Pierre Plateau

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTExchangeable proton NMR without base-line distorsion, using new strong-pulse sequencesPierre Plateau and Maurice GueronCite this: J. Am. Chem. Soc. 1982, 104, 25, 7310–7311Publication Date (Print):December 1, 1982Publication History Published online1 May 2002Published inissue 1 December 1982https://pubs.acs.org/doi/10.1021/ja00389a067https://doi.org/10.1021/ja00389a067research-articleACS PublicationsRequest reuse permissionsArticle Views1118Altmetric-Citations830LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts

The ppa gene for inorganic pyrophosphatase is essential for the growth of Escherichia coli. A recombinant with a chromosomal ppa::Kanr lesion and a temperature-sensitive replicon with a ppa+ gene showed a temperature-sensitive growth phenotype, and a mutant with the sole ppa+ gene under control of the lac promoter showed inducer-dependent growth. When the lacp-ppa mutant was subcultured without inducer, the pyrophosphatase level decreased, the PPi level increased, and growth stopped. Cellular PPi reached 16 mM about 6 h after growth arrest without loss of cell viability.

Administration of selenium in humans has anticarcinogenic effects. However, the boundary between cancer-protecting and toxic levels of selenium is extremely narrow. The mechanisms of selenium toxicity need to be fully understood. In Saccharomyces cerevisiae, selenite in the millimolar range is well tolerated by cells. Here we show that the lethal dose of selenite is reduced to the micromolar range by the presence of thiols in the growth medium. Glutathione and selenite spontaneously react to produce several selenium-containing compounds (selenodiglutathione, glutathioselenol, hydrogen selenide, and elemental selenium) as well as reactive oxygen species. We studied which compounds in the reaction pathway between glutathione and sodium selenite are responsible for this toxicity. Involvement of selenodiglutathione, elemental selenium, or reactive oxygen species could be ruled out. In contrast, extracellular formation of hydrogen selenide can fully explain the exacerbation of selenite toxicity by thiols. Indeed, direct production of hydrogen selenide with D-cysteine desulfhydrase induces high mortality. Selenium uptake by S. cerevisiae is considerably enhanced in the presence of external thiols, most likely through internalization of hydrogen selenide. Finally, we discuss the possibility that selenium exerts its toxicity through consumption of intracellular reduced glutathione, thus leading to severe oxidative stress.