Abstract
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.
Highlights
Oxidative stress reflects an imbalance between an organism’s excessive production of oxygen radicals and its reduced capacity to detoxify
We did not find hyperoside to be toxic to the evaluate impact of hyperoside on theand yeast cells, first determined celltolerance viability yeastTo cells withinthe thetoxic observed range of 10–40 mg/L, the cellswe continued to reachthe cells exposed to hyperoside for h
We did not find hyperoside to be toxic to the (Figure 2)
Summary
Oxidative stress reflects an imbalance between an organism’s excessive production of oxygen radicals and its reduced capacity to detoxify. It has been suggested that hyperoside target responding to oxidative stress, resulting in the functional decline of cells It has been suggested regulates the mitochondrial apoptotic pathway to prevent oxidative damage [20,21]. We used Saccharomyces cerevisiae as a model organism for studying protection because yeast has developed antioxidant defence systems, including an enzymatic ROS antioxidant protection because yeast has developed antioxidant defence systems, including an detoxification system that involves SOD, CTT1, GPX, and a non-enzymatic system mainly including enzymatic ROS detoxification system that involves SOD, CTT1, GPX, and a non-enzymatic system glutathione (GSH), to maintain intracellular redox status and ROS levels [2]. Gtt2∆) caused by oxidants (CdSO4, H2O2 and CCl4), and to provide further evidence for hyperoside to be used as and a health food product
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