ArticleMedical science monitor : international medical journal of experimental and clinical research2012
Altered expression of base excision repair genes in response to high glucose-induced oxidative stress in HepG2 hepatocytes.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- The protective role of resveratrol against high glucose-induced oxidative stress and apoptosis in HepG2 cells.Food science & nutrition · 2024Article
- Single-Nucleotide Polymorphisms in Base-Excision Repair-Related Genes Involved in the Risk of an Occurrence of Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2023Article
- Article
- Glucose Increases STAT3 Activation, Promoting Sustained XRCC1 Expression and Increasing DNA Repair.International journal of molecular sciences · 2022Article
- Flavonoids fromAging · 2020Article
- DNA repair deficiency and senescence in concussed professional athletes involved in contact sports.Acta neuropathologica communications · 2019Article
- Liraglutide improves lipid metabolism by enhancing cholesterol efflux associated with ABCA1 and ERK1/2 pathway.Cardiovascular diabetology · 2019Article
- Radiation-Induced Reactions in The Liver - Modulation of Radiation Effects by Lifestyle-Related Factors.International journal of molecular sciences · 2018Review
- Differential Impact of Flavonoids on Redox Modulation, Bioenergetics, and Cell Signaling in Normal and Tumor Cells: A Comprehensive Review.Antioxidants & redox signaling · 2018Review
- Cinnamomum osmophloeum Kanehira ethanol extracts prevents human liver-derived HepG2 cell death from oxidation stress by induction of ghrelin gene expression.Journal of biosciences · 2017Article
- Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study.Journal of clinical and diagnostic research : JCDR · 2017Article
- A novel method for determining human ex vivo submaximal skeletal muscle mitochondrial function.The Journal of physiology · 2015Article
- Roles of Sulfur Metabolism and Rhodanese in Detoxification and Anti-Oxidative Stress Functions in the Liver: Responses to Radiation Exposure.Medical science monitor : international medical journal of experimental and clinical research · 2015Review
- Differential Response to High Glucose in Skin Fibroblasts of Monozygotic Twins Discordant for Type 1 Diabetes.The Journal of clinical endocrinology and metabolism · 2015Article
- Oxidant stress and signal transduction in the nervous system with the PI 3-K, Akt, and mTOR cascade.International journal of molecular sciences · 2012Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt is widely accepted that chronic hyperglycemia induces DNA oxidative damage in type 2 diabetes, but little is known about the effect of hyperglycemia on the DNA repair system which plays a critical role in the maintenance of genomic DNA stability in diabetes. MATERIAL/
methodsTo investigate the alteration of base excision repair (BER) genes under hyperglycemia, the relative expression of the mRNAs of the BER genes--ogg1, polbeta, lig3, xrcc1, and parp1--were quantified using real-time PCR in HepG2 hepatocytes incubated with 5.5 mM or 30 mM glucose.
resultsHigh levels of glucose induced ROS accumulation and DNA damage, paralleling the dynamic alterations of BER mRNA expression. Compared to 5.5 mM glucose-treated cells, ogg1 and polbeta mRNA expression transiently increased at day 1 and decreased after day 4 in cells exposed to 30 mM glucose. Exposure to 30 mM glucose increased the activity of PARP1, which led to reduced cellular NAD content and insulin receptor phosphorylation.
conclusionsExposure to high concentrations of glucose initially led to the increased expression of BER mRNAs to counteract hyperglycemia-induced DNA damage; however, long-term exposure to high glucose concentrations reduced the expression of mRNA from BER genes, leading to accumulated DNA damage.
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