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J Cancer Prev. 2019 Mar;24(1):54-58. doi: 10.15430/JCP.2019.24.1.54. Epub 2019 Mar 30.

Astaxanthin Prevents Decreases in Superoxide Dismutase 2 Level and Superoxide Dismutase Activity in Helicobacter pylori-infected Gastric Epithelial Cells.

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Department of Food and Nutrition, Brian Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul, Korea.



Helicobacter pylori increases production of reactive oxygen species (ROS), which activates inflammatory and carcinogenesis-related signaling pathways in gastric epithelial cells. Therefore, reducing ROS, by upregulating antioxidant enzyme, such as superoxide dismutase (SOD), may be a novel strategy to prevent H. pylori-associated gastric diseases. Astaxanthin is an antioxidant carotenoid that prevents oxidative stress-induced cell injury. The present study was aimed to determine whether H. pylori decreases SOD activity by changing the levels of SOD1/SOD2 and whether astaxanthin prevents changes in SOD levels and activity in H. pylori-infected gastric epithelial AGS cells.


AGS cells were pre-treated with astaxanthin for 3 hours prior to H. pylori infection and cultured for 1 hour in the presence of H. pylori. SOD levels and activity were assessed by Western blot analysis and a commercial assay kit, respectively. Mitochondrial ROS was determined using MitoSOX fluorescence.


H. pylori decreased SOD activity and the SOD2 level, but increased mitochondrial ROS in AGS cells. The SOD1 level was not changed by H. pylori infection. Astaxanthin prevented H. pylori-induced decreases in the SOD2 level and SOD activity and reduced mitochondrial ROS in AGS cells.


Consumption of astaxanthin-rich food may prevent the development of H. pylori-associated gastric disorders by suppressing mitochondrial oxidative stress.


Astaxanthin; Gastric diseases; Helicobacter pylori; Reactive oxygen species; Superoxide dismutase

Conflict of interest statement

CONFLICTS OF INTEREST No potential conflicts of interest were disclosed.

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