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Dexamethasone‐induced apoptosis of mouse thymocytes: Prevention by native 7α‐hydroxysteroids

Dehydroepiandrosterone (DHEA) has been shown to decrease the dexamethasone (DEX)‐induced apoptosis of thymocytes and to be one of the native 3β‐hydroxysteroids extensively 7α‐hydroxylated in thymus. This led us to question whether DHEA or 7α‐hydroxy‐DHEA is responsible for the decrease in DEX‐induced apoptosis of thymocytes and whether this property is shared with other native 3β‐hydroxysteroids and their 7α‐hydroxylated metabolites. Treatment of mice with DHEA or 7α‐hydroxy‐DHEA prior to DEX led to a smaller decrease in thymus weight than with DEX alone and to a disappearance of the DEX‐induced changes in thymocyte phenotypes. Thymocyte apoptosis induced by DEX treatment was significantly lowered in DHEA‐ and 7α‐hydroxy‐DHEA‐treated thymi, even after 18 h culture with additional 10−6 mol/L DEX. Extensive apoptosis of thymocytes cultured with 10−7 mol/L DEX was brought back to control levels when 10−5 mol/L 7α‐hydroxy‐DHEA or 10−5 mol/L 7α‐hydroxy‐epiandrosterone was added. After use of DHEA and epiandrosterone or pregnenolone, less significant and no significant changes were obtained, respectively. These findings imply that the 7α‐hydroxylation of 3β‐hydroxysteroids may be a prerequisite for an exquisite regulation of the thymocyte‐positive selection driven by the glucocorticoids produced in thymic epithelial cells.