Manganese Homeostasis and Transport

Roth, Jerome A.; Ponzoni, Silvia; Aschner, Michael

doi:10.1007/978-94-007-5561-1_6

Cited by 71 publications

(47 citation statements)

References 217 publications

(253 reference statements)

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“…The inability of Mn depletion to correct the motor deficits in Slc39a14 −/− mice suggests that the motor impairments represent lasting effects of early-life Mn exposure. SLC39A14 | manganese | liver | pancreas M anganese (Mn) is an essential trace mineral required for normal growth and physiological processes, such as bone formation, immune response, and carbohydrate metabolism (1). The essentiality of Mn derives from its role as a cofactor in a variety of enzymes, including galactosyl transferase, Mnsuperoxide dismutase, xanthine oxidase, arginase and glutamine synthetase, and pyruvate decarboxylase.…”

mentioning

confidence: 99%

SLC39A14 deficiency alters manganese homeostasis and excretion resulting in brain manganese accumulation and motor deficits in mice

Jenkitkasemwong

Akinyode

Paulus

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

109

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Solute carrier family 39, member 14 (SLC39A14) is a transmembrane transporter that can mediate the cellular uptake of zinc, iron, and manganese (Mn). Studies of knockout () mice have documented that SLC39A14 is required for systemic growth, hepatic zinc uptake during inflammation, and iron loading of the liver in iron overload. The normal physiological roles of SLC39A14, however, remain incompletely characterized. Here, we report that mice spontaneously display dramatic alterations in tissue Mn concentrations, suggesting that Mn is a main physiological substrate for SLC39A14. Specifically, mice have abnormally low Mn levels in the liver coupled with markedly elevated Mn concentrations in blood and most other organs, especially the brain and bone. Radiotracer studies using Mn reveal that mice have impaired Mn uptake by the liver and pancreas and reduced gastrointestinal Mn excretion. In the brain of mice, Mn accumulated in the pons and basal ganglia, including the globus pallidus, a region susceptible to Mn-related neurotoxicity. Brain Mn accumulation in mice was associated with locomotor impairments, as assessed by various behavioral tests. Although a low-Mn diet started at weaning was able to reverse brain Mn accumulation in mice, it did not correct their motor deficits. We conclude that SLC39A14 is essential for efficient Mn uptake by the liver and pancreas, and its deficiency results in impaired Mn excretion and accumulation of the metal in other tissues. The inability of Mn depletion to correct the motor deficits in mice suggests that the motor impairments represent lasting effects of early-life Mn exposure.

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mentioning

confidence: 99%

SLC39A14 deficiency alters manganese homeostasis and excretion resulting in brain manganese accumulation and motor deficits in mice

Jenkitkasemwong

Akinyode

Paulus

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

109

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“…Mitochondria require manganese for protection against oxidative stress by the mitochondrial SOD2, the main antioxidant enzyme in mitochondria 32 and localized exclusively in the mitochondrial matrix, 33 and possibly non-SOD manganese antioxidants. 34 Similar to iron, manganese has been suggested to be delivered to yeast mitochondria by a kiss-and-run type mechanism of temporary contact (or fusion) with vesicles containing Smf2p, 35 Figure 4. Immunodetection of DMT1 in mitochondria isolated from a rat renal cortical cell line.…”

Section: Dmt1 Is Well Known As An Fementioning

confidence: 99%

Mitochondria represent another locale for the divalent metal transporter 1 (DMT1)

et al. 2014

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“…[2] The reason for the considerable interest in Mn II -based CAs can be attributed primarily to their higher safety profiles compared with those of Gd III -based CAs; manganese is an essential element, and the organs of living systems possess efficient mechanisms to manage the in vivo levels of this ion. [3] However, to fulfil the requirements for in vivo applications, the Mn II complexes should be characterized by high thermodynamic stability, kinetic inertness, and large relaxivity values (the change in the longitudinal relaxation rate of water protons, R 1 = 1/T 1 , normalized to the concentration of the paramagnetic ion). In principle, Mn II ).…”

Section: Introductionmentioning

confidence: 99%

A Bisamide Derivative of [Mn(1,4‐DO2A)] – Solution Thermodynamic, Kinetic, and NMR Relaxometric Studies

et al. 2016

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Manganese Homeostasis and Transport

Cited by 71 publications

References 217 publications

SLC39A14 deficiency alters manganese homeostasis and excretion resulting in brain manganese accumulation and motor deficits in mice

SLC39A14 deficiency alters manganese homeostasis and excretion resulting in brain manganese accumulation and motor deficits in mice

Mitochondria represent another locale for the divalent metal transporter 1 (DMT1)

A Bisamide Derivative of [Mn(1,4‐DO2A)] – Solution Thermodynamic, Kinetic, and NMR Relaxometric Studies

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