In Vivo Inhibition of Serum Dopamine-β-Hydroxylase by CaNa2 EDTA injection

Paris, Paola De; Caroldi, Stefano

doi:10.1177/096032719401300405

Cited by 5 publications

(3 citation statements)

References 6 publications

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“…Consequently, compounds with Fe chelating properties or those interfering with the Fenton’s reaction, such as polyphenol compounds, can be of potential pharmacological importance in the treatment of Mn toxicity [194–196]. Indeed, the treatment with a calcium disodium salt of the chelator EDTA (CaNa 2 EDTA) reduced Mn-induced DA autooxidation in vitro [197], enhanced urinary excretion of Mn in humans [198] and reduced Mn levels in the brain and liver of Mn-exposed rats [199]. However, there is still controversy regarding the amelioration provided by this chelating therapy [200, 201].…”

Section: Main Textmentioning

confidence: 99%

“Manganese-induced neurotoxicity: a review of its behavioral consequences and neuroprotective strategies”

Peres

Schettinger

Chen

et al. 2016

BMC Pharmacol Toxicol

284

183

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Manganese (Mn) is an essential heavy metal. However, Mn’s nutritional aspects are paralleled by its role as a neurotoxicant upon excessive exposure. In this review, we covered recent advances in identifying mechanisms of Mn uptake and its molecular actions in the brain as well as promising neuroprotective strategies. The authors focused on reporting findings regarding Mn transport mechanisms, Mn effects on cholinergic system, behavioral alterations induced by Mn exposure and studies of neuroprotective strategies against Mn intoxication. We report that exposure to Mn may arise from environmental sources, occupational settings, food, total parenteral nutrition (TPN), methcathinone drug abuse or even genetic factors, such as mutation in the transporter SLC30A10. Accumulation of Mn occurs mainly in the basal ganglia and leads to a syndrome called manganism, whose symptoms of cognitive dysfunction and motor impairment resemble Parkinson’s disease (PD). Various neurotransmitter systems may be impaired due to Mn, especially dopaminergic, but also cholinergic and GABAergic. Several proteins have been identified to transport Mn, including divalent metal tranporter-1 (DMT-1), SLC30A10, transferrin and ferroportin and allow its accumulation in the central nervous system. Parallel to identification of Mn neurotoxic properties, neuroprotective strategies have been reported, and these include endogenous antioxidants (for instance, vitamin E), plant extracts (complex mixtures containing polyphenols and non-characterized components), iron chelating agents, precursors of glutathione (GSH), and synthetic compounds that can experimentally afford protection against Mn-induced neurotoxicity.

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Section: Main Textmentioning

confidence: 99%

“Manganese-induced neurotoxicity: a review of its behavioral consequences and neuroprotective strategies”

Peres

Schettinger

Chen

et al. 2016

BMC Pharmacol Toxicol

284

183

View full text Add to dashboard Cite

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“…Polyaminocarboxylic acids mobilize Mn from internal organs, enhance its excretion, and prevent mortality induced by MnCl 2 in poisoned animals (Rodier et al 1954; Tandon and Khandelwal 1982). CaNa 2 EDTA decreases liver and brain Mn levels in Mn-intoxicated rats (Kosai and Boyle 1956); it also decreases Mn-induced dopamine autoxidation in vitro (Nachtman et al 1987) and inhibits serum dopamine- β -hydroxylase in humans (De Paris and Caroldi 1994), potentially preserving dopamine levels. EDTA and CaNa 2 EDTA increase urinary Mn excretion in humans (Cook et al 1974; Discalzi et al 2000; Herrero Hernández et al 2006; Sata et al 1998) and have been used with dubious justification to “prevent” occupational manganism (Ritter and Marti-Feced 1960; Wynter 1962).…”

Section: Diagnosismentioning

confidence: 99%

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

et al. 2009

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The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147–154, 2007) and Bowman et al. (Metals and neurodegeneration, 2009).

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“…Proper use of its calcium disodium salt (CaNa 2 EDTA) by trained personnel on a hospital basis and careful examination of the patients, as well as cautious management of the administration dosage, schedule and procedures have demonstrated protection of renal function and tissue integrity in Mn-induced parkinsonism [ 170 ]. Furthermore, CaNa 2 EDTA treatment reduced Mn-induced dopamine autooxidation in vitro [ 171 ], enhanced urinary excretion of Mn in humans [ 172 ] and reduced Mn levels in the brain and liver of Mn-exposed rats [ 173 ]. Nevertheless, other studies involving Mn-induced parkinsonism patients with extremely high occupational exposures have reported lack of clinical amelioration [ 174 , 175 , 176 ] or relinquished clinical amelioration [ 177 ] upon CaNa 2 EDTA treatment.…”

Section: Preventive and Treatment Strategies For Mn-induced Parkimentioning

confidence: 99%

Manganese-Induced Parkinsonism and Parkinson’s Disease: Shared and Distinguishable Features

Kwakye

Paoliello

Mukhopadhyay

et al. 2015

IJERPH

283

188

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Manganese (Mn) is an essential trace element necessary for physiological processes that support development, growth and neuronal function. Secondary to elevated exposure or decreased excretion, Mn accumulates in the basal ganglia region of the brain and may cause a parkinsonian-like syndrome, referred to as manganism. The present review discusses the advances made in understanding the essentiality and neurotoxicity of Mn. We review occupational Mn-induced parkinsonism and the dynamic modes of Mn transport in biological systems, as well as the detection and pharmacokinetic modeling of Mn trafficking. In addition, we review some of the shared similarities, pathologic and clinical distinctions between Mn-induced parkinsonism and Parkinson’s disease. Where possible, we review the influence of Mn toxicity on dopamine, gamma aminobutyric acid (GABA), and glutamate neurotransmitter levels and function. We conclude with a survey of the preventive and treatment strategies for manganism and idiopathic Parkinson’s disease (PD).

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In Vivo Inhibition of Serum Dopamine-β-Hydroxylase by CaNa2 EDTA injection

Cited by 5 publications

References 6 publications

“Manganese-induced neurotoxicity: a review of its behavioral consequences and neuroprotective strategies”

“Manganese-induced neurotoxicity: a review of its behavioral consequences and neuroprotective strategies”

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

Manganese-Induced Parkinsonism and Parkinson’s Disease: Shared and Distinguishable Features

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