PMID- 15695021
OWN - NLM
STAT- MEDLINE
DCOM- 20050315
LR  - 20231213
IS  - 0300-483X (Print)
IS  - 0300-483X (Linking)
VI  - 208
IP  - 3
DP  - 2005 Mar 30
TI  - The effects of gestational arsenic exposure and dietary selenium deficiency on 
      selenium and selenoenzymes in maternal and fetal tissues in mice.
PG  - 357-65
AB  - Although toxicological and metabolic interactions of arsenic (As) and selenium 
      (Se) have been suggested by epidemiolgical literatures, the past experimental 
      studies mostly focused on acute, high-dose interaction, leaving the long-term, 
      low-dose interaction unexplored. In the present study pregnant mice, fed either 
      Se-deficient or adequate (0 or 5 micromol Se/kg diet, respectively) diet, were 
      given oral gavage of sodium arsenite (0 or 58 micromol/kg per day; chosen as less 
      than half of the fetotoxic dose in this protocol) from gestational day (GD) 7-16. 
      The levels of As and Se as well as five selenoenzymes (glutathione peroxidase 
      (GPx), thioredoxin reductase (TRxR), and type-I, -II and -III iodothyronine 
      deiodinases (DI-I, -II and -III) were examined on GD17 in the tissues of dams and 
      of fetus. The Se-deficient mice showed significantly enhanced accumulation of As 
      compared to the Se-adequate mice in maternal liver (increased by 48%) and fetal 
      brain (by 31%). Although no direct evidence of the enhanced toxicity in the 
      Se-deficient group was obtained, the As exposure affected the levels of Se and 
      selenoenzymes, an effect which was more discernible in Se-deficient group. 
      Although most of theses changes were mild or moderate, the DI-II activity in 
      Se-deficient fetal brain showed a drastic four-fold increase by As exposure, 
      suggesting a possible disturbance of thyroid hormone environment in the fetus. 
      These data suggested that apparently non-toxic, in utero dose of As, showed 
      enhanced accumulation when combined with Se-deficiency and could affect the 
      metabolism/kinetics of Se in fetal brain, which might result in developmental 
      toxicity in mice.
FAU - Miyazaki, Kaori
AU  - Miyazaki K
AD  - Department of Public Health, Division of Environmental Medicine, Gunma University 
      Graduate School of Medicine, 3-39-22, Maebashi City, Gunma 371-8510, Japan. 
      kmiyazak@med.gunma-u.ac.jp
FAU - Watanabe, Chiho
AU  - Watanabe C
FAU - Mori, Kouki
AU  - Mori K
FAU - Yoshida, Katusmi
AU  - Yoshida K
FAU - Ohtsuka, Ryutaro
AU  - Ohtsuka R
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Arsenites)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Sodium Compounds)
RN  - 0 (Water Pollutants, Chemical)
RN  - 48OVY2OC72 (sodium arsenite)
RN  - EC 1.11.1.- (iodothyronine deiodinase type I)
RN  - EC 1.11.1.- (iodothyronine deiodinase type III)
RN  - EC 1.11.1.8 (Iodide Peroxidase)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.8.1.9 (Thioredoxin-Disulfide Reductase)
RN  - H6241UJ22B (Selenium)
SB  - IM
MH  - Animals
MH  - Arsenites/*toxicity
MH  - Brain/drug effects/enzymology
MH  - Diet
MH  - Enzyme Inhibitors/*toxicity
MH  - Female
MH  - Fetus/drug effects/metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Iodide Peroxidase/metabolism
MH  - Liver/drug effects/enzymology
MH  - Maternal Exposure
MH  - *Maternal-Fetal Exchange
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Placenta/drug effects/enzymology
MH  - Pregnancy
MH  - Selenium/analysis/*deficiency
MH  - Sodium Compounds/*toxicity
MH  - Thioredoxin-Disulfide Reductase/metabolism
MH  - Water Pollutants, Chemical/*toxicity
MH  - Iodothyronine Deiodinase Type II
EDAT- 2005/02/08 09:00
MHDA- 2005/03/16 09:00
CRDT- 2005/02/08 09:00
PHST- 2004/08/30 00:00 [received]
PHST- 2004/11/20 00:00 [revised]
PHST- 2004/11/22 00:00 [accepted]
PHST- 2005/02/08 09:00 [pubmed]
PHST- 2005/03/16 09:00 [medline]
PHST- 2005/02/08 09:00 [entrez]
AID - S0300-483X(04)00670-5 [pii]
AID - 10.1016/j.tox.2004.11.030 [doi]
PST - ppublish
SO  - Toxicology. 2005 Mar 30;208(3):357-65. doi: 10.1016/j.tox.2004.11.030.