4.7 Article

Genetic variants in telomerase-associated protein 1 are associated with telomere damage in PAH-exposed workers

Journal

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 223, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2021.112558

Keywords

Polycyclic aromatic hydrocarbons; Telomere length; TEP1 gene; Genetic polymorphism

Funding

  1. Programs for theCollaborative Innovation Major Project of Zhengzhou [20XTZX08017]
  2. National Natural Science Foundation of China [82002998, 81872597]
  3. Medical Science and Technology Research Project in Henan Province [LHGJ20190042]
  4. Youth Talent Support Project of Henan Province [2021HYTP045]

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This study suggests that exposure to polycyclic aromatic hydrocarbons (PAHs) in workers may lead to telomere shortening, while genetic variations in the TEP1 gene could affect telomere length. Specifically, carrying the TEP1 rs1760903 CC genotype may be protective against telomere shortening. These findings highlight the roles of environmental factors and genetic variations in telomere damage, providing a basis for early detection of susceptible populations and establishment of occupational standards.
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.

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