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Title:
Manganese Toxicity Upon Overexposure: a Decade in Review | Current Environmental Health Reports
Description:
Exposure to manganese (Mn) causes clinical signs and symptoms resembling, but not identical to, Parkinson’s disease. Since our last review on this subject in 2004, the past decade has been a thriving period in the history of Mn research. This report provides a comprehensive review on new knowledge gained in the Mn research field. Emerging data suggest that beyond traditionally recognized occupational manganism, Mn exposures and the ensuing toxicities occur in a variety of environmental settings, nutritional sources, contaminated foods, infant formulas, and water, soil, and air with natural or man-made contaminations. Upon fast absorption into the body via oral and inhalation exposures, Mn has a relatively short half-life in blood, yet fairly long half-lives in tissues. Recent data suggest Mn accumulates substantially in bone, with a half-life of about 8–9 years expected in human bones. Mn toxicity has been associated with dopaminergic dysfunction by recent neurochemical analyses and synchrotron X-ray fluorescent imaging studies. Evidence from humans indicates that individual factors such as age, gender, ethnicity, genetics, and pre-existing medical conditions can have profound impacts on Mn toxicities. In addition to body fluid-based biomarkers, new approaches in searching biomarkers of Mn exposure include Mn levels in toenails, non-invasive measurement of Mn in bone, and functional alteration assessments. Comments and recommendations are also provided with regard to the diagnosis of Mn intoxication and clinical intervention. Finally, several hot and promising research areas in the next decade are discussed.
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Topics {✒️}

metabolite n-acetyl-para-aminosalicylic acid synchrotron x-ray fluorescent synchrotron x-ray fluorescence x-ray fluorescence imaging neutron activation-based analysis t1-weighted mri signals pre-existing medical conditions store-operated calcium channels low-molecular-mass species [32 manganese-induced neuronal death sodium para-amino salicylate describe mn-induced hepatotoxicity parkinsonism-causing mutations block manganese-induced movement disorder mn-induced movement disorder high-molecular-mass fractions low-molecular-weight compounds neural stem/progenitor cells transporting para-aminosalicylic acid erythrocyte calcium-pump activity central nervous system mn-induced parkinsonian disorder soy-based infant formulas blood-csf barrier contributes mri enhancer mn-dpdp pre-existing neurological disease mn-dependent neurological disorders manganese-induced occupational parkinsonism mn-dpdp-overdosed patients [68] mn-induced cardiovascular toxicity proven anti-inflammatory effect low-level occupational exposure fairly long half-lives manganese-induced parkinsonism due chronic hepatic encephalopathy mn-dpdp enhanced mri n-acetyl-aspartate blood manganese-iron ratio fine motor coordination magnetic resonance imaging privacy choices/manage cookies low-level mn exposure transferrin-dependent transport mechanisms low-level mn exposures male sprague-dawley rats rbe4 cell types beneficial metal ions full-blown symptoms body fluid-based biomarkers para-aminosalicylic acid

Questions {❓}

A scientific review of age determination for a laboratory rat: how old is it in comparison with human age?
How does an occupational neurologist assess welders and steelworkers for a manganese-induced movement disorder?

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         description:Exposure to manganese (Mn) causes clinical signs and symptoms resembling, but not identical to, Parkinson’s disease. Since our last review on this subject in 2004, the past decade has been a thriving period in the history of Mn research. This report provides a comprehensive review on new knowledge gained in the Mn research field. Emerging data suggest that beyond traditionally recognized occupational manganism, Mn exposures and the ensuing toxicities occur in a variety of environmental settings, nutritional sources, contaminated foods, infant formulas, and water, soil, and air with natural or man-made contaminations. Upon fast absorption into the body via oral and inhalation exposures, Mn has a relatively short half-life in blood, yet fairly long half-lives in tissues. Recent data suggest Mn accumulates substantially in bone, with a half-life of about 8–9 years expected in human bones. Mn toxicity has been associated with dopaminergic dysfunction by recent neurochemical analyses and synchrotron X-ray fluorescent imaging studies. Evidence from humans indicates that individual factors such as age, gender, ethnicity, genetics, and pre-existing medical conditions can have profound impacts on Mn toxicities. In addition to body fluid-based biomarkers, new approaches in searching biomarkers of Mn exposure include Mn levels in toenails, non-invasive measurement of Mn in bone, and functional alteration assessments. Comments and recommendations are also provided with regard to the diagnosis of Mn intoxication and clinical intervention. Finally, several hot and promising research areas in the next decade are discussed.
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      headline:Manganese Toxicity Upon Overexposure: a Decade in Review
      description:Exposure to manganese (Mn) causes clinical signs and symptoms resembling, but not identical to, Parkinson’s disease. Since our last review on this subject in 2004, the past decade has been a thriving period in the history of Mn research. This report provides a comprehensive review on new knowledge gained in the Mn research field. Emerging data suggest that beyond traditionally recognized occupational manganism, Mn exposures and the ensuing toxicities occur in a variety of environmental settings, nutritional sources, contaminated foods, infant formulas, and water, soil, and air with natural or man-made contaminations. Upon fast absorption into the body via oral and inhalation exposures, Mn has a relatively short half-life in blood, yet fairly long half-lives in tissues. Recent data suggest Mn accumulates substantially in bone, with a half-life of about 8–9 years expected in human bones. Mn toxicity has been associated with dopaminergic dysfunction by recent neurochemical analyses and synchrotron X-ray fluorescent imaging studies. Evidence from humans indicates that individual factors such as age, gender, ethnicity, genetics, and pre-existing medical conditions can have profound impacts on Mn toxicities. In addition to body fluid-based biomarkers, new approaches in searching biomarkers of Mn exposure include Mn levels in toenails, non-invasive measurement of Mn in bone, and functional alteration assessments. Comments and recommendations are also provided with regard to the diagnosis of Mn intoxication and clinical intervention. Finally, several hot and promising research areas in the next decade are discussed.
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