Consequences of Disturbing Manganese Homeostasis

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(19), P. 14959 - 14959

Published: Oct. 6, 2023

Manganese (Mn) is an essential trace element with unique functions in the body; it acts as a cofactor for many enzymes involved energy metabolism, endogenous antioxidant enzyme systems, neurotransmitter production, and regulation of reproductive hormones. However, overexposure to Mn toxic, particularly central nervous system (CNS) due causing progressive destruction nerve cells. Exposure manganese widespread occurs by inhalation, ingestion, or dermal contact. Associations have been observed between accumulation neurodegenerative diseases such manganism, Alzheimer's disease, Parkinson's Huntington's amyotrophic lateral sclerosis. People genetic associated mutation gene impaired excretion, kidney iron deficiency, vegetarian diet are at particular risk excessive exposure Mn. This review has collected data on current knowledge source exposure, experimental supporting dispersive brain, controversies surrounding reference values biomarkers related status different matrices, competitiveness other metals, (Fe), magnesium (Mg), zinc (Zn), copper (Cu), lead (Pb), calcium (Ca). The disturbed homeostasis body connected susceptibility diseases, fertility, infectious diseases. evidence involvement metabolic type 2 diabetes mellitus/insulin resistance, osteoporosis, obesity, atherosclerosis, non-alcoholic fatty liver was discussed.

Language: Английский

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Neurotoxic effects of heavy metal pollutants in the environment: Focusing on epigenetic mechanisms

Environmental Pollution, Journal Year: 2024, Volume and Issue: 345, P. 123563 - 123563

Published: Feb. 13, 2024

Language: Английский

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Glial Perturbation in Metal Neurotoxicity: Implications for Brain Disorders

Neuroglia, Journal Year: 2025, Volume and Issue: 6(1), P. 4 - 4

Published: Jan. 6, 2025

Overexposure of humans to heavy metals and essential poses a significant risk for the development neurological neurodevelopmental disorders. The mechanisms through which these exert their effects include generation reactive oxygen species, mitochondrial dysfunction, activation inflammatory pathways, disruption cellular signaling. function glial cells in brain maintenance homeostasis cannot be overlooked. are particularly susceptible metal-induced neurotoxicity. Accumulation promotes microglial activation, triggering responses that can coincide with other neurotoxicity, inducing alteration synaptic transmission, cognitive deficit, neuronal damage. In this review, we highlighted role dysfunction some selected neurodegenerative diseases We further dive into how exposure such as nickel, manganese, methyl mercury, cadmium, iron, arsenic, lead affect functions microglia, astrocytes, oligodendrocytes they on relation Potential therapeutic interventions use new improved chelating agents antioxidant therapies might approach alleviating perturbations.

Language: Английский

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Ferroptosis as a mechanism of non-ferrous metal toxicity

Archives of Toxicology, Journal Year: 2022, Volume and Issue: 96(9), P. 2391 - 2417

Published: June 21, 2022

Language: Английский

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Manganese promotes α-synuclein amyloid aggregation through the induction of protein phase transition

Journal of Biological Chemistry, Journal Year: 2021, Volume and Issue: 298(1), P. 101469 - 101469

Published: Dec. 4, 2021

α-Synuclein (α-Syn) is the major protein component of Lewy bodies, a key pathological feature Parkinson's disease (PD). The manganese ion Mn2+ has been identified as an environmental risk factor PD. However, it remains unclear how regulates α-Syn aggregation. Here, we discovered that Mn2+accelerates amyloid aggregation through regulation phase separation. We found not only promotes liquid-to-solid transition but also directly induces soluble monomers to form solid-like condensates. Interestingly, lipid membrane integrated into condensates during Mn2+-induced transition; however, preformed Mn2+/α-syn can recruit lipids surface In addition, this largely facilitate Although do fuse, our results demonstrated they could existing Furthermore, observed chelator reverses stage. after maturation, becomes irreversible. These findings demonstrate facilitates accelerate formation aggregates and provide new insights for targeting separation in PD treatment. (α-Syn), cytoplasmic abundant presynaptic nerve terminals, implicated (PD), dementia with other synucleinopathies (1Baba M. Nakajo S. Tu P.H. Tomita T. Nakaya K. Lee V.M. Trojanowski J.Q. Iwatsubo Aggregation alpha-synuclein bodies sporadic bodies.Am. J. Pathol. 1998; 152: 879-884PubMed Google Scholar, 2Maroteaux L. Campanelli J.T. Scheller R.H. Synuclein: A neuron-specific localized nucleus terminal.J. Neurosci. 1988; 8: 2804-2815Crossref PubMed 3Bernal-Conde L.D. Ramos-Acevedo R. Reyes-Hernández M.A. Balbuena-Olvera A.J. Morales-Moreno I.D. Argüero-Sánchez Schüle B. Guerra-Crespo Alpha-synuclein physiology pathology: perspective on cellular structures organelles.Front. 2019; 13: 1399Crossref Scopus (41) Scholar). While monomer unstructured potential (4Fauvet Mbefo M.K. Fares M.B. Desobry C. Michael Ardah M.T. Tsika E. Coune P. Prudent Lion N. Eliezer D. Moore D.J. Schneider Aebischer El-Agnaf O.M. et al.α-Synuclein central nervous system from erythrocytes, mammalian cells, Escherichia coli exists predominantly disordered monomer.J. Biol. Chem. 2012; 287: 15345-15364Abstract Full Text PDF (387) 5Theillet F.X. Binolfi A. Bekei Martorana Rose H.M. Stuiver Verzini Lorenz van Rossum Goldfarb Selenko Structural disorder monomeric α-synuclein persists cells.Nature. 2016; 530: 45-50Crossref (525) 6Nguyen Derreumaux Structures intrinsically Aβ, tau proteins aqueous solution computer simulations.Biophys. 2020; 264: 106421Crossref (57) Scholar), multiple studies suggested forms α-helical tetramers physiologically resist (7Bartels Choi J.G. Selkoe occurs helically folded tetramer resists aggregation.Nature. 2011; 477: 107-110Crossref (847) 8Wang W. Perovic I. Chittuluru Kaganovich Nguyen L.T. Liao Auclair J.R. Johnson Landeru Simorellis A.K. Ju Cookson M.R. Asturias F.J. Agar J.N. Webb B.N. al.A construct dynamic tetramer.Proc. Natl. Acad. Sci. 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Jakes Goedert alpha-Synuclein bodies.Nature. 1997; 388: 839-840Crossref (5862) 13Nemani Lu Berge Nakamura Onoa Chaudhry F.A. Nicoll R.A. Edwards Increased expression reduces by inhibiting synaptic vesicle reclustering endocytosis.Neuron. 65: 66-79Abstract (735) toxic, numerous disclose oligomers fibrils causes toxicity (14Karpinar D.P. Balija Kügler Opazo F. Rezaei-Ghaleh Wender Kim H.Y. Taschenberger G. Falkenburger B.H. Heise Kumar Riedel Fichtner Voigt Braus G.H. al.Pre-fibrillar variants impaired beta-structure increase neurotoxicity models.EMBO 2009; 28: 3256-3268Crossref (341) 15Volpicelli-Daley L.A. Luk K.C. Patel T.P. Tanik S.A. Riddle D.M. Stieber Meaney D.F. Exogenous induce body pathology leading dysfunction neuron death.Neuron. 72: 57-71Abstract (899) Many pathway alternations, such oxidative stress, mitochondrial dysfunction, endoplasmic reticulum autophagy-lysosomal have linked cytotoxic effects (15Volpicelli-Daley 16Fields C.R. Bengoa-Vergniory Wade-Martins Targeting therapy disease.Front. Mol. 12: 299Crossref (96) 17Wong Y.C. Krainc neurodegeneration: Mechanism therapeutic strategies.Nat. Med. 2017; 23: 1-13Crossref (395) 18Guiney S.J. Adlard P.A. Lei Mawal C.H. Bush A.I. Finkelstein D.I. Ayton Fibrillar depends functional lysosomes.J. 295: 17497-17513Abstract (13) aggregations proteins, tau, IAPP, FUS, TDP-43, studied vitro decades 19Nguyen Sterpone Pouplana Campanera J.M. Dimerization mechanism Alzheimer Aβ(40) peptides: content intrapeptide-stabilized conformations A2V A2T heterozygous dimers retards formation.J. Phys. 120: 12111-12126Crossref (34) 20Ivanova M.I. Lin Y. Y.H. Biophysical processes underlying cross-seeding implications pathology.Biophys. 106507Crossref Protein targets amyloid-related 21Doig Inhibition small molecules.Curr. Opin. Struct. 2015; 30: 50-56Crossref (212) 22Savitt Jankovic disease: Progress towards development disease-modifying therapeutics.Drugs. 79: 797-810Crossref (45) addition α-Syn, contain components, including various organelles (20Ivanova 23Shahmoradian S.H. Lewis Genoud Hench Moors T.E. Navarro P.P. Castaño-Díez Schweighauser Graff-Meyer Goldie K.N. Sütterlin Huisman Ingrassia Gier Rozemuller A.J.M. al.Lewy consists crowded membranes.Nat. 22: 1099-1109Crossref (331) factors, lipids, coexist affect accumulation For example, activity glucocerebrosidase, lysosomal glycoprotein affects levels (24Muñoz S.S. Petersen Marlet F.R. Kücükköse Galvagnion interplay between human models disease.Biophys. 273: 106534Crossref (16) Recent Raman spectral imaging revealed colocalized cells (25Watson M.D. Flynn J.D. J.C. (13)C(2)H(15)N-labeled cells.Biophys. 106528Crossref (8) while regulations previously (26Galvagnion Meisl Michaels Vendruscolo Knowles Dobson C.M. Lipid vesicles trigger stimulating primary nucleation.Nat. 11: 229-234Crossref (358) 27Giehm Svergun Otzen D.E. Vestergaard Low-resolution structure disrupting oligomer accumulates fibrillation.Proc. 3246-3251Crossref (194) 28Kurochka A.S. Yushchenko D.A. Bouř Shvadchak V.V. Influence membranes aggregation.ACS 825-830Crossref (10) Metal ions Cu2+, Zn2+, concentrated brain bind (29González Arcos-López König Quintanar Menacho Márquez Outeiro T.F. Fernández C.O. Effects post-translational modifications metal binding.J. Neurochem. 150: 507-521Crossref (37) C-terminal domain which contains Asp Glu residues, interact di- trivalent 30Binolfi Rasia R.M. Bertoncini C.W. Ceolin Zweckstetter Griesinger Jovin T.M. Interaction divalent reveals differences: link structure, binding specificity fibrillation enhancement.J. Am. Soc. 2006; 128: 9893-9901Crossref (262) detailed information each metal-α-Syn still due lack high-resolution data. Manganese essential (31Pfalzer A.C. Bowman A.B. Relationships biology neurological disease.Curr. Environ. Health Rep. 4: 223-228Crossref 32Tinkov A.A. Paoliello M.M.B. Mazilina A.N. Skalny A.V. Martins Voskresenskaya O.N. Aaseth Santamaria Notova S.V. Tsatsakis Aschner Molecular manganese-induced neurotoxicity: five-year update.Int. 4646Crossref rise utility industry led increased pollution. imbalance homeostasis cause neurodegenerative diseases (33Guilarte T.R. New perspectives behavioral, neuroimaging, neuropathological humans non-human primates.Front. Aging 2013; 5: 23Crossref (136) 34Miah Ijomone Okoh C.O.A. O.K. Akingbade G.T. Ke Krum da Cunha Jr., Akinyemi Aranoff Antunes Soares overexposure health.Neurochem. Int. 135: 104688Crossref (35) Specially, epidemiological investigations indicate excessive exposure increases (34Miah 35Gorell C.C. Rybicki B.A. Peterson E.L. Kortsha G.X. Brown G.G. Richardson R.J. Occupational manganese, copper, lead, iron, mercury zinc disease.Neurotoxicology. 1999; 20: 239-247PubMed 36Lucchini R.G. Martin C.J. Doney B.C. From manganism parkinsonism: conceptual model based evolution exposure.Neuromolecular 311-321Crossref (125) Multiple occupational welding, mining, related industrial activities associated Parkinsonism (37Racette McGee-Minnich Moerlein S.M. Mink J.W. Videen T.O. Perlmutter J.S. Welding-related Clinical features, treatment, pathophysiology.Neurology. 2001; 56: 8-13Crossref (306) 38Jiang Y.M. Mo X.A. Du F.Q. Fu X. Zhu X.Y. Gao Xie J.L. F.L. Pira Effective treatment parkinsonism p-aminosalicylic acid: case 17-year follow-up study.J. Occup. 48: 644-649Crossref (108) 39Racette Tabbal S.D. Jennings Good Evanoff Prevalence relationship large sample Alabama welders.Neurology. 2005; 64: 230-235Crossref (150) 40Rutchik Jiang How does neurologist assess welders steelworkers movement disorder? An international team's experiences Guanxi, China part II.J. 54: 1562-1564Crossref (7) 41Rutchik China, I.J. 1432-1434Crossref (9) 42Racette Criswell S.R. Lundin J.I. Hobson Seixas Kotzbauer P.T. Zhang Sheppard Checkoway welding exposure.Neurotoxicology. 33: 1356-1361Crossref (105) 43Mortimer J.A. Borenstein A.R. Nelson L.M. Associations Parkinson Review meta-analysis.Neurology. 1174-1180Crossref (63) 44Al-Lozi Nielsen Hershey Birke Racette Cognitive control workers exposed manganese-containing fume.Am. Ind. 60: 181-188Crossref (15) Long-time level air may deficits cognitive (45Bowler Kornblith E.S. Gocheva Colledge Bollweg Beseler C.L. Wright Adams S.W. Lobdell D.T. Environmental air: functions.Neurotoxicology. 49: 139-148Crossref 46Carvalho C.F. Oulhote Martorelli Carvalho Menezes-Filho Argollo Abreu associations memory, executive functions, hyperactivity Brazilian children.Neurotoxicology. 2018; 69: 253-259Crossref (24) recent meta-analysis previous 22 significantly circulating patients, further demonstrating (47Du Liu M.Y. Pan Y.Z. Zhong Wei M.J. Association meta-analysis.Neurosci. Lett. 665: 92-98Crossref One induced (48Sun He Yang Liang Shi Ou injury via ATP-sensitive K(+) channels GABA receptors.Toxicol. 332: 164-170Crossref 49Liu Z.Q. Z.F. Cong Z. Li Deng Xu Manganese-induced overexpression aggravates damage repressing PINK1/parkin-mediated mitophagy.Food Toxicol. 112213Crossref (3) 50Verina Guilarte frontal cortex primates.Toxicol. 217: 177-183Crossref 51Cai Yao Chen Cao Shen Luo PC12 ERK activation.Brain Res. 1359: 201-207Crossref (47) 52Harischandra D.S. Rokad Neal Ghaisas Manne Sarkar Panicker Zenitsky Jin Huang Anantharam Kanthasamy A.G. prion-like cell-to-cell exosomal transmission α-synuclein.Sci. Signal. 12eaau4543Crossref (74) most these were cell culture, their relevance unknown. Biochemical showed shortens time (53Han J.Y. T.S. H.I. role Ca(2+) hard cations accelerated interfibrillar 1895Crossref (33) early stage elusive. protein–protein or protein–RNA condensed liquid droplets weak multivalent interactions, called liquid–liquid (LLPS). Proteins undergo LLPS, Tau protein, usually repetitive domains regions (IDR) (54Li Banjade Cheng H.C. Guo Llaguno Hollingsworth J.V. King Banani S.F. Russo P.S. Q.X. Nixon B.T. Rosen Phase transitions signalling proteins.Nature. 483: 336-340Crossref (1140) 55Conicella A.E. Dignon G.L. Zerze H.B. D'Ordine A.M. Rohatgi Ayala Mittal Fawzi N.L. TDP-43 tunes liquid-liquid function.Proc. 117: 5883-5894Crossref (102) 56Levone Lenzken S.C. Antonaci Maiser Rapp Conte Reber Mechtersheimer Ronchi Mühlemann O. Leonhardt Cardoso M.C. Ruepp Barabino S.M.L. FUS-dependent important DNA repair initiation.J. Cell 220e202008030Crossref 57Ambadipudi Biernat Mandelkow Liquid-liquid microtubule-binding repeats Alzheimer-related tau.Nat. Commun. 275Crossref (308) Numerous variety aggregation-prone initiate LLPS (58Wegmann Eftekharzadeh Tepper Zoltowska K.M. Bennett R.E. Dujardin Laskowski P.R. MacKenzie Kamath Commins Vanderburg Roe A.D. Fan Molliex Hernandez-Vega al.Tau aggregation.EMBO 37e98049Crossref (368) 59Tange Ishibashi Nakagaki Taguchi Kamatari Y.O. Ozawa Nishida full-length prion initiates conformational conversion vitro.J. 296: 100367Abstract (22) 60Pytowski Foley Vaux Jean diabetes-associated IAPP hydrogelation aggregation.Proc. 12050-12061Crossref 61Xing Nandakumar Kakinen Sun Davis P.C. Ding Amyloid under lens separation.J. 368-378Crossref (12) three IDRs low-complexity domains. reported undergoes aggregation, indicating be intermediate before (62Ray Singh Pandey Datta Mahato Panigrahi Navalkar Mehra Gadhe Chatterjee Sawner Maiti Bhatia nucleates separation.Nat. 705-716Crossref (147) 63Hardenberg Sinnige Casford Dada Poudel Robinson E.A. Fuxreiter Kaminksi Kaminski-Schierle G.S. Nollen E.A.A. Observation droplet state maturation body-like assemblies.J. 282-294PubMed 64Hoffmann Sansevrino Morabito Logan Vabulas Ulusoy Ganzella Milovanovic Synapsin alpha-synuclein.J. 433: 166961Crossref (20) work, examined whether LLPS. requirement crowding agents. efficiently transition, facilitating absence agents, bypassing step presence membrane. Lipids recruited Our proceed recruitment monomers. difficult disassemble mature aggregates, chelators reverse dimension understanding pathogenesis suggest target therapy. To study regulatory expressed (Fig. S1) conditions drives vitro. first labeled preparing EGFP-α-Syn fusion protein. unlabeled mixed at molar ratio 1:9 Using fluorescence microscopy, underwent relatively concentration S2) agent PEG-10000 S3). Ficoll 400, another macromolecular agent, promote although efficiency lower S4). By contrast, failed drive small-molecule ethylene glycol, supporting acts α-syn S5). Next, tested plays PEG, frequently used mimic environment, 200 μM formed typical smooth droplets. When included 2 mM Mn2+, morphology turned irregular 1A). dose-dependence experiments when was 400 above S6). Then performed recovery photobleaching (FRAP) examine intensity returned prebleaching 120 s laser bleaching, rapid fluidity inside 1, B C). contras

Language: Английский

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SIRT1/FOXO3-mediated autophagy signaling involved in manganese-induced neuroinflammation in microglia

Ecotoxicology and Environmental Safety, Journal Year: 2023, Volume and Issue: 256, P. 114872 - 114872

Published: April 5, 2023

Manganese (Mn), as one of the environmental risk factors for Parkinson's disease (PD), has been widely studied. Though autophagy dysfunction and neuroinflammation mainly are responsible causative issue Mn neurotoxicity, molecular mechanism parkinsonism caused by not explored clearly. The results in vivo vitro experiments showed that overexposure to impairment dysfunction, accompanied increase IL-1β, IL-6, TNF-α mRNA expression, nerve cell apoptosis, microglia activation, NF-κB poor neurobehavior performance. This is due Mn-induced downregulation SIRT1. Upregulation SIRT1 could alleviate neuroinflammation, yet these beneficial effects were abolished following 3-MA administration. Furthermore, we found interfered with acetylation FOXO3 BV2 cells, leading a decrease nuclear translocation FOXO3, its binding LC3B promoter transcription activity. be antagonized upregulation Finally, it proved SIRT1/FOXO3-LC3B signaling involves impairment.

Language: Английский

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Neurotoxicity of manganese via ferroptosis induced by redox imbalance and iron overload

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 278, P. 116404 - 116404

Published: May 4, 2024

Manganese (Mn) is an essential trace element for maintaining bodily functions. Excessive exposure to Mn can pose serious health risks humans and animals, particularly the nervous system. While has been implicated as a neurotoxin, exact mechanism of its toxicity remains unclear. Ferroptosis form programmed cell death that results from iron-dependent lipid peroxidation. It plays role in various physiological pathological cellular processes may be closely related Mn-induced neurotoxicity. However, ferroptosis neurotoxicity not thoroughly investigated. Therefore, this study aims investigate Using bioinformatics, we identified significant changes genes associated with Mn-exposed animal models. We then evaluated at both levels. Our findings suggest causes weight loss system damage mice. In vitro vivo experiments have shown increases malondialdehyde, reactive oxygen species, ferrous iron, while decreasing glutathione adenosine triphosphate. These leads increase peroxidation disrupts iron metabolism, resulting oxidative stress injury ferroptosis. Furthermore, assessed expression levels proteins mRNAs ferroptosis, confirming involvement

Language: Английский

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Manganese in autism spectrum disorder and attention deficit hyperactivity disorder: The state of the art

Current Research in Toxicology, Journal Year: 2024, Volume and Issue: 6, P. 100170 - 100170

Published: Jan. 1, 2024

The objective of the present narrative review was to synthesize existing clinical and epidemiological findings linking manganese (Mn) exposure biomarkers autism spectrum disorder (ASD) attention deficit hyperactivity (ADHD), discuss key pathophysiological mechanisms neurodevelopmental disorders that may be affected by this metal. Existing data demonstrated both direct inverse association between Mn body burden ASD, or lack any relationship. In contrast, majority studies revealed significantly higher levels in subjects with ADHD, as well relationship inattention scores children, although several reported contradictory results. laboratory impaired animals following associated dopaminergic dysfunction neuroinflammation. Despite evidence on Mn-induced neurobiological alterations patients ASD a plethora neurotoxic effects overexposure interfere pathogenesis inherent these disorders. Specifically, overload shown impair not only neurotransmission, but also affect metabolism glutamine/glutamate, GABA, serotonin, noradrenaline, thus affecting neuronal signaling. turn, its ability induce oxidative stress, apoptosis, neuroinflammation, and/or neurogenesis. Nonetheless, additional detailed are required evaluate environmental at wide range concentrations estimate potential dose-dependent effects, genetic factors association.

Language: Английский

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The Manganese–Bone Connection: Investigating the Role of Manganese in Bone Health

Journal of Clinical Medicine, Journal Year: 2024, Volume and Issue: 13(16), P. 4679 - 4679

Published: Aug. 9, 2024

The complex relationship between trace elements and skeletal health has received increasing attention in the scientific community. Among these minerals, manganese (Mn) emerged as a key element affecting bone metabolism integrity. This review examines multifaceted role of Mn health, including its effects on regeneration, mineralization, overall strength. article is based synthesis experimental models, epidemiologic studies, clinical trials mechanisms effect metabolism. Current research data show that actively involved processes remodeling by modulating activity osteoblasts osteoclasts, well main cells regulate formation resorption. ions have profound mineralization density intricately regulating signaling pathways enzymatic reactions cells. Additionally, superoxide dismutase (MnSOD), located mitochondria, plays crucial osteoclast differentiation function, protecting osteoclasts from oxidative damage. Understanding nuances Mn’s interaction with essential for optimizing strategies, potentially preventing managing diseases. Key findings include stimulation osteoblast proliferation differentiation, inhibition osteoclastogenesis, preservation mass through RANK/RANKL/OPG pathway. These results underscore importance maintaining highlight need further into therapeutic potential.

Language: Английский

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Cerebrovascular accidents association between serum trace elements and toxic metals level, a case-control study

PLoS ONE, Journal Year: 2025, Volume and Issue: 20(2), P. e0317731 - e0317731

Published: Feb. 3, 2025

Background Cerebrovascular accidents (CVAs) are among the most common complications of patients today. As prevalence ischemic CVAs rises, detecting related risk factors is crucial. Metal concentration has previously been considered a major factor in several neural complications, and this study, we will investigate this. Methods In case-control 70 CVA (clinically approved stroke cases by imaging NIH Stroke Scale (NIHSS)) individuals with no history controls were enrolled as control group. The serum level metals, including Fe (Iron), Co (Cobalt), Ni (Nickel), Cu (copper), Zn (Zinc), Mn (Manganese), Pb (lead), Hg (Mercury), assessed using Inductively coupled plasma mass spectrometry (ICP-MS) method. Logistic regression (LR) also used to determine association between metals’ levels occurrence. Results mean age group was 48.68 ± 15.25 years for non-CVA 47.89 9.65 years, result indicated that statically higher (respectively; P < 0.001 = 0.002) significantly lower (P 0.003). Other measured (Fe, Co, Ni, Mn, Hg) not different groups. LR model, all Cu, Pb, metals had value 0.03 an odd ratio (OR) confidence interval (CI) 1.34 (1.02–1.75), 1.19 (1.01–1.39) 1.01 (1.001–1.02) respectively. Conclusion Given some associated CVA, researchers physicians must better understand causes burden CVA. However, further studies larger population investigation exact pathogenesis these needed.

Language: Английский

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