Selenium spares ascorbate and alpha-tocopherol in cultured liver cell lines under oxidant stress

The selenoenzyme thioredoxin reductase (TR) can recycle ascorbic acid, whic h in turn can recycle alpha -tocopherol. Therefore, we evaluated the role o f selenium in ascorbic acid recycling and in protection against oxidant-ind uced loss of alpha -tocopherol in cultured liver cells. Treatment of HepG2 or H4IIE cultured liver cells for 48 h with sodium selenite (0-116 nmol/l) tripled the activity of the selenoenzyme TR, measured as aurothioglucose-se nsitive dehydroascorbic acid (DHA) reduction. However, selenium did not inc rease the ability of H4IIE cells to take up and reduce 2 mM DHA, despite a 25% increase in ascorbate-dependent ferricyanide reduction (which reflects cellular ascorbate recycling). Nonetheless, selenium supplements both spare d ascorbate in overnight cultures of H4IIE cells, and prevented loss of cel lular (x-tocopherol in response to an oxidant stress induced by either ferr icyanide or diazobenzene sulfonate. Whereas TR contributes little to ascorb ate recycling in H4IIE cells, selenium spares ascorbate in culture and oc-t ocopherol in response to an oxidant stress. (C) 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.