scholarly journals Microbially mediated reduction of FeIII and AsV in Cambodian sediments amended with 13C-labelled hexadecane and kerogen

2014 ◽  
Vol 11 (5) ◽  
pp. 538 ◽  
Author(s):  
Athanasios Rizoulis ◽  
Wafa M. Al Lawati ◽  
Richard D. Pancost ◽  
David A. Polya ◽  
Bart E. van Dongen ◽  
...  
Keyword(s):  
Organic Matter ◽  
Critical Role ◽  
Stable Isotope Probing ◽  
Mass Spectrometry Analysis ◽  
Gas Chromatography Mass Spectrometry ◽  
Organic Substrates ◽  
Spectrometry Analysis ◽  
Subsurface Sediments ◽  
Extractable Organic Matter ◽  
Long Chain

Environmental context The use of groundwater with elevated concentrations of arsenic for drinking, cooking or irrigation has resulted in the worst mass poisoning in human history. This study shows that organic compounds that can be found in arsenic rich subsurface sediments may be used by indigenous microorganisms, contributing to the release of arsenic from the sediments into the groundwater. This study increases our understanding of the range of organic substrates (and their sources) that can potentially stimulate arsenic mobilisation into groundwaters. Abstract Microbial activity is generally accepted to play a critical role, with the aid of suitable organic carbon substrates, in the mobilisation of arsenic from sediments into shallow reducing groundwaters. The nature of the organic matter in natural aquifers driving the reduction of AsV to AsIII is of particular importance but is poorly understood. In this study, sediments from an arsenic rich aquifer in Cambodia were amended with two 13C-labelled organic substrates. 13C-hexadecane was used as a model for potentially bioavailable long chain n-alkanes and a 13C-kerogen analogue as a proxy for non-extractable organic matter. During anaerobic incubation for 8 weeks, significant FeIII reduction and AsIII mobilisation were observed in the biotic microcosms only, suggesting that these processes were microbially driven. Microcosms amended with 13C-hexadecane exhibited a similar extent of FeIII reduction to the non-amended microcosms, but marginally higher AsIII release. Moreover, gas chromatography–mass spectrometry analysis showed that 65% of the added 13C-hexadecane was degraded during the 8-week incubation. The degradation of 13C-hexadecane was microbially driven, as confirmed by DNA stable isotope probing (DNA-SIP). Amendment with 13C-kerogen did not enhance FeIII reduction or AsIII mobilisation, and microbial degradation of kerogen could not be confirmed conclusively by DNA-SIP fractionation or 13C incorporation in the phospholipid fatty acids. These data are, therefore, consistent with the utilisation of long chain n-alkanes (but not kerogen) as electron donors for anaerobic processes, potentially including FeIII and AsV reduction in the subsurface.

Spectrophotometry Measurement of Polynuclear Aromatic Hydrocarbons in Hamilton Harbour Sediments

1991 ◽  
Vol 26 (1) ◽  
pp. 1-16 ◽  
Author(s):  
T.P. Murphy ◽  
H. Brouwer ◽  
M.E. Fox ◽  
E. Nagy
Keyword(s):  
Aromatic Hydrocarbons ◽  
Total Concentration ◽  
Coal Tar ◽  
Sediment Cores ◽  
Polynuclear Aromatic Hydrocarbons ◽  
Mass Spectrometry Analysis ◽  
Gas Chromatography Mass Spectrometry ◽  
Near Surface ◽  
Spectrometry Analysis ◽  
Hamilton Harbour

Abstract Eighty-one sediment cores were collected to determine the extent of coal tar contamination in a toxic area of Hamilton Harbour. Over 800 samples were analyzed by a UV spectrophotometric technique that was standardized with gas chromatography/mass spectrometry analysis. The coal tar distribution was variable. The highest concentrations were near the Stelco outfalls and the Hamilton-Wentworth combined sewer outfalls. The total concentration of the 16 polynuclear aromatic hydrocarbons (PAHs) in 48,300 m3 of near-surface sediments exceeded 200 µg/g.

scholarly journals Biodegradation and metabolic pathway of fenvalerate by Citrobacter freundii CD-9

AMB Express ◽  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jie Tang ◽  
Dan Lei ◽  
Min Wu ◽  
Qiong Hu ◽  
Qing Zhang
Keyword(s):  
Environmental Pollution ◽  
Environmental Remediation ◽  
High Efficiency ◽  
Mass Spectrometry Analysis ◽  
Gas Chromatography Mass Spectrometry ◽  
Citrobacter Freundii ◽  
16S Rrna Sequence ◽  
Intracellular Enzyme ◽  
Pyrethroid Insecticides ◽  
Spectrometry Analysis

Abstract Fenvalerate is a pyrethroid insecticide with rapid action, strong targeting, broad spectrum, and high efficiency. However, continued use of fenvalerate has resulted in its widespread presence as a pollutant in surface streams and soils, causing serious environmental pollution. Pesticide residues in the soil are closely related to food safety, yet little is known regarding the kinetics and metabolic behaviors of fenvalerate. In this study, a fenvalerate-degrading microbial strain, CD-9, isolated from factory sludge, was identified as Citrobacter freundii based on morphological, physio-biochemical, and 16S rRNA sequence analysis. Response surface methodology analysis showed that the optimum conditions for fenvalerate degradation by CD-9 were pH 6.3, substrate concentration 77 mg/L, and inoculum amount 6% (v/v). Under these conditions, approximately 88% of fenvalerate present was degraded within 72 h of culture. Based on high-performance liquid chromatography and gas chromatography-mass spectrometry analysis, ten metabolites were confirmed after the degradation of fenvalerate by strain CD-9. Among them, o-phthalaldehyde is a new metabolite for fenvalerate degradation. Based on the identified metabolites, a possible degradation pathway of fenvalerate by C. freundii CD-9 was proposed. Furthermore, the enzyme localization method was used to study CD-9 bacteria and determine that its degrading enzyme is an intracellular enzyme. The degradation rate of fenvalerate by a crude enzyme solution for over 30 min was 73.87%. These results showed that strain CD-9 may be a suitable organism to eliminate environmental pollution by pyrethroid insecticides and provide a future reference for the preparation of microbial degradation agents and environmental remediation.

Feline Spongy Encephalopathy With a Mutation in the ASPA Gene

2021 ◽  
pp. 030098582110021
Author(s):  
Yuta Takaichi ◽  
James K. Chambers ◽  
Moeko Shiroma-Kohyama ◽  
Makoto Haritani ◽  
Yumi Une ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Canavan Disease ◽  
Mass Spectrometry Analysis ◽  
Intensity Change ◽  
Gas Chromatography Mass Spectrometry ◽  
Clinical Genetic ◽  
Gene Encoding ◽  
Spongy Degeneration ◽  
Spectrometry Analysis ◽  
Dense Granules

Canavan disease is an autosomal recessive leukodystrophy caused by mutations in the gene encoding aspartoacylase (ASPA), which hydrolyses N-acetylaspartate (NAA) to acetate and aspartate. A similar feline neurodegenerative disease associated with a mutation in the ASPA gene is reported herein. Comprehensive clinical, genetic, and pathological analyses were performed on 4 affected cats. Gait disturbance and head tremors initially appeared at 1 to 19 months of age. These cats eventually exhibited dysstasia and seizures and died at 7 to 53 months of age. Magnetic resonance imaging of the brain revealed diffuse symmetrical intensity change of the cerebral cortex, brainstem, and cerebellum. Gas chromatography–mass spectrometry analysis of urine showed significant excretion of NAA. Genetic analysis of the 4 affected cats identified a missense mutation (c.859G>C) in exon 6 of the ASPA gene, which was not detected in 4 neurologically intact cats examined as controls. Postmortem analysis revealed vacuolar changes predominantly distributed in the gray matter of the cerebrum and brain stem as well as in the cerebellar Purkinje cell layer. Immunohistochemically, these vacuoles were surrounded by neurofilaments and sometimes contained MBP- and Olig2-positive cells. Ultrastructurally, a large number of intracytoplasmic vacuoles containing mitochondria and electron-dense granules were detected in the cerebral cortex. All 4 cats were diagnosed as spongy encephalopathy with a mutation in the ASPA gene, a syndrome analogous to human Canavan disease. The histopathological findings suggest that feline ASPA deficiency induces intracytoplasmic edema in neurons and oligodendrocytes, resulting in spongy degeneration of the central nervous system.

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