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Setup of Capillary Electrophoresis-Inductively Coupled Plasma Mass Spectrometry (CE-ICP-MS) for Quantification of Iron Redox Species (Fe(II), Fe(III))
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Manganese neurotoxicity and the role of reactive oxygen species

Ebany J Martinez-Finley1, Claire E Gavin2, Michael Aschner3

  • 1Division of Clinical Pharmacology and Pediatric Toxicology, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 37240, USA; Center in Molecular Toxicology, Vanderbilt University Medical Center, Nashville, TN 37240, USA.

Free Radical Biology & Medicine
|February 12, 2013
PubMed

Insights

Manganese (Mn) is essential but toxic in excess. Overexposure causes manganism through oxidative stress, mitochondrial dysfunction, and depleted antioxidants, impacting absorption, distribution, and excretion.

Area of Science:

  • Biochemistry
  • Toxicology
  • Nutritional Science

Background:

  • Manganese (Mn) is a vital dietary nutrient.
  • Excessive Mn exposure leads to toxicity and manganism.
  • Mn toxicity involves reactive oxygen species and mitochondrial dysfunction.

Purpose of the Study:

  • Review mechanisms of Mn toxicity.
  • Summarize scientific studies on Mn toxicity.
  • Provide an overview of Mn metabolism and transport.

Main Methods:

  • Literature review of scientific studies.
  • Analysis of Mn absorption, distribution, and excretion.
  • Examination of Mn compound stability and transport.

Main Results:

  • Mn toxicity mechanisms include oxidative stress, free radical production, and toxic metabolites.
  • Mitochondrial function and ATP production are altered by Mn.
  • Cellular antioxidant defenses are depleted by excessive Mn exposure.

Conclusions:

  • Mn toxicity is multifaceted, involving cellular damage and metabolic disruption.
  • Understanding Mn metabolism is crucial for preventing toxicity.
  • Further research on Mn transport and stability is warranted.
Keywords:
DA autoxidationFree radicalsManganeseManganismMitochondrial dysfunctionReactive oxygen species

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