Faculty of Nutrition, Federal University of Mato Grosso, Cuiabá, Mato Grosso, Brazil; Postgraduate Program in Health Sciences, Faculty of Medicine, Federal University of Mato Grosso, Cuiabá, Mato Grosso, Brazil.
Postgraduate Program in Health Sciences, Faculty of Medicine, Federal University of Mato Grosso, Cuiabá, Mato Grosso, Brazil.
J Nutr Biochem. 2022 Sep;107:109070. doi: 10.1016/j.jnutbio.2022.109070. Epub 2022 May 27.
The risk for cardiovascular diseases (CVR) has been associated with oxidative DNA damage, but the genetic and environmental factors involved in the antioxidant and DNA repair system contributing to this damage are unknown. The aim was to evaluate the levels of oxidative DNA damage in CVR subjects and how it is related with some genetic and nutritional factors. The cross-sectional study evaluated 136 individuals of both sexes, aged 20-59 years, with at least one cardiovascular risk factor. The global risk score was used to classify individuals at low, intermediate, and high cardiovascular risk. The dietary total antioxidant capacity (DTAC) was calculated using table with FRAP values. The oxidative DNA damage was verified by the comet assay. The variants null of Glutathione-S-transferases Mu1 and Theta 1(GSTM1 and GSTT1) and rs25487 of X-Ray Repair Cross Complementing Protein 1 (XRCC1) were analyzed by real-time PCR and PCR-RFLP, respectively. The oxidative DNA damage was higher in patients with intermediate/high CVR than in patients with low CVR (P=.01). Individuals with GSTT1/GSTM1 null genotypes or arg/gln+gln/gln genotypes of the XRCC1 (rs25487) gene showed similar levels of oxidative DNA damage compared wild genotype. Multivariate regression analysis demonstrated that oxidative DNA damage in individuals with CVR depends on serum levels of vitamin A, selenium, and DTAC independently of the other factors [F(6.110)=8.213; P<.001; R2=0.330]. These findings suggest that nutritional factors such as DTAC, vitamin A and selenium may have a protective effect against oxidative DNA damage in these individuals.
心血管疾病（CVR）的风险与氧化 DNA 损伤有关，但涉及抗氧化和 DNA 修复系统的遗传和环境因素尚不清楚。目的是评估 CVR 受试者的氧化 DNA 损伤水平，以及它与某些遗传和营养因素的关系。这项横断面研究评估了 136 名年龄在 20-59 岁之间的男女，他们至少有一个心血管危险因素。使用全球风险评分将个体分为低、中、高心血管风险。使用 FRAP 值表计算膳食总抗氧化能力（DTAC）。通过彗星试验验证氧化 DNA 损伤。谷胱甘肽 S-转移酶 Mu1 和 Theta 1（GSTM1 和 GSTT1）的无效变体和 X 射线修复交叉互补蛋白 1（XRCC1）的 rs25487 分别通过实时 PCR 和 PCR-RFLP 进行分析。中间/高 CVR 患者的氧化 DNA 损伤高于低 CVR 患者（P=.01）。GSTM1/GSTT1 无效基因型或 XRCC1（rs25487）基因的 arg/gln+gln/gln 基因型个体的氧化 DNA 损伤与野生基因型相似。多元回归分析表明，CVR 个体的氧化 DNA 损伤取决于血清中维生素 A、硒和 DTAC 的水平，而与其他因素无关[F(6.110)=8.213；P<.001；R2=0.330]。这些发现表明，DTAC、维生素 A 和硒等营养因素可能对这些个体的氧化 DNA 损伤具有保护作用。
