Toxno Substance Profile
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Substance Name

Manganese(II) oxide
Identification Number: CASRN | 1344-43-0

  Substance Attributes


  • Metabolic Interference or Disruption

    Interferes with human metabolism. This can be a very serious thing. Some of these interference mechanics are well established. However, often long term effects and health consequences remain largely unknown. Additionally an emerging area of concern and one that is not currently studied, is the combined synergistic effects these metabolically disrupting chemicals have on human health.


    Metabolic interference happens when the substance produces highly reactive and often damaging intermediates during detoxification or when the substance binds to specific enzymes, important structural groups on molecules, receptors and membranes or targets DNA or mimics key nutrients.

  • Exposure Produces Health Symptoms

    Symptoms maybe short term or long term depending on the exposure duration and intensity and effects areas like Cardiovascular, Gastrointestinal, Cognition, Fatigue. A substance with this attribute may cause an allergic skin reaction, serious eye irritation, allergy or asthma symptoms or breathing difficulties if inhaled.

These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.



  • CATEGORIES: Household Toxin | Pollutant | Airborne Pollutant | Food Toxin | Natural Toxin | EAFUS (Everything Added to Food in the United States) | Inert Pesticide Ingredient USA - Non Food Use Only
  • SUBSTANCE LINEAGE: Inorganic Compounds | Mixed Metal/Non-metal Compounds | Transition Metal Organides | Transition Metal Oxides | Transition Metal Oxides
  • SYNONYMS: Cassel green | Manganese green | Manganese monooxide | Manganese oxide | Manganese protoxide | Manganosite | Manganous oxide | Natural manganosite | Rosensthiel green
  • DESCRIPTION: Manganous oxide is an oxided of manganese. It occurs in nature as the rare mineral manganosite. Manganese is a naturally occurring metal with the symbol Mn and the atomic number 25. It does not occur naturally in its pure form, but is found in many types of rocks in combination with other substances such as oxygen, sulfur, or chlorine. Manganese occurs naturally in most foods and small amounts are needed to stay healthy, as manganese ions act as cofactors for a number of enzymes. (L228, L229, L235)
  • COMMENTS:
  • toxin chemical structure pubchem
  • FORMULA: MnO
  • DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | EAFUS | EPA USA - Pesticide Inerts
  • LAST UPDATE: 28/04/2018

  Health Associations

Mostly focused on Health Implications of Long Term Exposure to this substance

  • SYMPTOMS: Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (L228)
  • POSSIBLE HEALTH CONSEQUENCES: Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (L228) | Manganese is absorbed mainly via ingestion, but can also be inhaled. It binds to alpha-2-macroglobulin, albumin, or transferrin in the plasma and is distributed to the brain and all other mammalian tissues, though it tends to accumulate more in the liver, pancreas, and kidney. Manganese is capable of existing in a number of oxidation states and is believed to undergo changes in oxidation state within the body. Manganese oxidation state can influence tissue toxicokinetic behavior, and possibly toxicity. Manganese is excreted primarily in the faeces. (L228)
  • ACTION OF TOXIN: Manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions. It primarily targets the central nervous system, particularily the globus pallidus of the basal ganglia. It is believed that the manganese ion, Mn(II), enhances the autoxidation or turnover of various intracellular catecholamines, leading to increased production of free radicals, reactive oxygen species, and other cytotoxic metabolites, along with a depletion of cellular antioxidant defense mechanisms, leading to oxidative damage and selective destruction of dopaminergic neurons. In addition to dopamine, manganese is thought to perturbations other neurotransmitters, such as GABA and glutamate. In order to produce oxidative damage, manganese must first overwhelm the antioxidant enzyme manganese superoxide dismutase. The neurotoxicity of Mn(II) has also been linked to its ability to substitute for Ca(II) under physiological conditions. It can enter mitochondria via the calcium uniporter and inhibit mitochondrial oxidative phosphorylation. It may also inhibit the efflux of Ca(II), which can result in a loss of mitochondrial membrane integrity. Mn(II) has been shown to inhibit mitochondrial aconitase activity to a significant level, altering amino acid metabolism and cellular iron homeostasis. (L228) | Manganese interferes with amino acid metabolism by inhibiting aconitase, resulting in an increase in citrate levels. It is also believed that this direct disruption of the catalytic [4Fe-4S] cluster of aconitase by manganese produces iron regulary protein 1, resulting in alterations in cellular iron homeostasis. (A159)
  • TOXIN SITES OF ACTION IN CELL: "Cytoplasm", "Extracellular"
  • Additional Exposure Routes:

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  Exposure Routes

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