Topographical distribution of arsenic, manganese, and selenium in the normal human brain

Larsen, N. Agersnap; Pakkenberg, H.; Damsgaard, Else Marie; Heydorn, Κ.

doi:10.1016/0022-510x(79)90173-4

Cited by 79 publications

(18 citation statements)

References 19 publications

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“…We recommended MRI examination of the brain for these reasons: postoperative cholestasis or reflux cholangitis may occur after pancreatoduodenectomy, and Mn is cleared by the liver and excreted into bile [15]. After informed consent was obtained from the patient, MRI examination and determination of the blood Mn level were performed.…”

Section: Resultsmentioning

confidence: 99%

“…When Mn is administered parenterally, however (i.e., by an intravenous, inhalational, or intraperitoneal route), these regulatory mechanisms may be bypassed, allowing excessive absorption and tissue deposition of Mn [9]. Ninety-eight percent of the Mn absorbed is cleared by the liver and excreted into bile [15]. Biliary excretion occurs against a concentration gradient [33] and bile duct obstruction causes marked impairment of Mn elimination [34,35].…”

Section: Discussionmentioning

confidence: 99%

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Hyperintense Basal Ganglia on T1-Weighted Magnetic Resonance Images following Postoperative Parenteral Nutrition in a Pancreatoduodenectomized Patient

Iwase¹,

Kondoh²,

Higaki³

et al. 2000

Dig Surg

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hyperintense Basal Ganglia on T1-Weighted Magnetic Resonance Images following Postoperative Parenteral Nutrition in a Pancreatoduodenectomized Patient

Iwase¹,

Kondoh²,

Higaki³

et al. 2000

Dig Surg

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“…Manganese is known to accumulate in the globus pallidus and caudate nucleus, two areas highly susceptible to HD neurodegeneration. 45,46 This accumulation may highlight a specific necessity of manganese for proper function, and may also make these brain areas more susceptible to fluctuations in manganese levels.…”

Section: Manganese and Hdmentioning

confidence: 97%

Manganese and Huntington Disease

Tidball¹,

Bichell²,

Bowman³

2014

Manganese in Health and Disease

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Huntington's disease (HD) is a devastating neurodegenerative disease presenting with impaired movement, psychological and behavioral disturbances, and cognitive decline. The most pronounced symptoms are motor impairments caused by degeneration of the medium spiny neurons of the caudate and putamen. Heavy metals are closely linked with both function and dysfunction in these basal ganglia nuclei, and are, therefore, likely candidates to be the environmental modifiers for age of onset in HD. HD patient cortices and mouse in vitro and in vivo models of HD have shown decreases in accumulation of manganese (Mn2+). Manganese is a necessary cofactor for several enzymes vital to proper cellular functioning, including arginase, manganese superoxide dismutase, glutamine synthetase, and pyruvate carboxylase. Additionally, manganese has also been shown to alter cellular signaling, particularly in the IGF–AKT and ATM–p53 pathways. Manganese deficiency can result in many dysfunctional manifestations similar to Huntington's disease, including urea cycle dysfunction, altered glutamate regulation, increased oxidative stress, and metabolic disturbances, in which these enzymatic functions are crucial. In this chapter, we elaborate on the potential influence of manganese and other metals in Huntington's disease; we also investigate the potential role of manganese-dependent enzymes in HD pathophysiology.

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“…Although other physicochemical studies have shown that this brain region grossly contains large quantities of Fe 3+, Cu 2+, and Mn 2+ (Warren et al, 1960;Cumings, 1968;Earle, 1968;Larsen et al, 1979;Sofic et al, 1988;Dexter et al, 1989Dexter et al, , 1991Riederer et al, 1989;Uitti et al, 1989;Hirsch et al, 1991), histochemical studies have suggested that the metal ions are localized to storage granules within glial cells and are not endogenous to neuromelanin granules in neurons (Barden, 1971;Hill and Switzer, 1984;Connor et al, 1990;Jellinger et al, 1990;Sofic et al, 1991). However, our data have been confirmed recently by other sophisticated physicochemical techniques (Swartz et al, 1992;Perl and Good, 1992;Jellinger et al, 1992), indicating that histochemical staining reactions for metal ions may not be reliable when the ions are bound to melanin.…”

Section: Nature Of Neuromelaninmentioning

confidence: 99%

The roles of neuromelanin, binding of metal ions, and oxidative cytotoxicity in the pathogenesis of Parkinson's disease: A hypothesis

Enochs

Sarna²,

Zecca

et al. 1994

J Neural Transm Gen Sect

109

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A characteristic feature of both Parkinson's disease (idiopathic paralysis agitans) and normal aging is loss of pigmented neurons in the substantia nigra. This has been found to correlate with the accumulation of neuromelanin and with oxidative stress in this brain region, but a clear association between these factors has not been established. Based on our recent demonstration that neuromelanin is a true melanin, containing bound metal ions in situ, we present a general model for its accumulation in vivo and the hypotheses (1) that it has a cytoprotective function in the sequestration of redox-active metal ions under normal conditions but (2) that it has a cytotoxic role in the pathogenesis of Parkinson's disease. Thus, neuromelanin accumulates normally through the autooxidation of catecholamines and serves tightly to bind redox-active metal ions, processes which would accelerate under conditions of intracellular or extracellular oxidative stress. Based on the known properties of melanin, however, neuromelanin also has the potential for exacerbating oxidative stress, eg by generating H2O2 when it is intact or by releasing redox-active metal ions if it loses its integrity; these reactions also would modulate the reactivity of the neuromelanin. By overwhelming intracellular antioxidative defense mechanisms, such a positive-feedback cycle could turn a condition of chronic or repeated oxidative stress in vulnerable neurons into an acute crisis, leading to cellular death. If the cumulative stress in duration and/or degree is severe enough, neuronal depletion could be sufficient to cause Parkinson's disease during life. One possible trigger for this cascade is suggested by the increased nigral iron contents in postmortem parkinsonian brains and the correlation of this disease with urban living where exposure to heavy metal ions is high: the saturation of neuromelanin with redox-active metal ions. Parkinson's disease therefore may be a form of accelerated aging in the substantia nigra associated with environmental toxins in which neuromelanin has a central, active role.

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Topographical distribution of arsenic, manganese, and selenium in the normal human brain

Cited by 79 publications

References 19 publications

Hyperintense Basal Ganglia on T1-Weighted Magnetic Resonance Images following Postoperative Parenteral Nutrition in a Pancreatoduodenectomized Patient

Hyperintense Basal Ganglia on T1-Weighted Magnetic Resonance Images following Postoperative Parenteral Nutrition in a Pancreatoduodenectomized Patient

Manganese and Huntington Disease

The roles of neuromelanin, binding of metal ions, and oxidative cytotoxicity in the pathogenesis of Parkinson's disease: A hypothesis

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