Affiliations: Department of Nutrition Sciences, University of Nevada
Las Vegas, Las Vegas, NV, USA | Department of Nutrition, Hospitality, and Retailing,
Texas Tech University, Lubbock, TX, USA
Note: [] Address for correspondence: Jau-Jiin Chen, PhD, RD, Department
of Nutrition Sciences, University of Nevada Las Vegas, 4505 S. Maryland Pkwy,
Box 453026, Las Vegas, NV 89154-3026, USA. Tel.: +1 702 895 3946; Fax: +1 702
895 2616; E-mail: [email protected]
Abstract: The carcinostatic activities of selenium (Se) compounds have been
shown to be composition and concentration dependent. Several studies have
indicated that the ratios between glutathione (GSH) and Se may play an
important role in Se catalysis and toxicity. The present study examined the
catalytic effect of three selenium compounds on GSH oxidation using
lucigenin-dependent chemiluminescence (CL) as an indirect measure of superoxide
generation. Various GSH:Se ratios were assayed for the glutathione oxidase
activity of selenite, selenocystamine and diselenodipropionic acid. CL emitted
from the reaction of selenite with GSH increased more rapidly and was greater
than those from the diselenides, but the diselenide CL reactions were
sustainable. Both selenite- and diselenide-induced CL were markedly suppressed
by superoxide dismutase (SOD). Iodoacetic acid (IAc) effectively inhibited CL
generated from selenite-, selenocystamine- and diselenodipropionic
acid-catalyzed GSH oxidation. These results suggest that GSH oxidation
catalyzed by selenite, and the diselenides selenocystamine and
diselenodipropionic acid, generated the superoxide radical in which the CL was
inhibited by SOD. Furthermore, CL inhibition by IAc suggests that the catalytic
species producing superoxide were the GSSe^{-} or
RSe^{-} anion. This redox chemistry may be responsible for
selenite and organoselenium toxicity and apoptosis, making possible the design
and synthesis of organoselenium-containing pharmaceuticals.
