Effect of olive oil phenol hydroxytyrosol (HT) in patient cell model with mitochondrial complex deficiency

Abstract

Background: There is growing evidence suggesting that daily consumption of high phenolicscontaining extra-virgin olive oil (EVOO) has beneficial effects on preventing neurodegeneration related to the high level of antioxidants. Previous literature demonstrated that phenolics such as hydroxytyrosol (HT) in EVOO, with strong antioxidant properties, are potential dietary supplements against the oxidative stress in brain tissue and protective effect on both acute and chronic neurodegenerative diseases by in vitro study and animal models. Objective: In this study, we aim to investigate the effect of olive oil phenol, HT, on cell viability and oxidative stress induced by hydrogen peroxide in patient fibroblasts with mitochondrial complex IV deficiency, a neurodegenerative disease. Methods: Patient fibroblasts were pre-treated with different doses (1, 10 and 20 µM) of HT for 24 hours. For viability, cells were exposed to oxidative stress by 100 µM of hydrogen peroxide for 90 min and cell viability was measured by MTT assay. For reaction oxygen species (ROS) measurement, cells pre-treated and post-treated with HT were exposed to 100 µM of hydrogen peroxide and cellular ROS were quantified by fluorescent indicator dichlorodihydrofluorescein diacetate (H2DCFDA). Results: Exposure of patient fibroblasts to hydrogen peroxide in the presence of HT greatly reduced ROS level showing that HT possessed the ROS scavenging capacity. Cellular ROS induced by hydrogen hydroxide decreased when cells were pre-treated with hydroxytyrosol. Pre-treatment with 10 and 20 µM of HT for 24 hours significantly increased cell viability in patient fibroblasts after exposure to hydrogen hydroxide. Conclusion: The present study demonstrated that HT could protect patient cells against oxidative stress induced by hydrogen peroxide. In mitochondrial diseases, deficiencies in mitochondrial respiratory chain complexes result in alteration of cellular redox state and increase in ROS production. The protective effect of HT against oxidative stress indicated its therapeutical role in mitochondrial diseases.