaction is confirmed by examining IRE-containing luciferase activity, RNA electrophoretic mobility shift assay, and activation of IRPs. The labile iron pool is depleted but reversed by silencing of either Ft-H or Ft-L, suggesting increased iron storage by ferritin. Silencing of Ft-H or Ft-L promotes cell death, suggesting that ferritin acts to protect the renal cells from cisplatin-mediated toxicity. A differential increase of transcripts and equivalent increase of proteins of Ft-H and Ft-L and unaltered TfR1 and DMT1 transcripts are found in the kidneys of cisplatin-treated rats along with iron accumulation. Our results reveal that cisplatin does not influence the IRE–IRP interaction despite alteration of the cellular iron pool in renal cells. This insensitivity of the IRE–IRP system may be implicated in the accumulation of iron to contribute to cisplatin-induced nephropathy.

Alteration of osteoclast activity in childhood cancer survivors: Role of iron and of CB2/TRPV1 receptors.

Childhood cancer survivors (CCS) are predisposed to the onset of osteoporosis (OP). It is known that iron overload induces osteoclasts (OCs) overactivity and that the iron chelator Deferasirox (DFX) can counteract it. The Cannabinoid Receptor type 2 (CB2) and the transient receptor potential vanilloid type-1 (TRPV1) are potential therapeutic targets for OP. In this study we isolated OCs from peripheral blood of 20 CCS and investigated osteoclast biomarkers expression and iron metabolism evaluating iron release by OCs and the expression of several molecules involved in its regulation. Moreover, we analyzed the effects of CB2 and TRPV1 stimulation in combination with DFX on osteoclast activity and iron metabolism. We observed, for the first time, an osteoclast hyperactivation in CCS suggesting a role for iron in its development. Moreover, we confirmed the well-known role of CB2 and TRPV1 receptors in bone metabolism, suggesting the receptors as possible key biomarkers of bone damage. Moreover, we demonstrated a promising synergism between pharmacological compounds, stimulating CB2 or inhibiting/desensitizing TRPV1 and DFX, in counteracting osteoclast overactivity in CCS to improve their quality of life.

Long-term sulfate resistance of synthesized cement systems with variable C3A/C4AF ratio at low temperature or ambient conditions: Insights into the crystalline and amorphous phase assemblage

Synthesized cement systems made with variable C3A/C4AF ratios, containing C3S, gypsum and, optionally, calcite, were stored long-term at humid conditions at 5 or 20 °C, without any protection against atmospheric carbonation. Analytical techniques able to assess both the crystalline and amorphous phases were used. Experimental results were compared with thermodynamic simulations. The systems with C3A/C4AF < 1 better preserved the soundness of the CSH phase, which hosted iron, and prevented thaumasite formation. The addition of calcite in these systems inhibited carbonation. When occurred (mixtures without calcite), the carbonation was significantly more intense at ambient temperature. In the systems that underwent extensive deterioration, cross-linking of silicate structures, AFt decomposition, and iron release from the deteriorating CSH, occurred, while Al-incorporating amorphous silica, calcium carbonate polymorphs and hydrous iron oxide formed. The presence of unreacted C3A in the systems with C3A/C4AF = 1, suggested that CSH decomposition was contributed by available sulfates.

Microencapsulation of Erythrocytes Extracted from Cavia porcellus Blood in Matrices of Tara Gum and Native Potato Starch.

Ferropenic anemy is the leading iron deficiency disease in the world. The aim was to encapsulate erythrocytes extracted from the blood of Cavia porcellus, in matrices of tara gum and native potato starch. For microencapsulation, solutions were prepared with 20% erythrocytes; and encapsulants at 5, 10, and 20%. The mixtures were spray-dried at 120 and 140 °C. The iron content in the erythrocytes was 3.30 mg/g and between 2.32 and 2.05 mg/g for the encapsulates (p < 0.05). The yield of the treatments varied between 47.84 and 58.73%. The moisture, water activity, and bulk density were influenced by the temperature and proportion of encapsulants. The total organic carbon in the atomized samples was around 14%. The particles had diverse reddish tonalities, which were heterogeneous in their form and size; openings on their surface were also observed by SEM. The particle size was at the nanometer level, and the zeta potential (ζ) indicated a tendency to agglomerate and precipitation the solutions. The presence of iron was observed on the surface of the atomized by SEM-EDX, and FTIR confirmed the encapsulation due to the presence of the chemical groups OH, C-O, C-H, and N-H in the atomized. On the other hand, high percentages of iron release in vitro were obtained between 88.45 and 94.71%. The treatment with the lowest proportion of encapsulants performed at 140 °C obtained the best results and could potentially be used to fortify different functional foods.

The role of mitochondria in the recovery of neurons after injury.

The role of mitochondria in the recovery of neurons after injury.