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Over-expression of Senescence Marker Protein-30 Decreases Reactive Oxygen Species in Human Hepatic Carcinoma Hep G2 Cells
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- Handa Setsuko
- Aging Regulation, Tokyo Metropolitan Institute of Gerontology
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- Maruyama Naoki
- Aging Regulation, Tokyo Metropolitan Institute of Gerontology
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- Ishigami Akihito
- Aging Regulation, Tokyo Metropolitan Institute of Gerontology Department of Biochemistry, Faculty of Pharmaceutical Sciences, Toho University
Bibliographic Information
- Other Title
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- Over-expression of senescence marker protein-30 decreases reactive oxygen species in human carcinoma HepG2 cells
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Description
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.
Journal
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- Biological and Pharmaceutical Bulletin
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Biological and Pharmaceutical Bulletin 32 (10), 1645-1648, 2009
The Pharmaceutical Society of Japan
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Keywords
Details 詳細情報について
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- CRID
- 1390282679601720448
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- NII Article ID
- 130000116921
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- NII Book ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL BIB ID
- 10375681
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- PubMed
- 19801822
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- Text Lang
- en
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- Article Type
- journal article
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- Data Source
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- JaLC
- NDL Search
- Crossref
- CiNii Articles
- KAKEN
- OpenAIRE
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- Abstract License Flag
- Disallowed