Document Detail


Selenoprotein P inhibits radiation-induced late reactive oxygen species accumulation and normal cell injury.
MedLine Citation:
PMID:  24074935     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: Radiation is a common mode of cancer therapy whose outcome is often limited because of normal tissue toxicity. We have shown previously that the accumulation of radiation-induced late reactive oxygen species (ROS) precedes cell death, suggesting that metabolic oxidative stress could regulate cellular radiation response. The purpose of this study was to investigate whether selenoprotein P (SEPP1), a major supplier of selenium to tissues and an antioxidant, regulates late ROS accumulation and toxicity in irradiated normal human fibroblasts (NHFs).
METHODS AND MATERIALS: Flow cytometry analysis of cell viability, cell cycle phase distribution, and dihydroethidium oxidation, along with clonogenic assays, were used to measure oxidative stress and toxicity. Human antioxidant mechanisms array and quantitative real-time polymerase chain reaction assays were used to measure gene expression during late ROS accumulation in irradiated NHFs. Sodium selenite addition and SEPP1 overexpression were used to determine the causality of SEPP1 regulating late ROS accumulation and toxicity in irradiated NHFs.
RESULTS: Irradiated NHFs showed late ROS accumulation (4.5-fold increase from control; P<.05) that occurs after activation of the cell cycle checkpoint pathways and precedes cell death. The mRNA levels of CuZn- and Mn-superoxide dismutase, catalase, peroxiredoxin 3, and thioredoxin reductase 1 increased approximately 2- to 3-fold, whereas mRNA levels of cold shock domain containing E1 and SEPP1 increased more than 6-fold (P<.05). The addition of sodium selenite before the radiation treatment suppressed toxicity (45%; P<.05). SEPP1 overexpression suppressed radiation-induced late ROS accumulation (35%; P<.05) and protected NHFs from radiation-induced toxicity (58%; P<.05).
CONCLUSION: SEPP1 mitigates radiation-induced late ROS accumulation and normal cell injury.
Authors:
Jaimee C Eckers; Amanda L Kalen; Wusheng Xiao; Ehab H Sarsour; Prabhat C Goswami
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  International journal of radiation oncology, biology, physics     Volume:  87     ISSN:  1879-355X     ISO Abbreviation:  Int. J. Radiat. Oncol. Biol. Phys.     Publication Date:  2013 Nov 
Date Detail:
Created Date:  2013-09-30     Completed Date:  2013-11-18     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  7603616     Medline TA:  Int J Radiat Oncol Biol Phys     Country:  United States    
Other Details:
Languages:  eng     Pagination:  619-25     Citation Subset:  IM    
Copyright Information:
Copyright © 2013 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Cell Cycle Checkpoints / physiology,  radiation effects
Cell Death
Cell Survival
Dose-Response Relationship, Radiation
Ethidium / analogs & derivatives,  metabolism
Fibroblasts / metabolism,  radiation effects
Genes, vif
Humans
Oxidative Stress / genetics
Radiation Injuries / prevention & control*
Reactive Oxygen Species / metabolism*
Real-Time Polymerase Chain Reaction
Selenoprotein P / genetics,  metabolism,  physiology*
Sodium Selenite / pharmacology
Grant Support
ID/Acronym/Agency:
2R01CA111365/CA/NCI NIH HHS; P30 ES005605/ES/NIEHS NIH HHS; P42 ES013661/ES/NIEHS NIH HHS; P42ES013661/ES/NIEHS NIH HHS; R01 CA111365/CA/NCI NIH HHS; T32 CA078586/CA/NCI NIH HHS; T32CA078586/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 0/Selenoprotein P; 104821-25-2/dihydroethidium; EN464416SI/Ethidium; HIW548RQ3W/Sodium Selenite

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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