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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