Publication

Associations of DNA Base Excision Repair and Antioxidant Enzyme Genetic Risk Scores with Biomarker of Systemic Inflammation.

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Last modified
  • 07/03/2025
Type of Material
Authors
    Ziling Mao, Emory UniversityAbigail LH Gray, Emory UniversityMyron D Gross, University of MinnesotaBharat Thyagarajan, University of MinnesotaRoberd Bostick, Emory University
Language
  • English
Date
  • 2022
Publisher
  • Frontiers
Publication Version
Copyright Statement
  • © 2022 Mao, Gray, Gross, Thyagarajan and Bostick.
License
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 3
Start Page
  • 897907
End Page
  • 897907
Grant/Funding Information
  • This work was supported by the National Cancer Institute at the National Institutes of Health under Grant R01 CA66539; The Fullerton Foundation; and the Anne and Wilson P. Franklin Foundation. None of the funding agencies had any role in the conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.
Supplemental Material (URL)
Abstract
  • Background: Inflammation is implicated in the etiology of various aging-related diseases. Numerous dietary and lifestyle factors contribute to chronic systemic inflammation; genetic variation may too. However, despite biological plausibility, little is known about associations of antioxidant enzyme (AE) and DNA base excision repair (BER) genotypes with human systemic inflammation. Methods: We genotyped 22 single nucleotide polymorphisms (SNPs) in 3 AE genes, and 79 SNPs in 14 BER genes to develop inflammation-specific AE and BER genetic risk scores (GRS) in two pooled cross-sectional studies (n = 333) of 30-74-year-old White adults without inflammatory bowel disease, familial adenomatous polyposis, or a history of cancer or colorectal adenoma. Of the genotypes, based on their associations with a biomarker of systemic inflammation, circulating high sensitivity C-reactive protein (hsCRP) concentrations, we selected 2 SNPs of 2 genes (CAT and MnSoD) for an AE GRS, and 7 SNPs of 5 genes (MUTYH, SMUG1, TDG, UNG, and XRCC1) for a BER GRS. A higher GRS indicates a higher balance of variant alleles directly associated with hsCRP relative to variant alleles inversely associated with hsCRP. We also calculated previously-reported, validated, questionnaire-based dietary (DIS) and lifestyle (LIS) inflammation scores. We used multivariable general linear regression to compare mean hsCRP concentrations across AE and BER GRS categories, individually and jointly with the DIS and LIS. Results: The mean hsCRP concentrations among those in the highest relative to the lowest AE and BER GRS categories were, proportionately, 13.9% (p = 0.30) and 57.4% (p = 0.009) higher. Neither GRS clearly appeared to modify the associations of the DIS or LIS with hsCRP. Conclusion: Our findings suggest that genotypes of DNA BER genes collectively may be associated with systemic inflammation in humans.
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Research Categories
  • Health Sciences, Public Health

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