Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Optimized models of xenobiotic-induced oxidative stress in HepG2 cells

Yollada Sriset¹, Waranya Chatuphonprasert^1,2, Kanokwan Jarukamjorn¹

¹Research Group for Pharmaceutical Activities of Natural Products using Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Khon Kaen University, Khon Kaen 40002; ²Faculty of Medicine, Mahasarakham University, Mahasarakham 44000, Thailand.

For correspondence:- Kanokwan Jarukamjorn Email: kanok_ja@kku.ac.th Tel:+6643202379

Accepted: 24 April 2019 Published: 31 May 2019

Citation: Sriset Y, Chatuphonprasert W, Jarukamjorn K. Optimized models of xenobiotic-induced oxidative stress in HepG2 cells. Trop J Pharm Res 2019; 18(5):1001-1007 doi: 10.4314/tjpr.v18i5.13

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To evaluate the molecular impact of ethanol, sodium selenite, and tert-butyl hydroperoxide (TBHP) on oxidant-antioxidant balance in HepG2 cells to establish an optimized oxidative stress model of HepG2 cells.

Methods: HepG2 cells were treated with ethanol (10 - 500 mM) and sodium selenite (1 - 10 µM) for 24 and 48 h and with TBHP (50 - 200 µM) for 3 and 24 h, respectively. Biomarkers for cellular injury, ie, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA), and for antioxidant system, i.e., superoxide dismutase (SOD), catalase (CAT), and total glutathione content, were determined.

Results: All treatments increased the levels of LDH, AST, ALT, and MDA but decreased SOD and CAT activities and the total glutathione content in HepG2 cells. Oxidative stress was induced by these oxidative stressors in HepG2 cells via oxidant-antioxidant imbalance, with TBHP (100 µM, 3 h) acting as a powerful oxidant based on the minimal time to induce oxidative stress. The antioxidants, ascorbic acid and gallic acid, improved oxidant-antioxidant imbalance against xenobiotic-induced oxidative stress in HepG2 cells.

Conclusion: These oxidative stress models are suitable for investigating the antioxidant and/or hepatoprotective potential of chemicals, including natural compounds.

Keywords: Ethanol, Sodium selenite, Tert-butyl hydroperoxide, Oxidative stressor, Oxidant-antioxidant balance