Manganese in the Diet: Bioaccessibility, Adequate Intake, and Neurotoxicological Effects

Martins, Airton C.; Krum, Bárbara Nunes; Queirós, Libânia; Tinkov, Alexey A.; Skalny, Anatoly V.; Bowman, Aaron B.; Aschner, Michael

doi:10.1021/acs.jafc.0c00641

Cited by 78 publications

(30 citation statements)

References 130 publications

(223 reference statements)

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“…Alteration of these processes, under Mn deficiency or excess conditions, may result in severe metabolic dysfunction. However, the case for dietary Mn deficiency appears to be extremely rare in humans due to high levels of Mn in dietary products [7,8]. In contrast, Mn overexposure, which is far more common, may cause brain-associated disorders [9].…”

Section: Introductionmentioning

confidence: 99%

Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

Tinkov

Paoliello

Mazilina

et al. 2021

IJMS

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Understanding of the immediate mechanisms of Mn-induced neurotoxicity is rapidly evolving. We seek to provide a summary of recent findings in the field, with an emphasis to clarify existing gaps and future research directions. We provide, here, a brief review of pertinent discoveries related to Mn-induced neurotoxicity research from the last five years. Significant progress was achieved in understanding the role of Mn transporters, such as SLC39A14, SLC39A8, and SLC30A10, in the regulation of systemic and brain manganese handling. Genetic analysis identified multiple metabolic pathways that could be considered as Mn neurotoxicity targets, including oxidative stress, endoplasmic reticulum stress, apoptosis, neuroinflammation, cell signaling pathways, and interference with neurotransmitter metabolism, to name a few. Recent findings have also demonstrated the impact of Mn exposure on transcriptional regulation of these pathways. There is a significant role of autophagy as a protective mechanism against cytotoxic Mn neurotoxicity, yet also a role for Mn to induce autophagic flux itself and autophagic dysfunction under conditions of decreased Mn bioavailability. This ambivalent role may be at the crossroad of mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis. Yet very recent evidence suggests Mn can have toxic impacts below the no observed adverse effect of Mn-induced mitochondrial dysfunction. The impact of Mn exposure on supramolecular complexes SNARE and NLRP3 inflammasome greatly contributes to Mn-induced synaptic dysfunction and neuroinflammation, respectively. The aforementioned effects might be at least partially mediated by the impact of Mn on α-synuclein accumulation. In addition to Mn-induced synaptic dysfunction, impaired neurotransmission is shown to be mediated by the effects of Mn on neurotransmitter systems and their complex interplay. Although multiple novel mechanisms have been highlighted, additional studies are required to identify the critical targets of Mn-induced neurotoxicity.

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Section: Introductionmentioning

confidence: 99%

Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

Tinkov

Paoliello

Mazilina

et al. 2021

IJMS

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“…[8] Chronic overexposure to Mn is known to cause neurotoxicity, referred to as manganism, a parkinsonism-like disorder. [9] Severe outcomes of Zn dyshomeostasis are largely due to malnutrition, which is especially prevalent in the elderly population. Vural et al, for example, reported that an insufficient daily Zn intake (defined as below the estimated average requirement (EAR) of 6.8 mg Zn⋅day -1 for women and 9.4 mg Zn⋅day -1 for men) was observed in 31-66% of older adults.…”

Section: Introductionmentioning

confidence: 99%

“…[ 8 ] Chronic overexposure to Mn is known to cause neurotoxicity, referred to as manganism, a parkinsonism‐like disorder. [ 9 ]…”

Section: Introductionmentioning

confidence: 99%

Nutritive Manganese and Zinc Overdosing in Aging C. elegans Result in a Metallothionein‐Mediated Alteration in Metal Homeostasis

Baesler

Michaelis

Stiboller

et al. 2021

Molecular Nutrition Food Res

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Scope: Manganese (Mn) and zinc (Zn) are not only essential trace elements, but also potential exogenous risk factors for various diseases. Since the disturbed homeostasis of single metals can result in detrimental health effects, concerns have emerged regarding the consequences of excessive exposures to multiple metals, either via nutritional supplementation or parenteral nutrition. This study focuses on Mn-Zn-interactions in the nematode Caenorhabditis elegans (C. elegans) model, taking into account aspects related to aging and age-dependent neurodegeneration. Methods and Results: Chronic co-exposure of C. elegans to Mn and Zn increases metal uptake, exceeding levels of single metal exposures. Supplementation with Mn and/or Zn also leads to an age-dependent increase in metal content, a decline in overall mRNA expression, and metal co-supplementation induced expression of target genes involved in Mn and Zn homeostasis, in particular metallothionein 1 (mtl-1). Studies in transgenic worms reveal that mtl-1 played a prominent role in mediating age-and diet-dependent alterations in metal homeostasis. Metal dyshomeostasis is further induced in parkin-deficient nematodes (Parkinson's disease (PD) model), but this did not accelerate the age-dependent dopaminergic neurodegeneration. Conclusions: A nutritive overdose of Mn and Zn can alter interactions between essential metals in an aging organism, and metallothionein 1 acts as a potential protective modulator in regulating homeostasis.

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“…However, people who consume 28 mg/L of water containing high levels of elements such as Mn can develop toxicity [ 73 ]. Although Mn is an essential nutrient, especially regarding the reduction of oxidative stress, both Mn deficiency or overload is rare, whereas the excess is usually caused by environmental exposure [ 74 , 75 ].…”

Section: Resultsmentioning

confidence: 99%

Human Health Risk Assessment through Roasted Meats Consumption

Leite

Melo

Arakaki

et al. 2020

IJERPH

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Data on the content of metals and metalloids in roasted meats with different types of wood and charcoal are still scarce in the literature. The concentrations of metals (Al, Cr, Cd, Cu, Fe, Mg, Mn, Mo, Ni, V, and Zn) and metalloid (As) were determined by inductively coupled plasma mass spectrometry (ICP-OES) after microwave digestion, and the estimated daily intake (EDI) for adults was assessed to determine the hazard quotient (HQ). The concentrations of Al, Cr, Cu, and Fe in raw meats were below the data obtained in other countries. The concentration of As (0.17 ± 0.42–0.23 ± 0.10 mg/kg), Mg (206.77 ± 3.99–291.95 ± 8.87 mg/kg), V (0.42 ± 0.14–6.66 ± 0.80 mg/kg), and Zn (6.66 ± 0.80–48.13 ± 0.56 mg/kg) in raw meats exceeded the values in the literature. The concentrations of Mg, As, Cr, Fe, V, and Zn are high when the meat is roasted using wood. All levels of Al, As, Cr, Cu, Fe, Mg, Mn, Mo, V, and Zn in raw meats are lower than those of meat roasted with coal and wood. The content of As in meat roasted with Chromed Copper Arsenate (CCA) wood (15.10 ± 0.27–26.25 ± 1.47 mg/kg) is higher than meat roasted with charcoal (0.46 ± 0.09–1.16 ± 0.50 mg/kg). EDI and HQ values revealed a minimal exposure of the adult population to those metals through roasted-meats consumption. However, EDI values of As in some roasted meats are above standard limits. Roast meats with wood showed higher levels of major and trace elements than meats roasted with coal. High exposures, in the long-term, may cause damage to health.

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Manganese in the Diet: Bioaccessibility, Adequate Intake, and Neurotoxicological Effects

Cited by 78 publications

References 130 publications

Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

Nutritive Manganese and Zinc Overdosing in Aging C. elegans Result in a Metallothionein‐Mediated Alteration in Metal Homeostasis

Human Health Risk Assessment through Roasted Meats Consumption

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