Antioxidant Activity Evaluation of Dietary Flavonoid Hyperoside Using <i>Saccharomyces Cerevisiae</i> as a Model

• Main Authors: Yuting Gao, Lianying Fang, Xiangxing Wang, Ruoni Lan, Meiyan Wang, Gang Du, Wenqiang Guan, Jianfu Liu, Margaret Brennan, Hongxing Guo, Charles Brennan, Hui Zhao
• Format: Article
• Language: English
• Published: MDPI AG 2019-02-01
• Series: Molecules
• Subjects: hyperoside; oxidative damage; lipid peroxidation; intracellular ROS; <i>Saccharomyces cerevisiae</i>
• Online Access: https://www.mdpi.com/1420-3049/24/4/788

Oxidative stress leads to various diseases, including diabetes, cardiovascular diseases, neurodegenerative diseases, and even cancer. The dietary flavonol glycoside, hyperoside (quercetin-3-<i>O</i>-galactoside), exerts health benefits by preventing oxidative damage. To further understand its antioxidative defence mechanisms, we systemically investigated the regulation of hyperoside on oxidative damage induced by hydrogen peroxide, carbon tetrachloride, and cadmium in <i>Saccharomyces cerevisiae</i>. Hyperoside significantly increased cell viability, decreased lipid peroxidation, and lowered intracellular reactive oxygen species (ROS) levels in the wild-type strain (WT) and mutants <i>gtt1∆</i> and <i>gtt2∆</i>. However, the strain with <i>ctt1∆</i> showed variable cell viability and intracellular ROS-scavenging ability in response to the hyperoside treatment upon the stimulation of H₂O₂ and CCl₄. In addition, hyperoside did not confer viability tolerance or intercellular ROS in CdSO₄-induced stress to strains of <i>sod1∆</i> and <i>gsh1∆.</i> The results suggest that the antioxidative reactions of hyperoside in <i>S. cerevisiae</i> depend on the intercellular ROS detoxification system.