Increased oxidative stress and toxicity in ADH and CYP2E1 overexpressing human hepatoma VL-17A cells exposed to high glucose
Abstract
High glucose mediated oxidative stress and cell death is a well documented phenomenon. Using VL-17A cells which are HepG2 cells over-expressing alcohol dehydrogenase (ADH) and cytochrome P450 2E1 (CYP2E1) and control HepG2 cells, the association of ADH and CYP2E1 with high glucose mediated oxidative stress and toxicity in liver cells was investigated. Cell viability was measured and apoptosis or necrosis was determined through caspase-3 activity, Annexin V-propidium iodide staining and detecting decreases in mitochondrial membrane potential. Reactive oxygen species, lipid peroxidation and the formation of advanced glycated-end products were assessed. The levels of several antioxidants which included glutathione, glutathione peroxidase, catalase and superoxide dismutase were altered in high glucose treated VL-17A cells. Greater toxicity was observed in VL-17A cells exposed to high glucose when compared to HepG2 cells. Oxidative stress parameters were greatly increased in high glucose exposed VL-17A cells and apoptotic cell death was observed. Inhibition of CYP2E1 or caspase 3 or addition of the antioxidant trolox led to significant decreases in high glucose mediated oxidative stress and toxicity. Thus, the over-expression of ADH and CYP2E1 in liver cells is associated with increased high glucose mediated oxidative stress and toxicity.
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CYP2E1 was shown to be involved in the production of hepatic AA- and AA-MDA adducts.
“Since CYP2E1 was shown to be involved in the production of hepatic AA- and AA-MDA adducts137,181,250, it would be of interest to study the direct role of CYP2E1 in alcohol-mediated AGE production and GI pathologies.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [250]
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Xin, Y., Ligorio, C., O’Brien, M., Dong, S., Miller, A. F., Saiani, A., & Gough, J. E. (2023) · SSRN Electronic Journal · doi:10.2139/ssrn.4603487
- Authors
- Chandrasekaran, K., Swaminathan, K., Kumar, S. M., Clemens, D. L., & Dey, A.
- Affiliations
- Anna University, Chennai (IN)
- Omaha VA Medical Center (US)
- Corresponding author
- Dey, Aparajita
- Venue
- Integrative Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012
- Volume
- 4
- Issue
- 5
- Pages
- 550
- ISSN
- 1757-9694 (ISSN-L)
- 1757-9708
- OpenAlex
- W2057336314
- Cited by
- 18
- References
- 84
- Citations by year
- 2024: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2019: 1 · 2017: 2 · 2014: 3 · 2013: 6 · 2012: 1
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Integrative Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Nebraska Medical Center
- Royal Society
- Royal Society of Chemistry
- Department of Science and Technology, Ministry of Science and Technology, India
- Council of Scientific and Industrial Research, India
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- high glucose, oxidative stress, alcohol dehydrogenase, CYP2E1, hepatotoxicity, apoptosis, caspase-3, advanced glycation end products, lipid peroxidation, reactive oxygen species, antioxidant enzymes, Trolox, HepG2 cells, mitochondrial membrane potential
- MeSH terms
- Cytochrome P450 Family 2, Alcohol Dehydrogenase, Cell Survival, Cytochrome P-450 Enzyme System, Glucose, Carcinoma, Hepatocellular, Humans, Up-Regulation, Apoptosis, Oxidative Stress, Cell Line, Tumor
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