GENOME STABILITY AND TELOMERE DYNAMICS IN STRESS-INDUCED CELLULAR AGING MECHANISMS

Abstract

Background: Cellular senescence is closely related to genome instability and telomere shortening under oxidative and environmental stress conditions. Telomeres are critical for maintaining chromosomal integrity and determining cellular lifespan. Telomere dysfunction induced by stress contributes to aging-related cellular damage. 
Objective: The present study was designed to investigate the relation between oxidative stress, telomere dynamics and genome stability in cellular aging processes induced by stress.
Methodology: Human fibroblast cell lines were treated with oxidative stress by hydrogen peroxide (H2O2) in controlled laboratory conditions. Telomere length was analyzed by quantitative PCR and DNA damage was analyzed by γ-H2AX immunofluorescence assays. Cellular aging responses were also evaluated by measuring telomerase activity and senescence-associated β-galactosidase staining. 
Findings: Chronic exposure to stress reduced relative telomere length to 61% of control cells (100%). We found increased γ-H2AX signal intensity and increased senescence marker activity, suggesting increased DNA double strand breaks and accelerated cellular senescence. Under oxidative stress conditions, reduced telomerase activity was also observed.
Conclusion: Stress-induced telomere dysfunction plays a significant role in genome instability and aging of cells. These findings underscore telomere maintenance pathways as potential therapeutic targets for age-related diseases and strategies for genomic preservation.