The Essential Element Manganese, Oxidative Stress, and Metabolic Diseases: Links and Interactions

Li, Longman; Yang, Xiaobo

doi:10.1155/2018/7580707

Cited by 403 publications

(265 citation statements)

References 122 publications

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“…But in comparison to other essential micronutrients, such as iron (Fe) and zinc (Zn), whose deficiencies in humans are responsible for major health problems, Mn deficiency in humans is rare. However, Mn poisoning may be encountered more frequently upon overexposure to this metal causing hepatic cirrhosis, polycythemia, dystonia, and Parkinson-like symptoms (Li and Yang, 2018). In plants, Mn is one of the 17 essential elements for growth and reproduction.…”

Section: Introductionmentioning

confidence: 99%

Manganese in Plants: From Acquisition to Subcellular Allocation

et al. 2020

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Manganese (Mn) is an important micronutrient for plant growth and development and sustains metabolic roles within different plant cell compartments. The metal is an essential cofactor for the oxygen-evolving complex (OEC) of the photosynthetic machinery, catalyzing the water-splitting reaction in photosystem II (PSII). Despite the importance of Mn for photosynthesis and other processes, the physiological relevance of Mn uptake and compartmentation in plants has been underrated. The subcellular Mn homeostasis to maintain compartmented Mn-dependent metabolic processes like glycosylation, ROS scavenging, and photosynthesis is mediated by a multitude of transport proteins from diverse gene families. However, Mn homeostasis may be disturbed under suboptimal or excessive Mn availability. Mn deficiency is a serious, widespread plant nutritional disorder in dry, well-aerated and calcareous soils, as well as in soils containing high amounts of organic matter, where bio-availability of Mn can decrease far below the level that is required for normal plant growth. By contrast, Mn toxicity occurs on poorly drained and acidic soils in which high amounts of Mn are rendered available. Consequently, plants have evolved mechanisms to tightly regulate Mn uptake, trafficking, and storage. This review provides a comprehensive overview, with a focus on recent advances, on the multiple functions of transporters involved in Mn homeostasis, as well as their regulatory mechanisms in the plant's response to different conditions of Mn availability.

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Section: Introductionmentioning

confidence: 99%

Manganese in Plants: From Acquisition to Subcellular Allocation

et al. 2020

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“…Manganese is a cofactor of numerous metalloenzymes, including manganese superoxide dismutase (Mn-SOD) [244,245], pyruvate carboxylase [246], and glutamate synthetase [247,248]. Manganese is also required for mucopolysaccharide metabolism, oxidative phosphorylation, and oxidative stress [249]. Increased oxidative stress can result in higher levels of HIV-1 and increases in Mn-SOD have been observed in HIV-1 infection; increased Mn-SOD may help protect HIV-1-infected cells from cell death [250,251].…”

Section: Manganese (Mn 2+ ) and Magnesium (Mg 2+ )mentioning

confidence: 99%

Role of Divalent Cations in HIV-1 Replication and Pathogenicity

Khan

Chen

Geiger

2020

Viruses

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Divalent cations are essential for life and are fundamentally important coordinators of cellular metabolism, cell growth, host-pathogen interactions, and cell death. Specifically, for human immunodeficiency virus type-1 (HIV-1), divalent cations are required for interactions between viral and host factors that govern HIV-1 replication and pathogenicity. Homeostatic regulation of divalent cations’ levels and actions appear to change as HIV-1 infection progresses and as changes occur between HIV-1 and the host. In people living with HIV-1, dietary supplementation with divalent cations may increase HIV-1 replication, whereas cation chelation may suppress HIV-1 replication and decrease disease progression. Here, we review literature on the roles of zinc (Zn2+), iron (Fe2+), manganese (Mn2+), magnesium (Mg2+), selenium (Se2+), and copper (Cu2+) in HIV-1 replication and pathogenicity, as well as evidence that divalent cation levels and actions may be targeted therapeutically in people living with HIV-1.

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“…Excess accumulation of Mn in mitochondria disrupts mitochondrial homeostasis and alters mitochondrial bioenergetics . Although several mechanisms of Mn‐induced neurotoxicity have been reported, including oxidative stress, energy failure and the disturbance of neurotransmitter metabolism, and so forth, increasing evidence has indicated that mitochondrial damage is also the crucial mechanism of Mn‐induced neurotoxicity …”

Section: Introductionmentioning

confidence: 99%

“…5 Although several mechanisms of Mn-induced neurotoxicity have been reported, including oxidative stress, energy failure and the disturbance of neurotransmitter metabolism, and so forth, increasing evidence has indicated that mitochondrial damage is also the crucial mechanism of Mninduced neurotoxicity. 6,7 Mitochondria are double-membrane organelles exited in the cytoplasm of eukaryotic cells function as the power plant for the cell. 8 Mitochondria produce the energy necessary for | 537 LIU et aL.…”

Section: Introductionmentioning

confidence: 99%

Effect of trehalose on manganese‐induced mitochondrial dysfunction and neuronal cell damage in mice

Liu

Jing

Liu

et al. 2019

Basic Clin Pharma Tox

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Chronic overexposure to manganese (Mn) has been verified to induce mitochondrial dysfunction, which is related to oxidative damage. The autophagic‐lysosomal degradation pathway plays a vital role in the removal of impaired mitochondria through a specific quality control mechanism termed mitophagy. However, trehalose functions as an inducer of autophagy by an mTOR‐independent mechanism, and little data report its effect on Mn‐induced mitochondrial dysfunction. To explore the possibility that trehalose could be effective in interfering with the Mn‐induced mitochondrial dysfunction, we used trehalose (2% and 4% (g/vol (mL))) in a mouse model of manganism. Our data showed that mice developed weary motor and behavioural deficits after exposure to Mn for 6 weeks. Overexposure to Mn resulted in mitochondrial dysfunction and neuronal cell damage in the basal nuclei of mice, which could be ameliorated by trehalose pre‐treatment. Moreover, our results indicated that trehalose pre‐treatment significantly reduced the oxidative damage and enhanced the activation of mitophagy. The findings clearly demonstrated that trehalose could relieve Mn‐induced mitochondrial and neuronal cell damage through its antioxidative and mitophagy‐inducing effects.

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The Essential Element Manganese, Oxidative Stress, and Metabolic Diseases: Links and Interactions

Cited by 403 publications

References 122 publications

Manganese in Plants: From Acquisition to Subcellular Allocation

Manganese in Plants: From Acquisition to Subcellular Allocation

Role of Divalent Cations in HIV-1 Replication and Pathogenicity

Effect of trehalose on manganese‐induced mitochondrial dysfunction and neuronal cell damage in mice

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