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en The Status of Nitric Oxide and its Backup, Heme Oxygenase 1, in Thromboangiitis Obliterans بیوشیمی Biochemistry مقالات اصلی Original Article <div style="text-align: justify;">Background: Until recently, a gene polymorphism in the promoter region of endothelial nitric oxide synthase has been suggested as a risk factor for thromboangiitis obliterans (TAO) development. The aim of this study was to compare the metabolites of nitric oxide (NO) and its backup, heme-oxygenase-1 (HMOX1), between TAO patients and those of a smoking control group matched by race, age, sex, and smoking habits. Methods: Twenty-four male Caucasian TAO patients and 20 male Caucasian controls enrolled in the study. Their smoking habits were matched based on the serum cotinine levels of 17 of the TAO patients and the 20 controls. A colorimetric kit was used to measure NO, and an enzyme-linked immunosorbent assay kit was used to measure cotinine and HMOX1 levels. Results: The mean serum level of NO metabolites in the TAO group was significantly less than in the controls (p = 0.03) and also significantly less in the patients with below-knee amputations than in non-amputees (p= 0.018). Also, HMOX1 was significantly greater in the TAO patients than in the controls (p= 0.01). No significant correlation was found between NO and HMOX1 (p = 0.054). Conclusions: Nitric oxide may play a pivotal role in TAO development and its outcome. However, the intact HMOX1 pathway may demonstrate the unique role of NO, which cannot be compensated for by HMOX1 and whose absence may make patients susceptible to developing TAO. In addition, another pathway besides NO, with influence on vascular tone and hemostasis, might be involved in TAO development, such as the autonomic nervous system. Further studies are suggested regarding these issues.</div> Cotinine, Heme oxygenase 1, Nitric oxide, Peripheral arterial disease, Smoking, Thromboangiitis obliterans 197 202 http://rbmb.net/browse.php?a_code=A-10-106-1&slc_lang=en&sid=1 Ali Aliee alieea941@mums.ac.ir 10031947532846006310 10031947532846006310 No Department of Clinical Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran & Student Research Committee, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Farnaz Zahedi Avval zahediaf@mums.ac.ir 10031947532846006311 10031947532846006311 No Department of Clinical Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran & Metabolic Syndrome Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Hossein Taheri ht23766@yahoo.com 10031947532846006312 10031947532846006312 No General Surgery Department, Farabi Hospital, Kowsar Blvd, Mashhad, Iran. Saeedeh Mehraban Moghadam mehrabans1@mums.ac.ir 10031947532846006313 10031947532846006313 No Inflammation and Inflammatory Diseases Division of Immunology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Mohammad Soukhtanloo soukhtanloom@mums.ac.ir 10031947532846006314 10031947532846006314 No Department of Clinical Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Daryoush Hamidi Alamdari hamidiad@mums.ac.ir 10031947532846006315 10031947532846006315 No Surgical Oncology Research Center, Emam Reza Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Bahare Fazeli bahar.fazeli@gmail.com 10031947532846006316 10031947532846006316 Yes Inflammation and Inflammatory Diseases Division of Immunology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran & VAS, European Independent Foundation in Angiology/Vascular Medicine. Milan, Italy.