Antioxidant Activity Evaluation of Dietary Flavonoid Hyperoside Using Saccharomyces Cerevisiae as a Model.
Yuting GaoLianying FangXiangxing WangRuoni LanMeiyan WangGang DuWenqiang GuanJianfu LiuMargaret BrennanHongxing GuoCharles Stephen BrennanHui ZhaoPublished in: Molecules (Basel, Switzerland) (2019)
Oxidative stress leads to various diseases, including diabetes, cardiovascular diseases, neurodegenerative diseases, and even cancer. The dietary flavonol glycoside, hyperoside (quercetin-3-O-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 Saccharomyces cerevisiae. Hyperoside significantly increased cell viability, decreased lipid peroxidation, and lowered intracellular reactive oxygen species (ROS) levels in the wild-type strain (WT) and mutants gtt1∆ and gtt2∆. However, the strain with ctt1∆ 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 sod1∆ and gsh1∆. The results suggest that the antioxidative reactions of hyperoside in S. cerevisiae depend on the intercellular ROS detoxification system.
Keyphrases
- reactive oxygen species
- saccharomyces cerevisiae
- hydrogen peroxide
- dna damage
- cardiovascular disease
- cell death
- wild type
- oxidative stress
- healthcare
- type diabetes
- diabetic rats
- liver injury
- escherichia coli
- public health
- nitric oxide
- papillary thyroid
- adipose tissue
- drug induced
- mental health
- anti inflammatory
- risk assessment
- heavy metals
- stress induced
- social media
- health information
- glycemic control
- mass spectrometry
- endothelial cells
- induced apoptosis
- squamous cell
- replacement therapy