Sargassum horneri ethanol extract containing polyphenols attenuates PM-induced oxidative stress via ROS scavenging and transition metal chelation

• Published in: Journal of functional foods 2021-04, Vol.79, p.104401, Article 104401
• Main Authors: Kim, Hyo Jin, Herath, Kalahe Hewage Iresha Nadeeka Madushani, Dinh, Duong Thi Thuy, Kim, Hyun-Soo, Jeon, You-Jin, Kim, Hyun Jung, Jee, Youngheun
• Format: Article
• Language: English
• Subjects: Antioxidant mechanisms; Metal chelating; MLE-12 cells; Oxidative stress; Particulate matter (PM); Sargassum horneri
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2021.104401

[Display omitted] •SHE chelates PM-derived transition metals adhered to MLE-12 cells’ surfaces.•SHE attenuates PM-induced intracellular ROS generation in MLE-12 cells.•SHE helps to regulate antioxidant enzyme activities to suppress oxidative stress.•SHE reduces oxidative DNA damages in MLE-12 cells exposed to PM.•SHE is possibly used as an antioxidant against PM-induced lung damage. Particulate matter (PM) generate oxidative stress and damage to exposed cells. In this study, we investigated the antioxidant mechanisms of Sargassum horneri ethanol extract (SHE) against PM in lung epithelial cell, MLE-12 cells. We discovered that transition metals in PM adhered to the surfaces of MLE-12 cells, triggering intracellular ROS generation and lipid peroxidation. The PM-induced oxidative stress in turn reduced the antioxidant enzymes activities. This disturbance in redox balance further produced oxidative DNA damage and eventually led to apoptotic cell death as expected. However, we uncovered that SHE containing polyphenols chelated the transition metals (Si, Mg, Al, Ti, and Fe) on the surfaces of MLE-12 cells. In addition, SHE not only attenuated the intracellular ROS and lipid peroxidation but also regulated antioxidant enzymes to suppress the PM-induce oxidative DNA damage and apoptotic cell death. These results suggest that SHE containing polyphenols contribute to the alleviation of the PM-induced oxidative stress and apoptotic cell death via ROS scavenging and transition metals chelating.