ORIGINAL ARTICLE Oxidative stress in relation to telomere length maintenance in vascular smooth muscle cells following balloon angioplasty Gonen Ozsarlak-Sozer & Zeliha Kerry & Goksel Gokce & Ismail Oran & Zeki Topcu Received: 4 March 2010 / Accepted: 14 September 2010 / Published online: 6 October 2010 # University of Navarra 2010 Abstract Telomeres are specialized DNA–protein complexes found at the tips of linear chromosomes. In this study, we investigated the effects of oxidative stress on telomeric length distribution of proliferating vascular smooth muscle cells follow- ing balloon injury in single or combined treatment of rabbits with either buthionine sulfoximine or taurine. Exposure to oxidative stress increased the balloon injury whereas taurine treatment signifi- cantly diminished L-buthionine-sulfoximine-related intimal hyperplasia. Our results also showed that both variables had a significant influence on mean telomeric length distribution. Keywords Oxidative stress . Telomere length . Balloon angioplasty . Atherosclerosis Introduction Oxidative damage is an important factor in the accumulation of DNA damage. It can lead to mutagenesis and carcinogenesis among other biolog- ical effects [9]. Increased levels of reactive oxygen species (ROS) are found in atherosclerosis in all layers of the affected artery wall [24, 30, 38]. Oxidative damage was also proposed to have an impact on telomeric DNA ends as the accumulation of ROS can cause an accelerated telomere shortening [7, 36]. Telomeres are specialized G-rich repeat sequen- ces, playing an important role in the maintenance of genomic stability by preventing the natural ends from being recognized as damaged DNA [1, 3, 4, 13, 19]. Telomeric repeats are generated by a specialized reverse transcriptase, called telomerase, which is composed of an RNA component, serving as a template for the addition of telomeric repeats, and a protein component, which is the telomerase reverse- transcriptase catalytic subunit (Tert) [28]. The sensi- tivity of telomeric DNA ends to oxidative stress was attributed to their high guanine content [23, 24, 36]. As the single strand breaks at telomeric DNA cannot undergo a repair process, 8-oxo dG as a result of reactive oxygen species causes telomere shortening through replication [36]. Ataxia telangi- ectasia (A-T), an autosomal recessive disease, is an example of the relation between oxidative stress and telomere shortening [31]. J Physiol Biochem (2011) 67:35–42 DOI 10.1007/s13105-010-0046-2 G. Ozsarlak-Sozer : Z. Kerry : G. Gokce Department of Pharmacology, Ege University, 35100 Izmir, Turkey I. Oran Department of Radiology, Faculty of Medicine, Ege University, 35100 Izmir, Turkey Z. Topcu (*) Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Ege University, 35100 Izmir, Turkey e-mail: zeki.topcu@ege.edu.tr