Dataset Information

Rate-Limiting Mass Transfer in Micropollutant Degradation Revealed by Isotope Fractionation in Chemostat.

ABSTRACT: Biodegradation of persistent micropollutants like pesticides often slows down at low concentrations (?g/L) in the environment. Mass transfer limitations or physiological adaptation are debated to be responsible. Although promising, evidence from compound-specific isotope fractionation analysis (CSIA) remains unexplored for bacteria adapted to this low concentration regime. We accomplished CSIA for degradation of a persistent pesticide, atrazine, during cultivation of Arthrobacter aurescens TC1 in chemostat under four different dilution rates leading to 82, 62, 45, and 32 ?g/L residual atrazine concentrations. Isotope analysis of atrazine in chemostat experiments with whole cells revealed a drastic decrease in isotope fractionation with declining residual substrate concentration from ?(C) = -5.36 ± 0.20‰ at 82 ?g/L to ?(C) = -2.32 ± 0.28‰ at 32 ?g/L. At 82 ?g/L ?(C) represented the full isotope effect of the enzyme reaction. At lower residual concentrations smaller ?(C) indicated that this isotope effect was masked indicating that mass transfer across the cell membrane became rate-limiting. This onset of mass transfer limitation appeared in a narrow concentration range corresponding to about 0.7 ?M assimilable carbon. Concomitant changes in cell morphology highlight the opportunity to study the role of this onset of mass transfer limitation on the physiological level in cells adapted to low concentrations.

SUBMITTER: Ehrl BN

PROVIDER: S-EPMC6365907 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Rate-Limiting Mass Transfer in Micropollutant Degradation Revealed by Isotope Fractionation in Chemostat.

Ehrl Benno N BN Kundu Kankana K Gharasoo Mehdi M Marozava Sviatlana S Elsner Martin M

Environmental science & technology 20181219 3

Biodegradation of persistent micropollutants like pesticides often slows down at low concentrations (μg/L) in the environment. Mass transfer limitations or physiological adaptation are debated to be responsible. Although promising, evidence from compound-specific isotope fractionation analysis (CSIA) remains unexplored for bacteria adapted to this low concentration regime. We accomplished CSIA for degradation of a persistent pesticide, atrazine, during cultivation of Arthrobacter aurescens TC1 i ...[more]

PMID: 30514083

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Project description:Huntington's disease is an autosomal dominant neurodegenerative disease caused by abnormal polyglutamine expansion in huntingtin (Exp-HTT) leading to degeneration of striatal neurons. Altered brain cholesterol homeostasis has been implicated in Huntington's disease, with increased accumulation of cholesterol in striatal neurons yet reduced levels of cholesterol metabolic precursors. To elucidate these two seemingly opposing dysregulations, we investigated the expression of cholesterol 24-hydroxylase (CYP46A1), the neuronal-specific and rate-limiting enzyme for cholesterol conversion to 24S-hydroxycholesterol (24S-OHC). CYP46A1 protein levels were decreased in the putamen, but not cerebral cortex samples, of post-mortem Huntington's disease patients when compared to controls. Cyp46A1 mRNA and CYP46A1 protein levels were also decreased in the striatum of the R6/2 Huntington's disease mouse model and in SThdhQ111 cell lines. In vivo, in a wild-type context, knocking down CYP46A1 expression in the striatum, via an adeno-associated virus-mediated delivery of selective shCYP46A1, reproduced the Huntington's disease phenotype, with spontaneous striatal neuron degeneration and motor deficits, as assessed by rotarod. In vitro, CYP46A1 restoration protected SThdhQ111 and Exp-HTT-expressing striatal neurons in culture from cell death. In the R6/2 Huntington's disease mouse model, adeno-associated virus-mediated delivery of CYP46A1 into the striatum decreased neuronal atrophy, decreased the number, intensity level and size of Exp-HTT aggregates and improved motor deficits, as assessed by rotarod and clasping behavioural tests. Adeno-associated virus-CYP46A1 infection in R6/2 mice also restored levels of cholesterol and lanosterol and increased levels of desmosterol. In vitro, lanosterol and desmosterol were found to protect striatal neurons expressing Exp-HTT from death. We conclude that restoring CYP46A1 activity in the striatum promises a new therapeutic approach in Huntington's disease.

Dataset Information

Rate-Limiting Mass Transfer in Micropollutant Degradation Revealed by Isotope Fractionation in Chemostat.

Publications

Rate-Limiting Mass Transfer in Micropollutant Degradation Revealed by Isotope Fractionation in Chemostat.

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