Modeling the environmental fate of manganese from methylcyclopentadienyl manganese tricarbonyl in urban landscapes

Bhuie, A.K.; Ogunseitan, Oladele A.; White, Rodney R.; Sain, M.; Roy, D. N.

doi:10.1016/j.scitotenv.2004.06.012

Cited by 13 publications

(6 citation statements)

References 13 publications

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“…Mn poisoning, or manganism, typically occurs from occupational exposures in industrial settings, such as in welding, where Mn-containing fumes and/or products are abundant 10, 11 . Mn is also found as an antiknock agent methylcyclopentadienyl manganese tricarbonyl (MMT) in gasoline, but limited studies currently exist on the impact of Mn release from combustion on general human health 12, 13 . Certain pesticides also contain Mn, making surface runoff from these agricultural uses an additional source of overexposure 1 .…”

Section: Introductionmentioning

confidence: 99%

“…10,11 Mn is also found in the antiknock agent methylcyclopentadienyl manganese tricarbonyl (MMT) in gasoline, but limited studies currently exist on the impact of Mn release from combustion on general human health. 12,13 Certain pesticides also contain Mn, making surface runoff from these agricultural uses an additional source of overexposure. 1 Moreover, Mn toxicity can also affect other susceptible populations, including ill neonates receiving total parenteral nutrition (TPN) that is supplemented with a trace element solution containing Mn.…”

Section: Introductionmentioning

confidence: 99%

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Loss of pdr-1/parkin influences Mn homeostasis through altered ferroportin expression in C. elegans

et al. 2015

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Overexposure to the essential metal manganese (Mn) can result in an irreversible condition known as manganism that shares similar pathophysiology with Parkinson's disease (PD), including dopaminergic (DAergic) cell loss that leads to motor and cognitive impairments. However, the mechanisms behind this neurotoxicity and its relationship with PD remain unclear. Many genes confer risk for autosomal recessive, early-onset PD, including the parkin/PARK2 gene that encodes for the E3 ubiquitin ligase Parkin. Using Caenorhabditis elegans (C. elegans) as an invertebrate model that conserves the DAergic system, we previously reported significantly increased Mn accumulation in pdr-1/parkin mutants compared to wildtype (WT) animals. For the current study, we hypothesize that this enhanced accumulation is due to alterations in Mn transport in the pdr-1 mutants. While no change in mRNA expression of the major Mn importer proteins (smf-1-3) was found in pdr-1 mutants, significant downregulation in mRNA levels of the putative Mn exporter ferroportin (fpn-1.1) was observed. Using a strain overexpressing fpn-1.1 in worms lacking pdr-1, we show evidence for attenuation of several endpoints of Mn-induced toxicity, including survival, metal accumulation, mitochondrial copy number and DAergic integrity, compared to pdr-1 mutants alone. These changes suggest a novel role of pdr-1 in modulating Mn export through altered transporter expression, and provides further support of metal dyshomeostasis as a component of Parkinsonism pathophysiology.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Loss of pdr-1/parkin influences Mn homeostasis through altered ferroportin expression in C. elegans

et al. 2015

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“…Pure Mn does not occur naturally, but is a component of more than 100 minerals formed when Mn combines with other substances such as oxygen, sulfur, and chlorine. Mn compounds can change naturally or artificially from one compound to another, but the metal is generally stable in the environment [ 4 , 5 , 6 ]. Exposure to Mn can occur through inhalation or ingestion, but for most people, exposure to Mn is usually through diet because Mn is present in many foods, including tea, grains and cereals, and in drinking water [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Metallic Burden of Deciduous Teeth and Childhood Behavioral Deficits

Chan

Gutiérrez

Ogunseitan

2015

IJERPH

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Attention Deficit/Hyperactivity Disorder (ADHD) affects 5%–8% of children in the U.S. (10% of males and 4% of females). The contributions of multiple metal exposures to the childhood behavioral deficits are unclear, although particular metals have been implicated through their neurotoxicity. The objective of this study was to test the hypothesis that the body burden of Mn is positively correlated with ADHD symptoms. We also investigated the putative roles of Ca, Fe, Pb, and Hg. We collected shed molars from 266 children (138 boys and 128 girls) who lost a tooth between 11 and 13 years of age. The molars were analyzed for metals using ICP-OES. The third grade teacher of each child completed the Teacher’s Disruptive Behavior Disorders Rating Scale (DBD) to produce a score for “Total Disruptive Behavior” and subscale scores for “Attention Deficit Hyperactivity Disorder”, Hyperactivity/Impulsivity, Inattention, and Oppositional/Defiant. The mean Mn, Fe, Pb and Ca concentrations found in teeth was 3.1 ± 2.9 µg/g, 11.4 ± 12.1 µg/g, 0.5 ± 0.7 µg/g, and 3.0 × 105 ± 0.8 × 105 µg/g, respectively. Hg was not detected. No significant association was found between Mn and behavioral deficits. Ca was significantly negatively associated, and Pb showed a significant positive association with Hyperactivity/Impulsivity, Inattention, and Oppositional/Defiant Disorders. These findings call into question the putative independent association of manganese exposure and behavioral deficits in children, when the balance of other metallic burden, particularly Ca and Pb burdens play significant roles.

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“…During heavy rain and storm events, the concentration of metals entering into the watershed routinely exceeds the TMDL limits (8). Although metal TMDL for manganese in the watershed has not been established, manganese, like cadmium and lead, is a potentially toxic metal with demonstrated adverse effects on humans and aquatic life (9,10). Furthermore, Gonzales-Chavez et al (5).…”

Section: Introductionmentioning

confidence: 99%

Deposition of Glomalin-Related Soil Protein and Sequestered Toxic Metals into Watersheds

Chern

Tsai

Ogunseitan

2007

Environ. Sci. Technol.

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We hypothesized that glomalin-related soil proteins (GRSP) are eroded in sufficient quantities to influence metal loading into watersheds. We tested correlations among GRSP, Glomeromycota fungi, and metals (cadmium, iron, lead, and manganese) in proteins extracted from embankment soils at seven locations along an urban/coastal watershed. Immunoreactive (IRSP) and easily extractable (EE-IRSP) glomalin ranged from 0.007 to 2.9 mg g(-1) and from 0.006 to 0.63 mg g(-1) of soils, respectively. Glomalin-bound metals (microg mg(-1) protein) were Cd = 0.00-0.338; Fe = 0.5-227.7; Pb = 0.11-188.95; Mn = 2.23-784.42). Glomeromycota fungi were detected in 24% of all samples tested with PCR targeting the 18S and 28S ribosomal DNA extracted from soils. Specific assay for G. intraradices showed 3.08 x 10(7) copies g(-1) and 1.96 x 10(3) copies g(-1) of soil at two sites. Estimated annual glomalin loading into the watershed ranged from 5.48 x 10(2) to 7.22 x 10(4) kg of IRSP and from 2.57 x 102 to 2.86 x 10(4) kg of EE-IRSP; including 2.7 kg (Cd), 6.3 x 10(3) kg (Fe), 5.06 x 10(2) kg (Pb), and 1.80 x 10(3) kg (Mn). These data provide insights into the sources and ecological fate of a ubiquitous soil protein and its metals content.

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Modeling the environmental fate of manganese from methylcyclopentadienyl manganese tricarbonyl in urban landscapes

Cited by 13 publications

References 13 publications

Loss of pdr-1/parkin influences Mn homeostasis through altered ferroportin expression in C. elegans

Loss of pdr-1/parkin influences Mn homeostasis through altered ferroportin expression in C. elegans

Metallic Burden of Deciduous Teeth and Childhood Behavioral Deficits

Deposition of Glomalin-Related Soil Protein and Sequestered Toxic Metals into Watersheds

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