Metabolic Networks to Counter Al Toxicity<i>in Pseudomonas Fluorescens</i>: A Holistic View

Auger, Christopher; Appanna, Nishma D.; Appanna, Vasu D.

doi:10.1002/9781119004813.ch111

Cited by 2 publications

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“…However, after nZVI exposure, both normal cells and persistent phenotypic cells possess a high content of PE. PE involves in the metal detoxification in P. fluorescens, by immobilizing and expulsing intracellular metals, for example, iron and aluminum out of cells (Appanna and Finn, 1995;Auger et al, 2016). The higher PE content of nZVI-treated normal cells of P .putida F1 could explain the arrangement of nZVI both inside and on bacterial membrane (Figure 5.7E), similar to the study by Appanna et al which reported the deposit of iron around bacterial membrane (Appanna and Finn, 1995).…”

Section: 28) Phospholipid Headgroup Analysissupporting

confidence: 83%

“…The up-regulation of succinate dehydrogenase, an enzyme catalyzing the conversion of succinate to fumarate, potentially enhances the amount of fumarate (Table 4.3). Fumarate can be further converted oxaloacetate and citrate which can acts a metal chelation thus reducing metal toxicity (Auger et al, 2016;Auger et al, 2013). However, the upregulation of enzymes, for example, fumarase, malate dehydrogenase or citrate synthase was not observed in this study.…”

Section: Adenylosuccinate Lyase (Asl) Is An Enzyme In Purine Biosynth...contrasting

confidence: 57%

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Effect of nanoscale zero valent iron toward bacteria and their response

Kotchaplai

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Nanoscale zero valent iron or nZVI is a reactive iron nanoparticle which has been considered as a promising treatment agent for various contaminants due to its small size and high reactivity. While the successful in-situ environmental application of nZVI has been demonstrated, the increasing use of nZVI possibly leads to the potential environmental impact of nZVI. This research aims to understand the effect of nZVI particularly on environmental bacteria. In this study, Pseudomonas putida were selected as the model bacteria as they are ubiquitous in the environment. Exposure of P. putida to 1.0 g/L of reactive nZVI (R-nZVI) decreased the bacterial viability by three order of magnitude. Bacterial exposure to oxidized nZVI (O-nZVI), a non-toxic form remained in the environment, resulted in one-order of magnitude reduction in cell viability. Proteomic analysis revealed the significant effect of both forms of nZVI on bacterial membrane as suggested by the decreased abundance of membrane-bound proteins and the up-regulation of proteins playing a role in membrane protein folding. Prolonged exposure in the presence of carbon source resulted in the rebound in number of viable cells, suggesting that bacterial cells can adapt themselves to the nZVI-induced damage. According to TEM analysis, nZVI heavily adsorbed onto the bacterial surface and partially localized around the bacterial membrane, fluidizing bacterial membrane. Fatty acid profile analysis showed the significant conversion of cis-isomer to trans-unsaturated fatty acid upon nZVI exposure. The altered membrane composition resulted in the tightly packed bilayer, and more rigid membrane as confirmed by fluorescent anisotropy measurement. It is likely that this membrane rigidification is a bacterial adaptive response to counteract the membrane fluidizing effect of nZVI. Interestingly, repetitive exposures of bacteria to an environmentally relevant concentration of R-nZVI (0.1 g/L) induced the emergence of the small colony variant (SCV) of P. putida exhibiting much smaller colony size and higher persistence to nZVI exposure. Single bacterial exposure to higher concentration of R-nZVI (i.e. 0.5 and 1.0 g/L) also increased the number of this SCV phenotype by approximately ten-fold. It appears that nZVI-induced oxidative stress involves in the emergent SCV phenotype. While most of the SCV phenotype could revert back to normal phenotype in the absence of nZVI, the irreversible SCV phenotype was also detected. Characterization of this irreversible SCV phenotype reveals partial loss of the environmentally relevant traits including swimming motility and biofilm formation. While P. putida F1 is a model strain for toluene degradation study, its irreversible SCV phenotype is slightly more susceptible to toluene and showed four-fold longer lag phase of growth under toluene as sole carbon source, compared to the normal phenotype. Overall, this study unveils the significant effect of nZVI on bacterial membrane (i.e. membrane fluidizing effect) as well as bacterial adaptation responses to the occurred damage. It demonstrates that the bacterial adaptation should be considered for accurately predicting the toxicity of nZVI. The study on adaptability of other microorganisms is also required. Additionally, nZVI in-situ injection strategies (e.g. single and repetitive injection) should be taken into concern since it may induce the variation in bacterial phenotype.

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Section: 28) Phospholipid Headgroup Analysissupporting

confidence: 83%

Section: Adenylosuccinate Lyase (Asl) Is An Enzyme In Purine Biosynth...contrasting

confidence: 57%

Effect of nanoscale zero valent iron toward bacteria and their response

Kotchaplai

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Metabolic defence against oxidative stress: the road less travelled so far

et al. 2017

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SummaryBacteria have survived, and many have thrived, since antiquity in the presence of the highly-reactive chalcogen-oxygen (O 2 ). They are known to evoke intricate strategies to defend themselves from the reactive by-products of oxygenreactive oxygen species (ROS). Many of these detoxifying mechanisms have been extensively characterized; superoxide dismutase, catalases, alkyl hydroperoxide reductase and the glutathione (GSH)-cycling system are responsible for neutralizing specific ROS. Meanwhile, a pool of NADPH-the reductive engine of many ROS-combating enzymes-is maintained by metabolic enzymes including, but not exclusively, glucose-6 phosphate dehydrogenase (G6PDH) and NADPdependent isocitrate dehydrogenase (ICDH-NADP). So, it is not surprising that evidence continues to emerge demonstrating the pivotal role metabolism plays in mitigating ROS toxicity. Stemming from its ability to concurrently decrease the production of the pro-oxidative metabolite, NADH, while augmenting the antioxidative metabolite, NADPH, metabolism is the fulcrum of cellular redox potential. In this review, we will discuss the mounting evidence positioning metabolism and metabolic shifts observed during oxidative stress, as critical strategies microbes utilize to thrive in environments that are rife with ROS. The contribution of ketoacids-moieties capable of non-enzymatic decarboxylation in the presence of oxidants-as ROS scavengers will be elaborated alongside the metabolic pathways responsible for their homeostases. Further, the signalling role of the carboxylic acids generated following the ketoacid-mediated detoxification of the ROS will be commented on within the context of oxidative stress.

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Metabolic Networks to Counter Al Toxicityin Pseudomonas Fluorescens: A Holistic View

Cited by 2 publications

References 74 publications

Effect of nanoscale zero valent iron toward bacteria and their response

Effect of nanoscale zero valent iron toward bacteria and their response

Metabolic defence against oxidative stress: the road less travelled so far

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