RRC ID 38118
Author Anan Y, Kimura M, Hayashi M, Koike R, Ogra Y.
Title Detoxification of selenite to form selenocyanate in mammalian cells.
Journal Chem Res Toxicol
Abstract When human hepatoma HepG2 cells were exposed to sodium selenite, an unknown selenium metabolite was detected in the cytosolic fraction by HPLC-inductively coupled plasma mass spectrometry (ICP-MS). The unknown selenium metabolite was also detected in the mixture of HepG2 homogenate and sodium selenite in the presence of exogenous glutathione (GSH). The unknown selenium metabolite was identified as selenocyanate by electrospray ionization mass spectrometry (ESI-MS) and ESI quadrupole time-of-flight mass spectrometry (ESI-Q-TOF-MS). Because exogenous cyanide increased the amount of selenocyanate in the mixture, selenocyanate seemed to be formed by the reaction between selenide or its equivalent, the product of the reduction of selenite, and endogenous cyanide. Rhodanase, an enzyme involved in thiocyanate synthesis, was not required for the formation of selenocyanate. Selenocyanate was less toxic to HepG2 cells than selenite or cyanide, suggesting that it was formed to reduce the toxicity of selenite. However, selenocyanate could be assimilated into selenoproteins and selenometabolites in rats in the same manner as selenite. Consequently, selenite was metabolized to selenocyanate to temporarily ameliorate its toxicity, and selenocyanate acted as an intrinsic selenium pool in cultured cells exposed to surplus selenite.
Volume 28(9)
Pages 1803-14
Published 2015-9-21
DOI 10.1021/acs.chemrestox.5b00254
PMID 26243445
MeSH Animals Chromatography, High Pressure Liquid Cyanates / metabolism* Hep G2 Cells Humans Male Mass Spectrometry Rats Rats, Wistar Selenious Acid / metabolism* Selenium Compounds / metabolism*
IF 3.184
Times Cited 18
WOS Category CHEMISTRY, MEDICINAL TOXICOLOGY CHEMISTRY, MULTIDISCIPLINARY
Resource
Human and Animal Cells Hep G2(RCB1886)