Retention and distribution of manganese in the mouse brain following acute exposure on postnatal day 0, 7, 14 or 42: An autoradiographic and gamma counting study

Valois, Angelo A.; Webster, William S.

doi:10.1016/0300-483x(89)90119-4

Cited by 14 publications

(12 citation statements)

References 21 publications

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“…A higher accumulation of Mn is observed in CPs from neonatal animals, as compared to adult animals. This is in agreement with the developmental decrease in the intensity of the signal observed in the CPs by qualitative autoradiography following acute exposure to the metal (Valois and Webster 1989). Given the toxicological consequences of CP over‐exposure to Mn (see below), and the particular importance of the neuroprotective and trophic properties attributed to the CPs in the developing brain (Strazielle and Ghersi‐Egea 2000; Johansson et al.…”

Section: Discussionsupporting

confidence: 89%

“…Earlier work had shown that in vivo exposure to Mn leads to a preferential accumulation of this metal into the choroidal tissue (Valois and Webster 1989; Rabin et al. 1993; Ingersoll et al.…”

Section: Discussionmentioning

confidence: 99%

“…Earlier work had shown that in vivo exposure to Mn leads to a preferential accumulation of this metal into the choroidal tissue (Valois and Webster 1989;Rabin et al 1993;Ingersoll et al 1995). Part of the blood-borne Mn circulates as a non protein-bound divalent species (Rabin et al 1993;Crossgrove et al 2003).…”

Section: Discussionmentioning

confidence: 99%

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Active transport at the blood-CSF barrier contributes to manganese influx into the brain

Schmitt

Strazielle

Richaud

et al. 2011

Journal of Neurochemistry

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J. Neurochem. (2011) 117, 747–756. Abstract Manganese is an essential trace element, and a contrast agent of potential interest for brain magnetic resonance imaging. Brain overexposure to manganese, however induces a neurodegenerative syndrome. Imaging data suggest that manganese appearance into the CSF precedes its accumulation into the cerebral parenchyma. We therefore investigated manganese uptake and transport at the blood‐CSF barrier. Like lead, the non protein‐bound divalent manganese accumulated into the rat choroid plexus. The metal accumulation was especially high in developing animals. Using a differentiated cellular model of the blood‐CSF barrier, we demonstrated that manganese crosses the choroid plexus epithelium by a concentrating, unidirectional blood‐to‐CSF transport mechanism. This transport was inhibited by calcium, which is also transported into the CSF against its concentration gradient. The permeability barrier function towards lipid‐insoluble compound and the organic anion transport property of the blood‐brain interface were affected by exposure of the blood‐facing membrane of choroidal cells to micromolar concentrations of manganese, but its antioxidant capacity was not. The unidirectional transport of manganese across the choroid plexus provides the anatomo‐functional basis linking the systemic exposure to manganese with the spreading pattern of manganese accumulation observed in brain imaging, and explains the polarized sensitivity of choroidal epithelial cells to manganese toxicity.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

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Active transport at the blood-CSF barrier contributes to manganese influx into the brain

Schmitt

Strazielle

Richaud

et al. 2011

Journal of Neurochemistry

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“…The lack of any significant Mn 2+ leakage out of the cells after removal of the MnCl 2 and washing of the cells implies a relatively slow rate of Mn 2+ efflux out of the cells, similar to what has been reported in neuronal tissues [23], [49].…”

Section: Discussionsupporting

confidence: 82%

Human Tumor Cell Proliferation Evaluated Using Manganese-Enhanced MRI

et al. 2012

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BackgroundTumor cell proliferation can depend on calcium entry across the cell membrane. As a first step toward the development of a non-invasive test of the extent of tumor cell proliferation in vivo, we tested the hypothesis that tumor cell uptake of a calcium surrogate, Mn2+ [measured with manganese-enhanced MRI (MEMRI)], is linked to proliferation rate in vitro.Methodology/Principal FindingsProliferation rates were determined in vitro in three different human tumor cell lines: C918 and OCM-1 human uveal melanomas and PC-3 prostate carcinoma. Cells growing at different average proliferation rates were exposed to 1 mM MnCl2 for one hour and then thoroughly washed. MEMRI R1 values (longitudinal relaxation rates), which have a positive linear relationship with Mn2+ concentration, were then determined from cell pellets. Cell cycle distributions were determined using propidium iodide staining and flow cytometry. All three lines showed Mn2+-induced increases in R1 compared to cells not exposed to Mn2+. C918 and PC-3 cells each showed a significant, positive correlation between MEMRI R1 values and proliferation rate (p≤0.005), while OCM-1 cells showed no significant correlation. Preliminary, general modeling of these positive relationships suggested that pellet R1 for the PC-3 cells, but not for the C918 cells, could be adequately described by simply accounting for changes in the distribution of the cell cycle-dependent subpopulations in the pellet.Conclusions/SignificanceThese data clearly demonstrate the tumor-cell dependent nature of the relationship between proliferation and calcium influx, and underscore the usefulness of MEMRI as a non-invasive method for investigating this link. MEMRI is applicable to study tumors in vivo, and the present results raise the possibility of evaluating proliferation parameters of some tumor types in vivo using MEMRI.

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“…However, Mn does enter the brain, as numerous studies show that brain [Mn] increases after oral or systemic administration of the metal (Chandra et al, 1979;Autissier et al, 1982;Gianutsos et al, 1985;Kabata et al, 1989). Preliminary investigations of brain uptake using 54Mn or nuclear magnetic resonance spectroscopy demonstrate localization of Mn to specific areas of the CNS (London et al, 1989;Newland et al, 1989;Valois and Webster, 1989) and dependence of Mn uptake on Fe status (Mena, 1974;Aschner and Aschner, 1990). These findings imply that Mn moves across the blood-brain barrier and that this movement competes with Fe.…”

mentioning

confidence: 99%

Saturable Transport of Manganese(II) Across the Rat Blood‐Brain Barrier

Murphy¹,

Wadhwani²,

Smith³

et al. 1991

Journal of Neurochemistry

139

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Unanesthetized adult male rats were infused intravenously with solutions containing 54Mn (II) and one of six concentrations of stable Mn(II). The infusion was timed to produce a near constant [Mn] in plasma for up to 20 min. Plasma was collected serially and on termination of the experiment, samples of CSF, eight brain regions, and choroid plexus (CP) were obtained. Influx of Mn (JMn) was calculated from uptake of 54Mn into tissues and CSF at two different times. Plasma [Mn] was varied 1,000-fold (0.076-78 nmol/ml). Over this plasma concentration range, JMn increased 123 times into CP, 18-120 times into brain, and 706 times into CSF. CP and brain JMn values fit saturation kinetics with Km (nmol/ml) equal to 15 for CP and 0.7-2.1 for brain, and Vmax (10(-2) nmol.g-1.s-1) of 27 for CP and 0.025-0.054 for brain. Brain JMn except at cerebral cortex had a nonsaturable component. CSF JMn varied linearly with plasma [Mn]. These findings suggest that Mn transport into brain and CP is saturable, but transport into CSF is nonsaturable.

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Retention and distribution of manganese in the mouse brain following acute exposure on postnatal day 0, 7, 14 or 42: An autoradiographic and gamma counting study

Cited by 14 publications

References 21 publications

Active transport at the blood-CSF barrier contributes to manganese influx into the brain

Active transport at the blood-CSF barrier contributes to manganese influx into the brain

Human Tumor Cell Proliferation Evaluated Using Manganese-Enhanced MRI

Saturable Transport of Manganese(II) Across the Rat Blood‐Brain Barrier

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