Abstract
The aim of study is to determine the relationship between telomere length and telomerase activity with indicators of oxidative stress in patients with stage 1-3 cerebral atherosclerosis and type 2 diabetes.
 Material and methods. A total clinical and instrumental study involved 161 patients with grade 1–3 CA. Telomerase activity was determined using a tandem repeat amplification protocol with real-time detection. The relative telomere lengths were measured using real-time multiplex quantitative polymerase chain reaction.
 Results. A comparative analysis revealed that patients with stage 1-3 CA with long telomeres had a significantly higher catalase level than in the short telomere group, and the catalase and SOD levels in the group with high telomerase activity were significantly lower than in the group with low telomerase activity. A correlation analysis revealed significant direct relationships between telomere length and oxidative stress markers such as catalase and SOD (r = 0.23 and r = 0.21, respectively) and telomerase activity with GSH (r = 0.48). An inverse relationship between the telomere length and T2DM (r = -0.21) was also revealed. Telomere length and telomerase activity were not correlated with other markers of oxidative stress.
 Conclusion. In patients with stage 1-3 cerebral atherosclerosis, an association of some markers of oxidative stress (catalase, SOD, GSH) with telomere length and telomerase activity, regardless of the presence of concomitant type 2 diabetes mellitus, was revealed. In patients with stage 1-3 cerebral atherosclerosis with longer telomeres, catalase levels are statistically significantly higher than in patients with short telomeres. Stage 1-3 cerebral atherosclerosis patients with higher telomerase activity are characterized by statistically significantly lower levels of catalase and superoxide dismutase compared with patients with lower telomerase activity. The most stable direct correlation in this category of patients was found between GSH and telomerase activity (r = 0.48), which may indicate the key role of GSH in the rate of telomere shortening and the development of atherosclerosis.
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