National Engineering Laboratory for Internet Medical Systems and Applications, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China; Department of Occupational and Environmental Health, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan, China.
Department of nursing, Zhengzhou Health Vocational College, Zhengzhou 450100, Henan, China.
Ecotoxicol Environ Saf. 2021 Oct 15;223:112558. doi: 10.1016/j.ecoenv.2021.112558. Epub 2021 Jul 29.
Telomeres are functional complexes at the ends of linear chromosomes, and telomerase aids in their maintenance and replication. Additionally, accumulating evidence suggests that telomerase-associated protein 1 (TEP1) is a component of the telomerase ribonucleoprotein complex and is responsible for catalyzing the addition of new synthetic telomere sequences to chromosome ends. In our previous study, we found that genetic variants of the TERT gene participated in the regulation of telomere length. Exposure to particulate matter, environmental pollutants, oxidative stress, and pesticides is associated with shortening of telomere length. However, it is unknown whether genetic variants in the TEP1 gene may affect telomere length (TL) in polycyclic aromatic hydrocarbon (PAH)-exposed workers. Therefore, we measured the peripheral leukocyte TL and genotyped the polymorphism loci in the TEP1 gene among 544 PAH-exposed workers and 238 healthy controls. Covariance analysis showed that the individuals carrying TEP1 rs1760903 CC and TEP1 rs1760904 TT had longer TL in the control group (P < 0.05). In the generalized linear model, we found that rs1760903 CC was a protective factor against TL shortening, and PAH exposure could promote telomere shortening (P < 0.05). Thus, this study reinforces the roles of environmental factors and genetic variations in telomere damage, and provides a theoretical foundation for the early detection of susceptible populations and the establishment of occupational standards.
端粒是线性染色体末端的功能复合物,端粒酶有助于其维持和复制。此外,越来越多的证据表明,端粒酶相关蛋白 1(TEP1)是端粒酶核糖核蛋白复合物的一个组成部分,负责催化在染色体末端添加新的合成端粒序列。在我们之前的研究中,我们发现 TERT 基因的遗传变异参与了端粒长度的调节。暴露于颗粒物、环境污染物、氧化应激和杀虫剂会导致端粒长度缩短。然而,目前尚不清楚 TEP1 基因的遗传变异是否会影响多环芳烃(PAH)暴露工人的端粒长度(TL)。因此,我们测量了 544 名 PAH 暴露工人和 238 名健康对照者的外周血白细胞 TL,并对 TEP1 基因的多态性位点进行了基因分型。协方差分析显示,在对照组中,携带 TEP1 rs1760903 CC 和 TEP1 rs1760904 TT 的个体 TL 较长(P < 0.05)。在广义线性模型中,我们发现 rs1760903 CC 是 TL 缩短的保护因素,而 PAH 暴露可促进端粒缩短(P < 0.05)。因此,本研究强调了环境因素和遗传变异在端粒损伤中的作用,为易感人群的早期检测和职业标准的建立提供了理论依据。