Document Detail

Over-expression of Senescence Marker Protein-30 decreases reactive oxygen species in human hepatic carcinoma Hep G2 cells.
MedLine Citation:
PMID:  19801822     Owner:  NLM     Status:  MEDLINE    
Senescence Marker Protein-30 (SMP30) is an androgen-independent factor that decreases with aging. We recently characterized SMP30 as a gluconolactonase (GNL) involved in the biosynthetic pathway of vitamin C and established that SMP30 knockout mice could not synthesize vitamin C in vivo. Although mice normally synthesize vitamin C, humans are prevented from doing so by mutations that have altered the gluconolactone oxidase gene during evolution. Even the SMP30/GNL present abundantly in the human liver does not synthesize vitamin C in vivo. To clarify the functions of this SMP30/GNL, we transfected the human SMP30/GNL gene into the human liver carcinoma cell line, Hep G2. The resulting Hep G2/SMP30 cells expressed approximately 10.9-fold more SMP30/GNL than Hep G2/pcDNA3 mock-transfected control cells. Examination of SMP30/GNL's impact on the state of oxidative stress in these cells revealed that formation of the reactive oxygen species (ROS) of mitochondrial and post-mitochondrial fractions from Hep G2/SMP30 cells decreased by a significant 24.0% and 18.1%, respectively, compared to those from Hep G2/pcDNA3 cells. Lipid peroxidation levels in Hep G2/SMP30 cells similarly decreased. Moreover, levels of the antioxidants superoxide dismutase (SOD) and glutathione (GSH) in Hep G2/SMP30 cells were a significant 42.6% and 62.4% lower than those in Hep G2/pcDNA3 cells, respectively. Thus, over-expression of SMP30/GNL in Hep G2 cells contributed to a decrease of ROS formation accompanied by decreases of lipid peroxidation, SOD activity and GSH levels.
Setsuko Handa; Naoki Maruyama; Akihito Ishigami
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biological & pharmaceutical bulletin     Volume:  32     ISSN:  1347-5215     ISO Abbreviation:  Biol. Pharm. Bull.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-10-05     Completed Date:  2010-01-28     Revised Date:  2010-03-08    
Medline Journal Info:
Nlm Unique ID:  9311984     Medline TA:  Biol Pharm Bull     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  1645-8     Citation Subset:  IM    
Aging Regulation, Tokyo Metropolitan Institute of Gerontology, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Aging / metabolism
Antioxidants / metabolism*
Ascorbic Acid / biosynthesis
Calcium-Binding Proteins / genetics,  metabolism*
Carboxylic Ester Hydrolases / genetics,  metabolism
Carcinoma, Hepatocellular / metabolism
Gene Expression*
Glutathione / metabolism
Hep G2 Cells / metabolism
Intracellular Signaling Peptides and Proteins / genetics,  metabolism*
Lipid Peroxidation*
Liver / enzymology*
Liver Neoplasms / metabolism
Mice, Knockout
Mitochondria / metabolism
Oxidative Stress*
Reactive Oxygen Species / metabolism*
Superoxide Dismutase / metabolism
Reg. No./Substance:
0/Antioxidants; 0/Calcium-Binding Proteins; 0/Intracellular Signaling Peptides and Proteins; 0/Reactive Oxygen Species; 0/Rgn protein, mouse; 50-81-7/Ascorbic Acid; 70-18-8/Glutathione; EC Dismutase; EC 3.1.1.-/Carboxylic Ester Hydrolases; EC

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

Previous Document:  Oligovascular signaling in white matter stroke.
Next Document:  Chlorpyrifos induces delayed cytotoxicity after withdrawal in primary hippocampal neurons through ex...