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

Li X, Hill KE, Burk RF, May JM
FEBS Lett. 2001 508 (3): 489-92

PMID: 11728478 · DOI:10.1016/s0014-5793(01)03129-5

The selenoenzyme thioredoxin reductase (TR) can recycle ascorbic acid, which in turn can recycle alpha-tocopherol. Therefore, we evaluated the role of selenium in ascorbic acid recycling and in protection against oxidant-induced 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-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 alpha-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 alpha-tocopherol in response to an oxidant stress.

MeSH Terms (19)

alpha-Tocopherol Animals Ascorbic Acid Culture Media Dehydroascorbic Acid Diazonium Compounds Ferricyanides Hepatocytes Humans Oxidation-Reduction Oxidative Stress Oxidoreductases Rats Selenocysteine Sodium Selenite Sulfanilic Acids Thioredoxin-Disulfide Reductase Thioredoxins Tumor Cells, Cultured

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