Literature DB >> 29766003

The Status of Nitric Oxide and its Backup, Heme Oxygenase 1, in Thromboangiitis Obliterans.

Ali Aliee1,2, Farnaz Zahedi Avval1,3, Hossein Taheri4, Saeedeh Mehraban Moghadam5, Mohammad Soukhtanloo1, Daryoush Hamidi Alamdari6, Bahare Fazeli5,7.   

Abstract

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).
CONCLUSION: 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.

Entities:  

Keywords:  Cotinine; Heme oxygenase 1; Nitric oxide; Peripheral arterial disease; Smoking; Thromboangiitis obliterans

Year:  2018        PMID: 29766003      PMCID: PMC5941125     

Source DB:  PubMed          Journal:  Rep Biochem Mol Biol        ISSN: 2322-3480


  26 in total

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Journal:  Environ Res       Date:  2016-01-29       Impact factor: 6.498

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5.  Heme oxygenase-1-derived carbon monoxide contributes to the suppression of acute hypertensive responses in vivo.

Authors:  R Motterlini; A Gonzales; R Foresti; J E Clark; C J Green; R M Winslow
Journal:  Circ Res       Date:  1998-09-07       Impact factor: 17.367

Review 6.  Carbon monoxide and bilirubin: potential therapies for pulmonary/vascular injury and disease.

Authors:  Stefan W Ryter; Danielle Morse; Augustine M K Choi
Journal:  Am J Respir Cell Mol Biol       Date:  2006-09-15       Impact factor: 6.914

7.  Plasma heme oxygenase-1 is decreased in peripheral artery disease patients.

Authors:  Salvatore Santo Signorelli; Guido Li Volsi; Valerio Fiore; Marco Mangiafico; Ignazio Barbagallo; Rosalba Parenti; Manfredi Rizzo; Giovanni Li Volti
Journal:  Mol Med Rep       Date:  2016-08-19       Impact factor: 2.952

8.  Nitric oxide: link between endothelial dysfunction and inflammation in patients with peripheral arterial disease of the lower limbs.

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9.  Heme oxygenase 2: endothelial and neuronal localization and role in endothelium-dependent relaxation.

Authors:  R Zakhary; S P Gaine; J L Dinerman; M Ruat; N A Flavahan; S H Snyder
Journal:  Proc Natl Acad Sci U S A       Date:  1996-01-23       Impact factor: 11.205

Review 10.  Biomarkers of environmental tobacco smoke exposure.

Authors:  N L Benowitz
Journal:  Environ Health Perspect       Date:  1999-05       Impact factor: 9.031

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