Interactions Between Manganese and Brain Dopamine

Cotzias, George C.; Miller, Samuel T.; Papavasiliou, Paul S.; Tang, Lei-Han

doi:10.1016/s0025-7125(16)31856-9

Cited by 56 publications

(22 citation statements)

References 24 publications

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“…Biliary excretion is poorly developed in neonatal animals, and exposure during this period may result in increased delivery of Mn into the brain and other tissues. In mice, rats, and kittens, there is an almost complete absence of biliary Mn excretion during the neonatal period (Cotzias et al, 1976). Pancreatic excretion of Mn contributes only a small fraction of the absorbed Mn dose (Davis et al, 1993).…”

Section: The Absorption Distribution and Elimination Of Oral Manganesementioning

confidence: 99%

Nutritional aspects of manganese homeostasis

Aschner

2005

Molecular Aspects of Medicine

747

555

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Manganese (Mn) is an essential mineral. It is present in virtually all diets at low concentrations. The principal route of intake for Mn is via food consumption, but in occupational cohorts, inhalation exposure may also occur (this subject will not be dealt with in this review). Humans maintain stable tissue levels of Mn. This is achieved via tight homeostatic control of both absorption and excretion. Nevertheless, it is well established that exposure to high oral, parenteral or ambient air concentrations of Mn can result in elevations in tissue Mn levels. Excessive Mn accumulation in the central nervous system (CNS) is an established clinical entity, referred to as manganism. It resembles idiopathic Parkinson's disease (IPD) in its clinical features, resulting in adverse neurological effects both in laboratory animals and humans. This review focuses on an area that to date has received little consideration, namely the potential exposure of parenterally fed neonates to exceedingly high Mn concentrations in parenteral nutrition solutions, potentially increasing their risk for Mn-induced adverse health sequelae. The review will consider (1) the essentiality of Mn; (2) the concentration ranges, means and variation of Mn in various foods and infant formulas; (3) the absorption, distribution, and elimination of Mn after oral exposure and (4) the factors that raise a theoretical concern that neonates receiving total parenteral nutrition (TPN) are exposed to excessive dietary Mn.

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Section: The Absorption Distribution and Elimination Of Oral Manganesementioning

confidence: 99%

Nutritional aspects of manganese homeostasis

Aschner

2005

Molecular Aspects of Medicine

747

555

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“…However, it was evident that significant stimulatory effects already occurred at levels as low as 0.1 mM. Mn 2ϩ is an important element biologically and has been shown to be essential to the activity of a number of enzymes in a variety of organisms (12,38,39). For example, it is central to the function of superoxide dismutase, an enzyme that protects against oxidative damage in tissues (12,8).…”

Section: Physiological Relevance Of the Stimulation Of Sulfating Actimentioning

confidence: 99%

Manganese Stimulation and Stereospecificity of the Dopa (3,4-Dihydroxyphenylalanine)/Tyrosine-sulfating Activity of Human Monoamine-form Phenol Sulfotransferase

Pai

Ohkimoto

Sakakibara

et al. 2002

Journal of Biological Chemistry

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“…Decreased striatal dopamine has historically been considered a hallmark neurochemical outcome of Mn neurotoxicity (Cotzias et al, 1976), based in part on the similarities in motor symptoms between Manganism and Parkinson's disease. However, recent studies have indicated that GABAergic nuclei of the basal ganglia such as the globus pallidus and the striatum may be early, more sensitive targets of Mn (Wolters et al, 1989;Spadoni et al, 2000;Gwiazda et al, 2002;Kim et al, 2005;Liu et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Low-level manganese exposure alters glutamate metabolism in GABAergic AF5 cells

2007

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Recent studies have suggested that the globus pallidus may be a particularly sensitive target of manganese (Mn), however, in vitro studies of the effects of Mn on GABAergic neurons have been restricted by the lack of a cell model expressing GABAergic properties. Here we investigated the effects of low-level Mn treatment on cellular GABA and glutamate metabolism using the newly characterized AF5 rat neural-derived cell line, which displays GABAergic properties during culture in vitro. Intracellular GABA and glutamate levels were measured along with measurement of the release of GABA and glutamate into the culture medium, glutamine uptake from the culture medium, and the specific effects of Mn on the enzymes directly responsible for the synthesis and degradation of GABA, glutamate decarboxylase (GAD) and GABA transaminase (GABA-T). Our results demonstrate that Mn had no effect on the activities of GAD or GABA-T. Similarly, low-level Mn treatment of AF5 cultures had only a small effect on intracellular GABA levels (114% of control) and no effect on the release of GABA. In contrast, intracellular and extracellular glutamate levels were enhanced to 170% and 198% of control during Mn treatment, respectively, while extracellular glutamine decreased to 73% of controls. Together, these results suggest that glutamate homeostasis may be preferentially affected over GABA in AF5 cells during low-level Mn treatment, suggesting a novel mechanism by which Mn-induced excitotoxicity might arise.

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Interactions Between Manganese and Brain Dopamine

Cited by 56 publications

References 24 publications

Nutritional aspects of manganese homeostasis

Nutritional aspects of manganese homeostasis

Manganese Stimulation and Stereospecificity of the Dopa (3,4-Dihydroxyphenylalanine)/Tyrosine-sulfating Activity of Human Monoamine-form Phenol Sulfotransferase

Low-level manganese exposure alters glutamate metabolism in GABAergic AF5 cells

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