Journal of Nutrition and Health

The Korean Nutrition Society (한국영양학회)
권호 표지
DOI QR코드

DOI QR Code

A plant-based multivitamin, multimineral, and phytonutrient supplementation enhances the DNA repair response to metabolic challenges

  • Yeo, Eunji (Department of Food and Nutrition, Hannam University) ;
  • Hong, Jina (Access Business Group International, LLC) ;
  • Kang, Seunghee (Department of Nutritional Science and Food Management, Ewha Womans University) ;
  • Lee, Wonyoung (Department of Food and Nutrition, Hannam University) ;
  • Kwon, Oran (Department of Nutritional Science and Food Management, Ewha Womans University) ;
  • Park, Eunmi (Department of Food and Nutrition, Hannam University)
  • Received : 2022.05.31
  • Accepted : 2022.08.08
  • Published : 2022.08.31
Download PDF
⟨ Previous Next ⟩

Abstract

Purpose: DNA damage and repair responses are induced by metabolic diseases and environmental stress. The balance of DNA repair response and the antioxidant system play a role in modulating the entire body's health. This study uses a high-fat and high-calorie (HFC) drink to examine the new roles of a plant-based multivitamin/mineral supplement with phytonutrients (PMP) for regulating the antioxidant system and cellular DNA repair signaling in the body resulting from metabolic stress. Methods: In a double-blind, randomized, parallel-arm, and placebo-controlled trial, healthy adults received a capsule containing either a PMP supplement (n = 12) or a placebo control (n = 12) for 8 weeks. Fasting blood samples were collected at 0, 1, and 3 hours after consuming a HFC drink (900 kcal). The blood samples were analyzed for the following oxidative stress makers: areas under the curve reactive oxygen species (ROS) levels, plasma malondialdehyde (MDA), erythrocytes MDA, urinary MDA, oxidized low-density lipoprotein, and the glutathione:oxidized glutathione ratio at the time points. We further examined the related protein levels of DNA repair signaling (pCHK1 (Serine 345), p-P53 (Serine 15), and 𝛄H2AX expression) in the plasma of subjects to evaluate the time-dependent effects of a HFC drink. Results: In a previous study, we showed that PMP supplementation for eight weeks reduces the ROS and endogenous DNA damage in human blood plasma. Results of the current study further show that PMP supplementation is significantly correlated with antioxidant defense. Compared to the placebo samples, the blood plasma obtained after PMP supplementation showed enhanced DNA damage response genes such as pCHK1(Serine 345) (a transducer of DNA response) and 𝛄H2AX (a hallmark of DNA damage) during the 8 weeks trial on metabolic challenges. Conclusion: Our results indicate that PMP supplementation for 8 weeks enhances the antioxidant system against oxidative stress and prevents DNA damage signaling in humans.

Keywords

Acknowledgement

This study was supported by Amway Korea, Ltd. (Seoul, Korea).

References

  1. Shimizu I, Yoshida Y, Suda M, Minamino T. DNA damage response and metabolic disease. Cell Metab 2014; 20(6): 967-977. https://doi.org/10.1016/j.cmet.2014.10.008
  2. Barzilai A, Yamamoto K. DNA damage responses to oxidative stress. DNA Repair (Amst) 2004; 3(8-9): 1109-1115. https://doi.org/10.1016/j.dnarep.2004.03.002
  3. Al-Aubaidy HA, Jelinek HF. Oxidative DNA damage and obesity in type 2 diabetes mellitus. Eur J Endocrinol 2011; 164(6): 899-904. https://doi.org/10.1530/EJE-11-0053
  4. Elledge SJ. Cell cycle checkpoints: preventing an identity crisis. Science 1996; 274(5293): 1664-1672. https://doi.org/10.1126/science.274.5293.1664
  5. Kang S, Lim Y, Kim YJ, Jung ES, Suh DH, Lee CH, et al. Multivitamin and mineral supplementation containing phytonutrients scavenges reactive oxygen species in healthy subjects: a randomized, double-blinded, placebo-controlled trial. Nutrients 2019; 11(1): E101.
  6. Stroeve JH, van Wietmarschen H, Kremer BH, van Ommen B, Wopereis S. Phenotypic flexibility as a measure of health: the optimal nutritional stress response test. Genes Nutr 2015; 10(3): 13.
  7. Cho J, Park E. Ferulic acid maintains the self-renewal capacity of embryo stem cells and adipose-derived mesenchymal stem cells in high fat diet-induced obese mice. J Nutr Biochem 2020; 77: 108327.
  8. Tukey JW. Exploratory data analysis. Boston (MA): Addison-Wesley; 1977.
  9. Kardinaal AF, van Erk MJ, Dutman AE, Stroeve JH, van de Steeg E, Bijlsma S, et al. Quantifying phenotypic flexibility as the response to a high-fat challenge test in different states of metabolic health. FASEB J 2015; 29(11): 4600-4613. https://doi.org/10.1096/fj.14-269852
  10. Zhang Y, Hunter T. Roles of Chk1 in cell biology and cancer therapy. Int J Cancer 2014; 134(5): 1013-1023. https://doi.org/10.1002/ijc.28226
  11. Wellen KE, Thompson CB. Cellular metabolic stress: considering how cells respond to nutrient excess. Mol Cell 2010; 40(2): 323-332. https://doi.org/10.1016/j.molcel.2010.10.004
  12. Rajgopal A, Roloff SJ, Burns CR, Fast DJ, Scholten JD. The cytoprotective benefits of a turmeric, quercetin, and rosemary blend through activation of the oxidative stress pathway. Pharmacogn Mag 2019; 15(66): 449.
  13. Missler SR, Rajgopal A, Roloff SJ, Scholten JD, Burns CR, Patterson JA, et al. Synergistic activation of the Nrf2-ARE oxidative stress response pathway by a combination of botanical extracts. Planta Medica International Open 2016; 3(02): e27-e30. https://doi.org/10.1055/s-0036-1585165
  14. Lopez-Otin C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell 2013; 153(6): 1194-1217. https://doi.org/10.1016/j.cell.2013.05.039
  15. Tchkonia T, Zhu Y, van Deursen J, Campisi J, Kirkland JL. Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. J Clin Invest 2013; 123(3): 966-972. https://doi.org/10.1172/JCI64098
  16. Bartek J, Lukas J. Chk1 and Chk2 kinases in checkpoint control and cancer. Cancer Cell 2003; 3(5): 421-429. https://doi.org/10.1016/S1535-6108(03)00110-7
  17. Sorensen CS, Syljuasen RG, Falck J, Schroeder T, Ronnstrand L, Khanna KK, et al. Chk1 regulates the S phase checkpoint by coupling the physiological turnover and ionizing radiation-induced accelerated proteolysis of Cdc25A. Cancer Cell 2003; 3(3): 247-258. https://doi.org/10.1016/S1535-6108(03)00048-5
  18. McGowan CH. Checking in on Cds1 (Chk2): a checkpoint kinase and tumor suppressor. BioEssays 2002; 24(6): 502-511. https://doi.org/10.1002/bies.10101
  19. Wittlinger M, Grabenbauer GG, Sprung CN, Sauer R, Distel LV. Time and dose-dependent activation of p53 serine 15 phosphorylation among cell lines with different radiation sensitivity. Int J Radiat Biol 2007; 83(4): 245-257. https://doi.org/10.1080/09553000701275432