Journals / Kafkas Üniversitesi Veteriner Fakültesi Dergisi / 2016 / Cilt: 22 - Sayı: 6

Vitamin E'nin HepG2 Hücrelerinde Antioksidan Enzim AktivitesiÜzerine Etkileri

The Effects of Vitamin E on Antioxidant Enzyme Activity in HepG2 Cells [1]

Pages
865–869
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

It was determined that vitamin E has a dose-dependent effect on antioxidant enzyme activity in HepG2 cells

📌 3 Key Takeaways

🎯
Objective & Hypothesis:It is aimed to investigate the effect of vitamin E, powerful antioxidant (alpha-tocopherol succinate) on antioxidant enzyme activities in hepatocellular carcinoma (HepG2) cells.
📊
Key Findings & Data:The hepatocellular carcinoma cell line HepG2 was used and the cells were cultured in the absence (control) or presence of different dose of vitamin E (50 mM, 50 ?M and 10 ?M vitamin E) for 24 h.
💡
Conclusion & Impact:It was determined that vitamin E has a dose-dependent effect on antioxidant enzyme activity in HepG2 cells
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

It is aimed to investigate the effect of vitamin E, powerful antioxidant (alpha-tocopherol succinate) on antioxidant enzyme activities in hepatocellular carcinoma (HepG2) cells. The hepatocellular carcinoma cell line HepG2 was used and the cells were cultured in the absence (control) or presence of different dose of vitamin E (50 mM, 50 ?M and 10 ?M vitamin E) for 24 h. The effect of vitamin E (alpha-tocopherol succinate) on catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities in hepatocarcinoma cells were measured by spectrophotometry. A significant decrease in GPx activity was detected in 50 mM vitamin E treated HepG2 cells. However a significant decrease occurred in 10 µM and 50µM vitamin E applied HepG2 cells. SOD activity in study groups were lower than in control cells. In addition to this, the decrease in SOD activity in 50 mM vitamin E applied cells was significant. CAT enzyme activity in 50 ?m vitamin E applied HepG2 cells was higher and, in 10 ?M and 50 mM vitamin E applied HepG2 cells were lower than in control group. It was determined that vitamin E has a dose-dependent effect on antioxidant enzyme activity in HepG2 cells

Özet

Güçlü bir antioksidan olan vitamin E'nin (alfa-tokoferolsüksinat) HepG2 hücrelerinde antioksidan enzim aktiviteleri üzerine etkisinin araştırılması amaçlanmıştır. Çalışma materyali olarak HepG2 hücre hattı kullanılmıştır. Vitamin E uygulanan hücreler çalışma grubunu vitamin E uygulaması yapılmayan hücreler kontrol grubunu oluşturmuştur. Çalışma grubu hücrelerine 10 µM, 50 µM, 50 mM dozlarda vitamin E uygulaması yapılarak, 24 saat sonunda HepG2 hücrelerinde antioksidan enzimlerden katalaz (CAT), süperoksitdismutaz (SOD) ve glutasyonperoksidaz (GPx) aktiviteleri spektrofotometrik olarak ölçülmüştür. 50 mM vitamin E uygulanan HepG2 hücrelerinde GPx enzim aktivitesinde anlamlı bir artış saptanmıştır. Ancak, 10 µM ve 50 µM vitamin E uygulanan HepG2 hücrelerinde ise anlamlı bir azalma meydana gelmiştir. Vitamin E uygulaması yapılan hücrelerdeki SOD aktivitesi vitamin E uygulaması yapılmayan kontrol grubuna göre daha düşük ölçülürken, 50 µM vitamin E uygulanan HepG2 hücrelerinde SOD aktivitesinde anlamlı azalma tespit edilmiştir. 50 µM vitamin E uygulanan HepG2 hücrelerindeki CAT enzim aktivitesi kontrol grubuna göre daha yüksek bulunurken, 10 ?M ve 50 mM vitamin E uygulanan hücrelerdeki CAT enzim aktivitesi kontrol grubuna göre daha düşük tespit edilmiştir. Vitamin E'nin HepG2 hücrelerinde antioksidan enzim aktiviteleri üzerinde doz-bağımlı etkisinin olduğu belirlenmiştir

🔖

Cite This Article

KISMALI, G., ALPAY, M., SAYINER, S., TURAN, D., BALKAN, A. B., SALMANOĞLU, B., KARAGÜL, H., SEL, T., BALKAN, B. M. (2016). Vitamin E'nin HepG2 Hücrelerinde Antioksidan Enzim AktivitesiÜzerine Etkileri. Kafkas Üniversitesi Veteriner Fakültesi Dergisi, Cilt: 22 - Sayı: 6, 865–869. https://ajindex.com/articles/272457

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (8)

  1. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D: Global cancerstatistics. CA Cancer J Clin, 61, 69-90, 2011. DOI: 10.3322/caac.20107 Verma RS, Mehta A, Srivastava N: In vivo chlorpyrifos induced oxidative stress: Attenuation by antioxidant vitamins. Pestic Biochem Phys,, 191-196, 2007. DOI: 10.1016/j.pestbp.2006.11.002 IUPAC-IUB JointCommission on BiochemicalNomenclature (JCBN): Nomenclature of tocopherols and related compounds. Recomendations Eur J Biochem, 123, 473-475, 1982. DOI: 10.1111/j.1432-1033.1982. tb06554.x Sheppard AJ, Pennington JAT, Weihrauch JL: Analysis and distribution of vitamin E in vegetable oils and foods. In, Packer L, Fuchs J (Eds): Vitamin E in Health and Disease. 9-31,
  2. CRC Press,
  3. Marcel Dekker Inc., New York, 1993.
  4. Traber MG, Atkinson J: Vitamin E, antioxidant and nothing more. Free Radic Biol Med, 43, 4-15, 2007. DOI: 10.1016/j.freeradbiomed.2007.03.024 Pathak SK, Sharma RA, Steward WP, Mellon JK, Griffiths TR, Gescher AJ: Oxidative stress and cyclooxygenase activity in prostate carcinogenesis: targets for chemopreventive strategies. Eur J Cancer, 41, 70, 2005. DOI: 10.1016/j.ejca.2004.09.028 D'Archivio M, Santangelo C, Scazzocchio B, Vari R, Filesi C, Masella R, Giovannini C: Modulatory effects of polyphenols on apoptosis induction: Relevance for cancer prevention. Int J Mol Sci, 9, 213-228, 2008. DOI: 10.3390/ijms9030213 Stampfer M, Hennekens C, Manson J, Colditz G, Rosner B, Willett W: Vitamin E consumption and the risk of coronary disease in women. N Engl J Med, 328, 1444-1449, 1993. DOI: 10.1056/NEJM199305203282003
  5. Rimm ER, Stampfer MJ, Ascherio A, Giovannucci E, Colditz GA, Willett WC: Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med, 328, 1450-1456, 1993. DOI: 10.1056/ NEJM199305203282004
  6. Upston JM, Terentis AC, Stocker R: Tocopherol-mediated peroxidation (TMP) of lipoproteins: Implications for vitamin E as a potential anti- atherogenic supplement. FASEB J, 13, 977-994, 1999.
  7. Heisler T, Towfigh S, Simon N, Liu C, McFadden DW: Peptide YY augments gross inhibition by vitamin E succinate of human pancreatic cancer cell growth. J Surg Res, 88, 23-25, 2000. DOI: 10.1006/jsre. 1999.
  8. Heukamp I, Kilian M, Gregor JI, Neumann A, Jacobi CA, Guski H, Schimke I, Walz MK, Wenger FA: Effects of the antioxidative vitamins A, C and E on liver metastasis and intrametastatic lipid peroxidation in BOP- induced pancreatic cancer in Syrian hamsters. Pancreatology, 5, 403-409, DOI: 10.1159/000086541 Peng L