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Talavera, Enrique; Arcaya, José-Luis; Giraldoth, Debora; Suárez, Jacqueline; Bonilla, Ernesto

doi:10.1023/a:1021064711866

Cited by 20 publications

(2 citation statements)

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“…Although manganese (Mn) is an essential transition metal (Anderson et al 2008; Erikson et al 2007; Talavera et al 1999), exposure to excessive Mn levels in either occupational or environmental settings may cause neurological dysfunction of the basal ganglia (Aschner et al 2009; Kinawy 2009; Takeda 2003). The major neurological disorder caused by excessive Mn exposure, manganism, consists of many symptoms that are similar to Parkinson’s disease (PD), i.e., postural instability, rigidity, and speech disturbances (Cersosimo and Koller 2006; Lucchini et al 2009; Pal et al 1999; Rajput et al 1991).…”

Section: Introductionmentioning

confidence: 99%

Brain deposition and neurotoxicity of manganese in adult mice exposed via the drinking water

et al. 2013

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Natural leaching processes and/or anthropogenic contamination can result in ground water concentrations of the essential metal manganese (Mn) that far exceed the current regulatory standards. Neurological consequences of Mn drinking water (DW) overexposure to experimental animals, i.e. mice, including its brain deposition/distribution and behavioral effects are understudied. Adult male C57BL/6 mice were exposed to Mn via the DW for 8 weeks. After 5 weeks of Mn exposure, magnetic resonance imaging revealed significant Mn deposition in all examined brain regions; the degree of Mn deposition did not increase further a week later. Behaviorally, early hyperactivity and more time spent in the center of the arenas in an open field test, decreased forelimb grip strength and less time swimming in a forced swim test were observed after 6 weeks of Mn DW exposure. Eight-week Mn DW exposure did not alter striatal dopamine, its metabolites, or the expression of key dopamine homeostatic proteins, but it significantly increased striatal 5-hydroxyindoleacetic acid (a serotonin metabolite) level, without affecting the levels of serotonin itself. Increased expression (mRNA) of glial fibrillary acidic protein (GFAP, an astrocyte activation marker), heme oxygenase-1 and inducible nitric oxide synthase (oxidative and nitrosative stress markers, respectively) were observed 8 weeks post Mn DW exposure in the substantia nigra. Besides mRNA increases, GFAP protein expression was increased in the substantia nigra pars reticulata. In summary, the neurobehavioral deficits, characterized by locomotor and emotional perturbations, and nigral glial activation associated with significant brain Mn deposition are among the early signs of Mn neurotoxicity caused by DW overexposure.

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Section: Introductionmentioning

confidence: 99%

Brain deposition and neurotoxicity of manganese in adult mice exposed via the drinking water

et al. 2013

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“…and neurobehavioral changes induced by Mn could be The neurotoxicity of Mn has been reproduced and correlated with the differential accumulation of the characterized in various animal species including metal in different regions of the brain [6,20]. Plasma, mainly rats and mice [4][5][6][7][8] with few studies in the bone and tissue levels of Mn are additionally used as avian species [9,10]. The neurobehavioral effects of diagnostic or biomarker endpoints of exposure [21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Single intramuscular dose toxicokinetics of manganese in broiler chicks

Al-Zubaidy¹,

Mohammad²

2012

Vet. World

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Aim: Manganese (Mn) produces neurobehavioral toxicity in various animal species including the young chicks. The present study examines toxicokinetics of Mn in 7-10-day old chicks after an intramuscular injection at 20 mg/kg. Materials and Methods: Samples of the blood, whole brain, liver and kidney were obtained from chicks (5/each time period) at 0 time (base-line) and then at times between 0.17 to 4 h. The concentrations of Mn in the plasma and tissues were determined by atomic absorption spectrometry. Toxicokinetic parameters of Mn were calculated from the mean metal concentrations in the plasma by a non-compartmental analysis using a Windows-based computer program. Results: Injection of Mn significantly increased the metal levels in the plasma, whole brain, liver and kidney of the chicks when compared to respective base-line control values at times 0.17 to 4 h after the injection (with the exception at 2 and 4 h in the brain). The highest concentration of Mn in the plasma and the whole brain appeared one h after the injection, whereas those of the liver and kidney appeared 4 h post-injection. The concentrations of Mn in the plasma ranged between 0.43 to 1.2 µg/ml within 0.17 to 4 h. Those of the whole brain, liver and kidney were 0.11-0.46, 6.3-15 and 5.3-22.9 µg/g, respectively. The elimination half-life of Mn was 3.02 h with steady state volume of distribution 24.34 L/kg and total body clearances of 4.78 L/h/kg. The mean residence time of Mn was 5.09 h and its area under the plasma concentration-time curve (0-) was 4.18 µg.h/ml. The elimination half-life of Mn from the brain was 3.12 h with an elimination rate constant of 0.22 h-1. Conclusion: The data suggest that Mn is well absorbed and rapidly distributed after an intramuscular administration in chicks and further support the reported neurobehavioral toxic effects of the metal which are observed within one h after treatment.

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