Manganese-Induced Hydroxyl Radical Formation in Rat Striatum Is Not Attenuated by Dopamine Depletion or Iron Chelationin Vivo

Sloot, W.N.; Korf, Jakob; Koster, J.F.; Wit, L. Elly A. de; Gramsbergen, Jan Bert

doi:10.1006/exnr.1996.0062

Cited by 48 publications

(28 citation statements)

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“…Other aftereffects of manganese intoxication include psychotic episodes, anxiety, liver cirrhosis, and so-called ''manganese madness'' (Tanaka and Lieben 1969;Cook et al 1974;Chandra et al 1981). It appears that manganese neurotoxicity is mediated by oxygen radicals (Donaldson 1987;Ali et al 1995;Sloot et al 1996), and that it is dependent on catecholamine oxidation (Archibald and Tyre 1987). The CNS of neonatal rats is more sensitive to manganese-induced neurotoxicity, as compared to adult rats, thus affecting receptor interaction and dopaminergic transmission (Kontur and Fechter 1998).…”

Section: Discussionmentioning

confidence: 96%

Ontogenetic Exposure of Rats to Pre- and Post-Natal Manganese Enhances Behavioral Impairments Produced by Perinatal 6-Hydroxydopamine

et al. 2010

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Rats lesioned shortly after birth with 6-hydroxydopamine (6-OHDA; 134 μg icv) represent a near-ideal model of severe Parkinson's disease because of the near-total destruction of nigrostriatal dopaminergic fibers. The element manganese, an essential cofactor for many enzymatic reactions, itself in toxic amount, replicates some clinical features similar to those of Parkinson's disease. The aim of this study was to examine the effect of neonatal manganese exposure on 6-OHDA modeling of Parkinson's disease in rats. Manganese (MnCl(2)·4H(2)O) 10,000 ppm was included in the drinking water of pregnant Wistar rats from the time of conception until the 21st day after delivery, the age when neonatal rats were weaned. Control rats consumed tap water. Other groups of neonatal rat pups, on the 3rd day after birth, were pretreated with desipramine (20 mg/kg ip 1 h) prior to bilateral icv administration of 6-OHDA (30, 60, or 137 μg) or its vehicle saline-ascorbic (0.1%) (control). At 2 months after birth, in rats lesioned with 30, 60, or 134 μg 6-OHDA, endogenous striatal dopamine (DA) content was reduced, respectively, by 66, 92, and 98% (HPLC/ED), while co-exposure of these groups to perinatal manganese did not magnify the DA depletion. However, there was prominent enhancement of DA D(1) agonist (i.e., SKF 38393)-induced oral activity in the group of rats exposed perinatally to manganese and also treated neonatally with the 30 mg/kg dose of 6-OHDA. The 30 mg/kg 6-OHDA group, demonstrating cataleptogenic responses to SCH 23390 (0.5 mg/kg) and haloperidol (0.5 mg/kg ip), developed resistance if co-exposed to perinatal manganese. In the group exposed to manganese and lesioned with the 60 mg/kg dose of 6-OHDA, there was a reduction in D(2) agonist (i.e., quinpirole, 0.1 mg/kg)-induced yawning. The series of findings demonstrate that ontogenetic exposure to manganese results in an enhancement of behavioral toxicity to a moderate dose of 6-OHDA, despite the fact that there is no enhanced depletion of striatal DA depletion by the manganese treatment.

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Section: Discussionmentioning

confidence: 96%

Ontogenetic Exposure of Rats to Pre- and Post-Natal Manganese Enhances Behavioral Impairments Produced by Perinatal 6-Hydroxydopamine

et al. 2010

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“…It appears that manganese neurotoxicity is mediated by oxygen radicals (Donaldson 1987;Ali et al 1995;Sloot et al 1996), and that it is dependent on catecholamine oxidation (Archibald and Tyre 1987). The CNS of neonatal rats is more sensitive to manganese-induced neurotoxicity, as compared to adult rats, thus affecting receptor interaction and dopaminergic transmission (Kontur and Fechter 1988).…”

Section: Discussionmentioning

confidence: 98%

Effect of Pre- and Postnatal Manganese Exposure on Brain Histamine Content in a Rodent Model of Parkinson’s Disease

et al. 2011

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Rats lesioned shortly after birth with 6-hydroxydopamine (6-OHDA; 134 μg icv) represent a near-ideal model of severe Parkinson's disease because of the near-total destruction of nigrostriatal dopaminergic fibers. There are scarce data that in Parkinson's disease, activity of the central histaminergic system is increased. The element manganese, an essential cofactor for many enzymatic reactions, itself in toxic amount, replicates some clinical features similar to those of Parkinson's disease. The aim of this study was to examine the effect of neonatal manganese exposure on 6-OHDA modeling of Parkinson's disease in rats, and to determine effects on histamine content in the brain of these rats in adulthood. Manganese (MnCl₂·4H₂O; 10,000 ppm) was included in the drinking water of pregnant Wistar rats from the time of conception until the 21st day after delivery, the age when neonatal rats were weaned. Control rats consumed tap water. Other groups of neonatal rat pups, on the 3rd day after birth, were pretreated with desipramine (20 mg/kg ip 1 h) prior to bilateral icv administration of 6-OHDA (60 or 134 μg) or its vehicle saline-ascorbic (0.1%) (control). At 2 months after birth, in rats lesioned with 60 or 134 μg 6-OHDA, endogenous striatal dopamine (DA) content was reduced, respectively, by 92 and 98% (HPLC/ED), while co-exposure of these groups to perinatal manganese did not magnify the DA depletion. However, there was prominent enhancement of histamine content in frontal cortex, hippocampus, hypothalamus, and medulla oblongata of adult rat brain after 6-OHDA (60 and 134 μg) injection on the day 3rd postnatal day. These findings indicate that histamine and the central histaminergic system are altered in the brain of rats lesioned to model Parkinson's disease, and that manganese enhances effects of 6-OHDA on histamine in brain.

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“…Oxidative stress is one of many factors implicated in Mninduced neurotoxicity (Aschner, 1997). Dopamine oxidation by Mn is a potential mechanism for Mn-induced oxidative stress, especially since Mn preferentially accumulates in dopamine-rich brain regions (e.g., basal ganglia) (Sloot et al, 1996). It has also been suggested given its sequestration by mitochondria, Mn interferes with proper respiration, thereby leading to excessive production of reactive oxygen species (ROS).…”

Section: The Essentiality Of Manganesementioning

confidence: 99%

Nutritional aspects of manganese homeostasis

Aschner

2005

Molecular Aspects of Medicine

767

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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Manganese-Induced Hydroxyl Radical Formation in Rat Striatum Is Not Attenuated by Dopamine Depletion or Iron Chelationin Vivo

Cited by 48 publications

References 50 publications

Ontogenetic Exposure of Rats to Pre- and Post-Natal Manganese Enhances Behavioral Impairments Produced by Perinatal 6-Hydroxydopamine

Ontogenetic Exposure of Rats to Pre- and Post-Natal Manganese Enhances Behavioral Impairments Produced by Perinatal 6-Hydroxydopamine

Effect of Pre- and Postnatal Manganese Exposure on Brain Histamine Content in a Rodent Model of Parkinson’s Disease

Nutritional aspects of manganese homeostasis

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