title: Effects of selenium status and supplementary seleno-chemical sources on mouse T-cell mitogenesis.
abstract: Although selenium is thought to be essential for various immune responses, the excess supplementation may have an adverse effect on certain immunological functions. The present study was designed to determine the effective chemical forms of selenium and their optimal levels on T-cell mitogenesis with splenic cells from mice given a selenium-deficient diet for 8 weeks to avoid effects of cellular selenium sources. Although selenium in tissues, except for spleen and thymus, was almost depleted by feeding selenium-deficient diet, the lymphoid organs still contained low levels of selenium. Both activities of cellular glutathione peroxidase (cGPx) and thioredoxin reductase (TR) in liver and splenic cells showed a tendency to decrease by selenium deficiency. However, splenic cells were tolerant against decrease of the selenoenzyme activities, and TR was also more tolerant than cGPx. T-cell proliferation of the selenium-insufficient splenic cells induced by concanavalin A was increased by addition of Na2SeO3, Na2SeO4, Na2Se, seleno-DL-cystine, seleno-L-methionine and selenocystamine. Their promoting action was observed at levels lower than 0.1 micromol/L and was completely suppressed at the highest concentration (1 micromol/L), except for selenocystamine. Na2SeO3 was one of the efficient selenocompounds for the mitogenesis, which was concomitant with the significant induction of cGPx and TR. However, recovery of cGPx activity in the selenium-insufficient cells by supplementary Na2SeO3 was only partial,while TR activity was readily recovered from selenium deficiency. These results therefore indicate that only low levels of selenium is essential for T-cell mitogenesis even in selenium-insufficient splenic cells, and TR, which is readily recovered by Na2SeO3, may be the critical enzyme.
authors.affiliation: Faculty of Pharmaceutical Sciences, Setsunan University, 45-1, Nagaotoge-cho, Hirakata, Osaka 573-0101, Japan. ueno@pharm.setsunan.ac.jp
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ueno
authors.forename: Gohki
authors.initials: G
authors.lastname: Hasegawa
authors.forename: Ryoko
authors.initials: R
authors.lastname: Ido
authors.forename: Tomofumi
authors.initials: T
authors.lastname: Okuno
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Nakamuro
mesh_terms: D000818:Animals; D005979:Glutathione Peroxidase / Q000378:metabolism; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D016566:Organoselenium Compounds / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D018038:Sodium Selenite / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D013154:Spleen / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism
chemical_list: D016566:Organoselenium Compounds; D005979:Glutathione Peroxidase; D013880:Thioredoxin-Disulfide Reductase; D018038:Sodium Selenite