Abstract
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.
Highlights
Laryngeal cancer (LC) represents about 30% of the malignant tumors of head and neck cancers, and this corresponds to 8% of all cancer types worldwide [1]
The aim of the current study was to evaluate the possible relation of NOS3 G894T genotypes with the levels various protein and lipid oxidation markers and antioxidant status such as protein carbonyl groups (PCO), Advanced oxidation protein products (AOPPs), LHP, total thiol protein thiol, nonprotein thiol, and Cu, Zn-superoxide dismutase (Cu, Zn-SOD) in patients with LC
The plasma levels of oxidative stress parameters were determined with manual colorimetric methods according to NOS3 genotypes in LC patients and their respective controls
Summary
Laryngeal cancer (LC) represents about 30% of the malignant tumors of head and neck cancers, and this corresponds to 8% of all cancer types worldwide [1]. Similar to other cancer types, LC is a multifactorial disease which can be induced by both genetic and environmental factors [2]. Among the various etiological factors sharing in the development of laryngeal tumors, increased production of reactive oxygen species (ROS) is playing an important role in the development of an impaired redox homeostasis [3]. Nitric oxide synthase (NOS) is the main source of the NO∙ production which produces NO∙ while converting Larginine to L-citrulline. NOS3 was first defined in vascular endothelial cells; later studies showed that this isoform can be found in other cell types such as airway epithelia, neurons, and certain types of tumors [6, 8].
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