Articles: manganese.
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Sci. Total Environ. · Jun 2013
Review Meta AnalysisAssociation of arsenic, cadmium and manganese exposure with neurodevelopment and behavioural disorders in children: a systematic review and meta-analysis.
The aim of this study was to analyse the scientific evidence published to date on the potential effects on neurodevelopment and behavioural disorders in children exposed to arsenic, cadmium and manganese and to quantify the magnitude of the effect on neurodevelopment by pooling the results of the different studies. We conducted a systematic review of original articles from January 2000 until March 2012, that evaluate the effects on neurodevelopment and behavioural disorders due to pre or post natal exposure to arsenic, cadmium and manganese in children up to 16 years of age. We also conducted a meta-analysis assessing the effects of exposure to arsenic and manganese on neurodevelopment. ⋯ Moreover a 50% increase of manganese levels in hair would be associated with a decrease of 0.7 points in the IQ of children aged 6-13 years. There is evidence that relates arsenic and manganese exposure with neurodevelopmental problems in children, but there is little information on cadmium exposure. Few studies have evaluated behavioural disorders due to exposure to these compounds, and manganese is the only one for which there is more evidence of the existence of association with attention deficit disorder with hyperactivity.
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Review
Manganese toxicity in the central nervous system: the glutamine/glutamate-γ-aminobutyric acid cycle.
Manganese (Mn) is an essential trace element that is required for maintaining proper function and regulation of numerous biochemical and cellular reactions. Despite its essentiality, at excessive levels Mn is toxic to the central nervous system (CNS). ⋯ Its toxicity is associated with disruption of the glutamine (Gln)/glutamate (Glu)-γ-aminobutyric acid (GABA) cycle (GGC) between astrocytes and neurons, thus leading to changes in Glu-ergic and/or GABAergic transmission and Gln metabolism. Here we discuss the common mechanisms underlying Mn-induced neurotoxicity and their relationship to CNS pathology and GGC impairment.
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To comparatively evaluate the efficiency of preventive treatment with various iron preparations on copper, manganese, and iron metabolic features in adult athletes. ⋯ Dietary addition of foods containing large amounts of ferrous iron, copper, and manganese is indicated for athletes exposed to higher intensity exercises.
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Circ Cardiovasc Imaging · Sep 2011
Comparative StudyDual manganese-enhanced and delayed gadolinium-enhanced MRI detects myocardial border zone injury in a pig ischemia-reperfusion model.
Gadolinium (Gd)-based delayed-enhancement MRI (DEMRI) identifies nonviable myocardium but is nonspecific and may overestimate nonviable territory. Manganese (Mn(2+))-enhanced MRI (MEMRI) denotes specific Mn(2+) uptake into viable cardiomyocytes. We performed a dual-contrast myocardial assessment in a porcine ischemia-reperfusion (IR) model to test the hypothesis that combined DEMRI and MEMRI identifies viable infarct border zone (BZ) myocardium in vivo. ⋯ The dual-contrast MEMRI-DEMRI detects BZ viability within DEMRI infarct zones. This approach may identify injured, at-risk myocardium in ischemic cardiomyopathy.
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Noise exposure at high intensities leads to a temporary shift of hearing thresholds (TTS) and is followed by a permanent threshold shift (PTS). Permanent threshold shift is not only associated with cochlear damage as the primary site-of-lesion, but also with subsequent structural and functional changes within the central auditory pathway. The aim of the present study was to monitor neuronal activity within central auditory structures in mice after noise exposure at different time intervals using manganese-enhanced magnetic resonance imaging (MEMRI). ⋯ Sustained manganese accumulation was present in the auditory brainstem after moderate acoustic stimulation as well without PTS induction. The long-lasting enhancement of MEMRI signals suggests a noise-induced activity increase of various calcium-dependent processes of different origin (such as neuroprotective mechanisms). The present findings could be helpful to better understand the time-course of different symptoms in NIHL and the individual susceptibility to noise.