Selenium spares ascorbate and α‐tocopherol in cultured liver cell lines under oxidant stress

Abstract

The selenoenzyme thioredoxin reductase (TR) can recycle ascorbic acid, which in turn can recycle α-tocopherol. Therefore, we evaluated the role of selenium in ascorbic acid recycling and in protection against oxidant-induced loss of α-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-sensitive dehydroascorbic acid (DHA) reduction. However, selenium did not increase 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 spared ascorbate in overnight cultures of H4IIE cells, and prevented loss of cellular α-tocopherol in response to an oxidant stress induced by either ferricyanide or diazobenzene sulfonate. Whereas TR contributes little to ascorbate recycling in H4IIE cells, selenium spares ascorbate in culture and α-tocopherol in response to an oxidant stress