Tellurite reduction by Escherichia coli NDH-II dehydrogenase results in superoxide production in membranes of toxicant-exposed cells

Díaz-Vásquez, Waldo A.; Abarca-Lagunas, María José; Arenas, Felipe; Pinto, Camilo A.; Cornejo, Fabián A.; Wansapura, Poorna T.; Appuhamillage, Gayan A.; Chasteen, Thomas G.; Vásquez, Claudio C.

doi:10.1007/s10534-013-9701-8

Cited by 24 publications

(16 citation statements)

References 53 publications

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“…The nitrate reductases do not appear to be a factor in the current work, as the addition of nitrite or nitrate did not provide any change in MIC of tellurite toxicity and would not have been expected as the experiments here were performed aerobically. In E. coli 6-phosphoguconate dehydrogenase (Sandoval et al, 2015 ) and NDH-II dehydrogenase (Díaz-Vásquez et al, 2014 , 2015 ) appear to have tellurite reduction activity. In these studies, this reduction leads to superoxide production that affects aerobic electron transport chains leading to a move into an anaerobic respiratory state (Molina-Quiroz et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Selenite Protection of Tellurite Toxicity Toward Escherichia coli

Vrionis

Wang

Haslam

et al. 2015

Front. Mol. Biosci.

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In this work the influence of selenite on metal resistance in Escherichia coli was examined. Both synergistic and antagonistic resistance and toxicities were found upon co exposure with selenite. In wild type cells co-exposure to selenite had little effect on arsenic resistance, decreased resistance to cadmium and mercury but led to a dramatically increased resistance to tellurite of 32-fold. Due to the potential importance of thiol chemistry in metal biochemistry, deletion strains in γ-glutamylcysteine synthetase (key step in glutathione biosynthesis, encoded by gshA), thioredoxin (trxA), glutaredoxin (grxA), glutathione oxidoreductase (gor), and the periplasmic glutathione transporter (cydD) were also evaluated for resistance to various metals in the presence of selenite. The protective effect of selenite on tellurite toxicity was seen in several of the mutants and was pronounced in the gshA mutant were resistance to tellurite was increased up to 1000-fold relative to growth in the absence of selenite. Thiol oxidation studies revealed a faster rate of loss of reduced thiol content in the cell with selenite than with tellurite, indicating differential thiol reactivity. Selenite addition resulted in reactive oxygen species (ROS) production equivalent to levels associated with H2O2 addition. Tellurite addition resulted in considerably lower ROS generation while vanadate and chromate treatment did not increase ROS production above that of background. This work shows increased resistance toward most oxyanions in mutants of thiol redox suggesting that metalloid reaction with thiol components such as glutathione actually enhances toxicity of some metalloids.

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Section: Discussionmentioning

confidence: 99%

Selenite Protection of Tellurite Toxicity Toward Escherichia coli

Vrionis

Wang

Haslam

et al. 2015

Front. Mol. Biosci.

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“…In addition, the expression of other genes shown to be involved in TeO 3 2− reduction such as ndh (encoding NDH-II dehydrogenase) (Díaz-Vásquez et al, 2014) and lpdA (encoding lipoamide dehydrogenase) (Reinoso et al, 2012) is upregulated upon toxicant exposure in E. coli. Further work to better characterize the global cell response to tellurite is being carried out in our laboratory.…”

Section: Discussionmentioning

confidence: 99%

Escherichia coli 6-phosphogluconate dehydrogenase aids in tellurite resistance by reducing the toxicant in a NADPH-dependent manner

Sandoval

Arenas

García

et al. 2015

Microbiological Research

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Exposure to the tellurium oxyanion tellurite (TeO3(2-)) results in the establishment of an oxidative stress status in most microorganisms. Usually, bacteria growing in the presence of the toxicant turn black because of the reduction of tellurite (Te(4+)) to the less-toxic elemental tellurium (Te(0)). In vitro, at least part of tellurite reduction occurs enzymatically in a nicotinamide dinucleotide-dependent reaction. In this work, we show that TeO3(2-) reduction by crude extracts of Escherichia coli overexpressing the zwf gene (encoding glucose-6-phosphate dehydrogenase) takes place preferentially in the presence of NADPH instead of NADH. The enzyme responsible for toxicant reduction was identified as 6-phosphogluconate dehydrogenase (Gnd). The gnd gene showed a subtle induction at short times after toxicant exposure while strains lacking gnd were more susceptible to the toxicant. These results suggest that both NADPH-generating enzymes from the pentose phosphate shunt may be involved in tellurite detoxification and resistance in E. coli.

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“…Samples were diluted 10-fold with 10% HNO 3 and the whole volume was used for Te determination using a Spectro CIROS Vision ICP-OES apparatus as previously described (Díaz-Vásquez et al, 2014a). A calibration curve was constructed with commercially-available tellurium standards (Sigma).…”

Section: Te Quantification By Inductively Coupled Plasma Optical Emismentioning

confidence: 99%

The ActP acetate transporter acts prior to the PitA phosphate carrier in tellurite uptake by Escherichia coli

Elías

Díaz-Vásquez

Abarca-Lagunas

et al. 2015

Microbiological Research

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The tellurium oxyanion tellurite is harmful for most microorganisms. Since its toxicity occurs chiefly once the toxicant reaches the intracellular compartment, unveiling the toxicant uptake process is crucial for understanding the whole phenomenon of tellurium toxicity. While the PitA phosphate transporter is thought to be one of the main paths responsible for toxicant entry into Escherichia coli, genetic and physiological evidence have identified the ActP acetate carrier as the main tellurite importer in Rhodobacter capsulatus. In this work, new background on the role of these transporters in tellurite uptake by E. coli is presented. It was found that, similar to what occurs in R. capsulatus, ActP is able to mediate toxicant entry to this bacterium. Lower reactive oxygen species levels were observed in E. coli lacking the actP gene. Antioxidant enzyme catalase and fumarase C activity was almost unchanged after short exposure of E. coli ΔactP to sublethal tellurite concentrations, suggesting a low antioxidant response. In this strain, tellurite uptake decreased significantly during the first 5 min of exposure and inductively coupled plasma optical emission spectroscopy assays using an actP-overexpressing strain confirmed that this carrier mediates toxicant uptake. Relative gene expression experiments by qPCR showed that actP expression is enhanced at short times of tellurite exposure, while pitA and pitB genes are induced later. Summarizing, the results show that ActP is involved in tellurite entry to E. coli and that its participation occurs mainly at early stages of toxicant exposure.

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Tellurite reduction by Escherichia coli NDH-II dehydrogenase results in superoxide production in membranes of toxicant-exposed cells

Cited by 24 publications

References 53 publications

Selenite Protection of Tellurite Toxicity Toward Escherichia coli

Selenite Protection of Tellurite Toxicity Toward Escherichia coli

Escherichia coli 6-phosphogluconate dehydrogenase aids in tellurite resistance by reducing the toxicant in a NADPH-dependent manner

The ActP acetate transporter acts prior to the PitA phosphate carrier in tellurite uptake by Escherichia coli

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