4.4 Article

Astaxanthin protects oxidative stress mediated DNA damage and enhances longevity in Saccharomyces cerevisiae

Journal

BIOGERONTOLOGY
Volume 22, Issue 1, Pages 81-100

Publisher

SPRINGER
DOI: 10.1007/s10522-020-09904-9

Keywords

Astaxanthin; ROS; Mutation; DNA damage

Funding

  1. DST [EMR/2016/008025]
  2. DBT, under the DBT-IPLS program Govt. of India [BT/PR14554/INF/22/125/2010]

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The study demonstrates that astaxanthin enhances the cell growth of DNA repair-deficient mutant cells, protects them from oxidative stress, reduces DNA damage caused by oxidative stress, and decreases apoptosis. Additionally, astaxanthin lowers the accumulation of mutation rate and prolongs the lifespan of DNA repair-deficient mutant cells.
Reactive oxygen species (ROS) have long been found to play an important role in oxidative mediated DNA damage. Fortunately, cells possess an antioxidant system that can neutralize ROS. However, oxidative stress occurs when antioxidants are overwhelmed by ROS or impaired antioxidant pathways. This study was carried out to find the protective effect of astaxanthin on the yeast DNA repair-deficient mutant cells under hydrogen peroxide stress. The results showed that astaxanthin enhances the percent cell growth of rad1 increment , rad51 increment , apn1 increment , apn2 increment and ogg1 increment cells. Further, the spot test and colony-forming unit count results confirmed that astaxanthin protects DNA repair mutant cells from oxidative stress. The DNA binding property of astaxanthin studied by in silico and in vitro methods indicated that astaxanthin binds to the DNA in the major and minor groove, and that might protect DNA against oxidative stress induced by Fenton's reagent. The intracellular ROS, 8-OHdG level and the DNA fragmentation as measured by comet tail was reduced by astaxanthin under oxidative stress. Similarly, reduced nuclear fragmentation and chromatin condensation results suggest that astaxanthin might reduce apoptosis. Finally, we show that astaxanthin decreases the accumulation of mutation rate and enhances the longevity of DNA repair-deficient mutants' cells during a chronological lifespan.

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