Oxidative stress reactions induced in beans (Phaseolus vulgaris) following exposure to uranium

Vandenhove, Hildegarde; Cuypers, Ann; Hees, May Van; Koppen, Gudrun; Wannijn, Jean

doi:10.1016/j.plaphy.2006.10.013

Cited by 70 publications

(47 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such a GSH consuming process and an excess of ROS activate GSH synthesis (reviewed in Foyer and Noctor 2005). A higher GSH level was also observed in primary leaves of U treated beans (Phaseolus vulgaris) (0.1-100 lM U) (Vandenhove et al 2006).…”

Section: Discussionmentioning

confidence: 93%

“…Consequently, exposure to U could be associated with changes in the cellular redox status. Recent studies in beans (Phaseolus vulgaris) and Arabidopsis thaliana suggested oxidative reactions caused by U indicated by altered levels of the glutathione pool and increased capacities of antioxidative enzymes like peroxidases (Vandenhove et al 2006;Vanhoudt et al 2008).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Impact of uranium (U) on the cellular glutathione pool and resultant consequences for the redox status of U

2011

View full text Add to dashboard Cite

Uranium (U) as a redox-active heavy metal can cause various redox imbalances in plant cells. Measurements of the cellular glutathione/glutathione disulfide (GSH/GSSG) by HPLC after cellular U contact revealed an interference with this essential redox couple. The GSH content remained unaffected by 10 μM U whereas the GSSG level immediately increased. In contrast, higher U concentrations (50 μM) drastically raised both forms. Using the Nernst equation, it was possible to calculate the half-cell reduction potential of 2GSH/GSSG. In case of lower U contents the cellular redox environment shifted towards more oxidizing conditions whereas the opposite effect was obtained by higher U contents. This indicates that U contact causes a consumption of reduced redox equivalents. Artificial depletion of GSH by chlorodinitrobenzene and measuring the cellular reducing capacity by tetrazolium salt reduction underlined the strong requirement of reduced redox equivalents. An additional element of cellular U detoxification mechanisms is the complex formation between the heavy metal and carboxylic functionalities of GSH. Because two GSH molecules catalyze electron transfers each with one electron forming a dimer (GSSG) two UO(2) (2+) are reduced to each UO(2) (+) by unbound redox sensitive sulfhydryl moieties. UO(2) (+) subsequently disproportionates to UO(2) (2+) and U(4+). This explains that in vitro experiments revealed a reduction to U(IV) of only around 33% of initial U(VI). Cellular U(IV) was transiently detected with the highest level after 2 h of U contact. Hence, it can be proposed that these reducing processes are an important element of defense reactions induced by this heavy metal.

show abstract

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Impact of uranium (U) on the cellular glutathione pool and resultant consequences for the redox status of U

2011

View full text Add to dashboard Cite

show abstract

“…Like copper, uranyl may interfere with natural metal-binding sites of enzymes, but the molecular mechanism of uranyl toxicity is expected to be more complex because uranium possesses four oxidation states, U(III), U(IV), U(V), and U(VI). The toxicity of uranium has been linked to oxidative stress, as deduced from effects on intracellular GSH levels in plants (24,25). It has been shown that uranyl affects the levels of both GSH and its oxidized form, GSSG, in cultured plant cells (26) and animals (27).…”

mentioning

confidence: 99%

Mechanism of Attenuation of Uranyl Toxicity by Glutathione in Lactococcus lactis

Obeid

Oertel

Solioz

et al. 2016

Appl Environ Microbiol

View full text Add to dashboard Cite

b ABSTRACTBoth prokaryotic and eukaryotic organisms possess mechanisms for the detoxification of heavy metals, and these mechanisms are found among distantly related species. We investigated the role of intracellular glutathione (GSH), which, in a large number of taxa, plays a role in protection against the toxicity of common heavy metals. Anaerobically grown Lactococcus lactis containing an inducible GSH synthesis pathway was used as a model organism. Its physiological condition allowed study of putative GSH-dependent uranyl detoxification mechanisms without interference from additional reactive oxygen species. By microcalorimetric measurements of metabolic heat during cultivation, it was shown that intracellular GSH attenuates the toxicity of uranium at a concentration in the range of 10 to 150 M. In this concentration range, no effect was observed with copper, which was used as a reference for redox metal toxicity. At higher copper concentrations, GSH aggravated metal toxicity. Isothermal titration calorimetry revealed the endothermic binding of U(VI) to the carboxyl group(s) of GSH rather than to the reducing thiol group involved in copper interactions. The data indicate that the primary detoxifying mechanism is the intracellular sequestration of carboxyl-coordinated U(VI) into an insoluble complex with GSH. The opposite effects on uranyl and on copper toxicity can be related to the difference in coordination chemistry of the respective metal-GSH complexes, which cause distinct growth phase-specific effects on enzyme-metal interactions. IMPORTANCEUnderstanding microbial metal resistance is of particular importance for bioremediation, where microorganisms are employed for the removal of heavy metals from the environment. This strategy is increasingly being considered for uranium. However, little is known about the molecular mechanisms of uranyl detoxification. Existing studies of different taxa show little systematics but hint at a role of glutathione (GSH). Previous work could not unequivocally demonstrate a GSH function in decreasing the presumed uranyl-induced oxidative stress, nor could a redox-independent detoxifying action of GSH be identified. Combining metabolic calorimetry with cell number-based assays and genetics analysis enables a novel and general approach to quantify toxicity and relate it to molecular mechanisms. The results show that GSH-expressing microorganisms appear advantageous for uranyl bioremediation.T he natural abundance of uranium and the increasing health risks that originate from its anthropogenic release to the environment have generated a high demand for understanding the molecular mechanisms of uranium toxicity. Its radiotoxicity is of minor ecological relevance compared to its toxicity due to chemical interference with metabolism (1, 2). The latter is caused mostly by the displacement of Ca 2ϩ and Mg 2ϩ from functionally important binding sites in enzymes (3). The water-soluble uranyl cation UO 2 2ϩ is the most commonly found contaminant, which contains uranium in its highest ...

show abstract

“…1). Vandenhove et al [5] also reported an increasing trend in growth parameters for Phaseolus vulgaris after application of 0-10 M uranium, and a decrease (not significant) after exposure to 1000 M uranium. Inhibition of leaf expansion and/or growth was also reported by several authors after exposure of Phaseolus vulgaris to cadmium [6], zinc [14] and copper [15].…”

Section: Resultsmentioning

confidence: 93%

“…[3,4]. Exposure to heavy metals can disrupt the cellular redox balance, resulting in an increase/decrease of the capacity of the antioxidative defense mechanism as was shown by several authors [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Induction of oxidative stress related responses inArabidopsis thalianafollowing uranium exposure

et al. 2009

Self Cite

View full text Add to dashboard Cite

Abstract. The reactive oxygen species (ROS)-signaling pathway is very important in heavy metal toxicity. Induction of the antioxidative defense mechanism, comprising ROS-scavenging enzymes and metabolites, in plants after environmental uranium contamination has been insufficiently studied in the past. This study aimed to analyze oxidative stress related responses in Arabidopsis thaliana after uranium exposure. Seventeen-day-old seedlings were exposed to 0, 0.1, 1, 10 and 100 M uranium for 3 days. After exposure to 100 M uranium, a decrease in fresh weight for leaves and roots was observed, leaves colored anthocyanous and roots were stunted and yellow. To reveal the importance of oxidative stress in uranium toxicity, alterations in ROS-scavenging enzymes were studied at protein and transcriptional level. Superoxide dismutase (SOD) capacities increased in leaves and roots after exposure to 100 M uranium but no differences were observed for catalase (CAT) capacities. Transcript levels of different SODs located at various cellular compartments were affected depending on the place of action. Gene expression of CAT in leaves and roots was also affected after uranium exposure. Results indicate that oxidative stress plays an important role in uranium toxicity but suggest that plant responses differ for leaves and roots.

show abstract

Oxidative stress reactions induced in beans (Phaseolus vulgaris) following exposure to uranium

Cited by 70 publications

References 46 publications

Impact of uranium (U) on the cellular glutathione pool and resultant consequences for the redox status of U

Impact of uranium (U) on the cellular glutathione pool and resultant consequences for the redox status of U

Mechanism of Attenuation of Uranyl Toxicity by Glutathione in Lactococcus lactis

Induction of oxidative stress related responses inArabidopsis thalianafollowing uranium exposure

Contact Info

Product

Resources

About