Association between DNA repair capacity and body mass index in women

IF 1.5 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2023-01-01 DOI:10.1016/j.mrfmmm.2022.111813

Ian Crespo-Orta , Carmen Ortiz , Jarline Encarnación , Erick Suárez , Jaime Matta

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引用次数: 1

Abstract

Objective

Examine whether DNA repair capacity (DRC) levels are associated with body mass index (BMI) in adult women.

Design and participants

A nested study composed of 539 women without breast cancer (BC) from a case-control BC study in addition to 104 that were recruited later for a total of 643.

Measurements

DRC levels were measured in lymphocytes using a host-cell reactivation assay with a luciferase reporter gene damaged by UVC. This assay measures the efficiency of nucleotide excision repair (NER). Log-binomial regression model was used. The prevalence ratio (PR) was used to evaluate the magnitude of the association between the BMI and DRC levels. An assessment of interaction terms was performed with the likelihood ratio test. The confounding effect was assessed by comparing the point estimates of the crude and adjusted PR.

Results

The 75th percentiles of DRC levels of the women with a BMI between 18 and 25 and > 25 showed statistically significant differences. The prevalence of a DRC ≤ 5 % among women with BMI > 25 is 1.24 (95 % CI: 1.03, 1.48) times the prevalence of having a DRC ≤ 5 % among the women with BMI ≤ 25 after adjustments for different covariates. This excess was statistically significant (p < 0.05). Women with a family history of cancer had an estimated PR of 1.25 (95 % CI, 0.87–1.39; P ≥ 0.05); and women with no family history of cancer, the estimated PR was 1.6 (95 % CI, 1.14–2.22; p ≤ 0.05).

Conclusions

Women with BMI > 25 tend to have lower DRC levels. When having a family history of cancer, the PR of low DRC levels in overweight/obese individuals was not statistically significant. However, the PR of low levels of DRC in overweight/obese individuals with no family history of cancer was statistically significant.

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女性DNA修复能力与体重指数的关系

目的探讨成年女性的DNA修复能力（DRC）水平是否与体重指数（BMI）有关。设计和参与者一项嵌套研究由539名没有患癌症（BC）的女性组成，这些女性来自一项病例对照BC研究，另外104名后来被招募，共643人。测量使用宿主细胞再激活试验测量淋巴细胞中的RC水平，该试验使用被UVC损伤的荧光素酶报告基因。该测定法测量核苷酸切除修复（NER）的效率。采用对数二项回归模型。患病率（PR）用于评估BMI和DRC水平之间的关联程度。使用似然比检验对交互项进行评估。通过比较粗PR和调整PR的点估计值来评估混杂效应。结果BMI在18-25之间且>；25例差异有统计学意义。在BMI>；的女性中，DRC的患病率≤5%；在对不同协变量进行调整后，BMI≤25的女性中，25是DRC≤5%患病率的1.24倍（95%CI:1.03，1.48）。这一超出具有统计学意义（p＜0.05）。有癌症家族史的女性的估计PR为1.25（95%CI，0.87-1.39；p≥0.05）；与无癌症家族史的女性相比，估计PR为1.6（95%CI，1.14–2.22；p≤0.05）；25的DRC水平往往较低。当有癌症家族史时，超重/肥胖个体的低DRC水平的PR在统计学上不显著。然而，在没有癌症家族史的超重/肥胖个体中，低水平DRC的PR具有统计学意义。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis 生物-毒理学

CiteScore

4.90

自引率

0.00%

发文量

审稿时长

51 days

期刊介绍： Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.