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Previous studies have shown that WEHI7.2 cell variants with an increased antioxidant defense exhibit increased resistance to dexamethasone\u2010induced apoptosis, suggesting that oxidative stress may play a role in glucocorticoid\u2010induced apoptosis. In this work we compared metabolic profiles of WEHI7.2 parental cells with those of WEHI7.2 variants with an increased antioxidant defense or overexpressing bcl\u20102, to determine whether bolstering the antioxidant defense results in altered metabolic parameters that could translate into increased resistance to dexamethasone\u2010induced apoptosis. WEHI7.2 parental cells and cells overexpressing catalase, thioredoxin or bcl\u20102, or selected for resistance to 200\u2005\u00b5<jats:sc>M<\/jats:sc> H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> were cultured in low\u2010glucose DMEM medium supplemented with 10% calf serum, and extracted using chloroform\u2013methanol\u2013water (1:1:1). Metabolites contained in the aqueous and organic phases of the extracts were processed separately and subjected to high\u2010resolution <jats:sup>31<\/jats:sup>P NMR spectroscopy. In most of the steroid\u2010resistant variants, ATP levels and energetic status were decreased compared with the steroid\u2010sensitive parental cell line, while the concentrations of hexose and triose phosphates were increased. Furthermore, the ratio of choline\u2010containing phospholipids to ethanolamine\u2010containing phospholipids was generally reduced in steroid\u2010resistant cells. Phosphatidylethanolamine and its derivatives contain a higher amount of polyunsaturated fatty acids (PUFA) than the choline\u2010containing analogs, and PUFA are readily oxidized by reactive oxygen species. Therefore, an increased initial amount of phosphatidylethanolamine may increase the \u2018buffering capacity\u2019 of this antioxidant and may thus contribute to the steroid resistance of WEHI7.2 variants. Copyright \u00a9 2002 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/nbm.790","type":"journal-article","created":{"date-parts":[[2002,8,26]],"date-time":"2002-08-26T21:28:02Z","timestamp":1030397282000},"page":"356-366","source":"Crossref","is-referenced-by-count":16,"title":["Changes in phosphate metabolism in thymoma cells suggest mechanisms for resistance to dexamethasone\u2010induced apoptosis. A <sup>31<\/sup>P NMR spectroscopic study of cell extracts"],"prefix":"10.1002","volume":"15","author":[{"given":"N. W.","family":"Lutz","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. E.","family":"Tome","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N. R.","family":"Aiken","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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