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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 4985063, 8 pages
Research Article

Relation between Endothelial Nitric Oxide Synthase Genotypes and Oxidative Stress Markers in Larynx Cancer

1Department of Medical Biochemistry, Cerrahpaşa Faculty of Medicine, İstanbul University, 34098 İstanbul, Turkey
2Department of Otorhinolaryngology/Head and Neck Surgery, Haydarpaşa Numune Educational and Research Hospital, 34668 İstanbul, Turkey
3Department of Molecular Medicine, Institute of Experimental Medicine, Istanbul University, 34393 İstanbul, Turkey
4Cerrahpaşa Faculty of Medicine, İstanbul University, 34098 Istanbul, Turkey
5Department of Neuroscience, Institute of Experimental Medicine, Istanbul University, 34393 İstanbul, Turkey

Received 11 June 2015; Revised 10 August 2015; Accepted 11 August 2015

Academic Editor: Luciano Saso

Copyright © 2016 K. Yanar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Nitric oxide synthase (eNOS/NOS3) is responsible for the endothelial synthesis of nitric oxide (NO). G894T polymorphism leads to the amino acid substitution from Glu298Asp that causes lower NOS3 activity and basal NO production in NOS3 894T (298Asp) allele carriers compared with the GG homozygotes. NO acts as an antioxidant protecting against Fenton’s reaction which generates highly reactive hydroxyl radicals. Allelic variation of NOS3 may influence an individual’s risk of laryngeal cancer (LC). In the current study we have examined the possible relationship between NOS3 G894T genotypes and various systemic oxidative damage markers such as protein carbonyl, advanced oxidation protein products, Cu, Zn-superoxide dismutase, thiol group fractions, and lipid hydroperoxides in LC patients. Genotyping was carried out by PCR-RFLP. In LC patients with TT genotype, Cu, Zn-superoxide dismutase activities and nonprotein thiol levels were significantly higher than the controls. In patients with GT and GG genotype, high levels of lipid hydroperoxides showed statistical significance when compared to controls. Our results indicate a potential relationship among G894T polymorphism of NOS3, and impaired redox homeostasis. Further studies are required to determine the role of NOS3 gene polymorphism and impaired plasma redox homeostasis.