Oxidative stress in severe pulmonary hypertension.

Severe pulmonary hypertension (PH) occurs in a primary or "unexplained" form and in a group of secondary forms associated with a number of diseases. Because the lung tissue from patients with severe PH demonstrates complex vascular lesions, which contain inflammatory cells, we wondered whether the lung tissue from patients with severe PH was "under oxidative stress." We used immunohistochemistry to localize nitrotyrosine and 8-hydroxy guanosine in the lung tissue sections from patients with primary and secondary PH. In some lung tissue extracts, the eicosanoid metabolites 5-oxo-eicosatetraenoic acid, leukotriene B4 5-hydroxyeicosatetraenoic acid (HETE), 12-HETE, and 15-HETE were measured using mass spectroscopy, and superoxide dismutase amount and activity were measured. Nitrotyrosine expression was ubiquitous in all PH lungs, and 5-oxo-eicosatetraenoic acid and HETE levels were elevated in the lungs of patients with severe PH but not in those lungs that were from the patients with severe PH treated chronically with prostacyclin. We conclude that indeed the lungs from patients with severe PH are under oxidative stress and that chronic prostacyclin infusion has an antiinflammatory effect on the lung tissue.

[1]  S. Hazen,et al.  Oxidative and nitrosative events in asthma. , 2003, Free radical biology & medicine.

[2]  N. Voelkel,et al.  Oxidative stress and apoptosis interact and cause emphysema due to vascular endothelial growth factor receptor blockade. , 2003, American journal of respiratory cell and molecular biology.

[3]  H. Kasai Chemistry-based studies on oxidative DNA damage: formation, repair, and mutagenesis. , 2002, Free radical biology & medicine.

[4]  R. Hotchkiss,et al.  Myeloperoxidase produces nitrating oxidants in vivo. , 2002, The Journal of clinical investigation.

[5]  J. K. Hurst Whence nitrotyrosine? , 2002, The Journal of clinical investigation.

[6]  D. Bullard,et al.  Endothelial transcytosis of myeloperoxidase confers specificity to vascular ECM proteins as targets of tyrosine nitration. , 2001, The Journal of clinical investigation.

[7]  G. Semenza,et al.  Expression of angiogenesis‐related molecules in plexiform lesions in severe pulmonary hypertension: evidence for a process of disordered angiogenesis , 2001, The Journal of pathology.

[8]  J. Cracowski,et al.  Increased lipid peroxidation in patients with pulmonary hypertension. , 2001, American journal of respiratory and critical care medicine.

[9]  J. Davis,et al.  Recombinant human superoxide dismutase enhances the effect of inhaled nitric oxide in persistent pulmonary hypertension. , 2001, American journal of respiratory and critical care medicine.

[10]  H. Niedermüller,et al.  Levels of 8-hydroxy-2′-deoxyguanosine in cellular DNA from 12 tissues of young and old Sprague–Dawley rats , 2001, Experimental Gerontology.

[11]  N. Voelkel,et al.  Severe pulmonary hypertension after the discovery of the familial primary pulmonary hypertension gene. , 2001, The European respiratory journal.

[12]  N. Voelkel,et al.  Generation of oxidative stress contributes to the development of pulmonary hypertension induced by hypoxia. , 2001, Journal of applied physiology.

[13]  N. Voelkel,et al.  Gene Expression Patterns in the Lungs of Patients With Primary Pulmonary Hypertension: A Gene Microarray Analysis , 2001, Circulation research.

[14]  Elias S. J. Arnér,et al.  Physiological functions of thioredoxin and thioredoxin reductase. , 2000, European journal of biochemistry.

[15]  R. Murphy,et al.  A Novel Glutathione Containing Eicosanoid (FOG7) Chemotactic for Human Granulocytes* , 2000, The Journal of Biological Chemistry.

[16]  David S. McClintock,et al.  Role of Oxidants in NF-κB Activation and TNF-α Gene Transcription Induced by Hypoxia and Endotoxin1 , 2000, The Journal of Immunology.

[17]  N. Chandel,et al.  Role of oxidants in NF-kappa B activation and TNF-alpha gene transcription induced by hypoxia and endotoxin. , 2000, Journal of immunology.

[18]  C. Kunsch,et al.  Oxidative stress as a regulator of gene expression in the vasculature. , 1999, Circulation research.

[19]  A. Al-Mehdi,et al.  Endothelial NADPH oxidase as the source of oxidants in lungs exposed to ischemia or high K+. , 1998, Circulation research.

[20]  A. Arroliga,et al.  Biochemical reaction products of nitric oxide as quantitative markers of primary pulmonary hypertension. , 1998, American journal of respiratory and critical care medicine.

[21]  R. Murphy,et al.  Activation of human polymorphonuclear leukocytes by products derived from the peroxidation of human red blood cell membranes. , 1998, Chemical research in toxicology.

[22]  N. Voelkel,et al.  Pulmonary hypertension and inflammation. , 1998, The Journal of laboratory and clinical medicine.

[23]  M. Humbert,et al.  Nitric oxide deficiency in fenfluramine- and dexfenfluramine-induced pulmonary hypertension. , 1998, American journal of respiratory and critical care medicine.

[24]  N. Voelkel,et al.  5-Lipoxygenase and 5-lipoxygenase activating protein (FLAP) immunoreactivity in lungs from patients with primary pulmonary hypertension. , 1998, American journal of respiratory and critical care medicine.

[25]  G. FitzGerald,et al.  Localization of distinct F2-isoprostanes in human atherosclerotic lesions. , 1997, The Journal of clinical investigation.

[26]  W. Powell,et al.  Effects of 5-oxo-6,8,11,14-eicosatetraenoic acid on expression of CD11b, actin polymerization, and adherence in human neutrophils. , 1997, Journal of immunology.

[27]  W. Glasgow,et al.  Mammalian arachidonate 12-lipoxygenases. , 1997, Advances in experimental medicine and biology.

[28]  R. J. Waugh,et al.  Mass spectrometric analysis of four regioisomers of F2-isoprostanes formed by free radical oxidation of arachidonic acid , 1996, Journal of the American Society for Mass Spectrometry.

[29]  E. Stadtman,et al.  Peroxynitrite disables the tyrosine phosphorylation regulatory mechanism: Lymphocyte-specific tyrosine kinase fails to phosphorylate nitrated cdc2(6-20)NH2 peptide. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[30]  O. Rådmark Arachidonate 5-lipoxygenase. , 2002, Journal of lipid mediators and cell signalling.

[31]  M. Humbert,et al.  Increased interleukin-1 and interleukin-6 serum concentrations in severe primary pulmonary hypertension. , 1995, American journal of respiratory and critical care medicine.

[32]  S. Matalon,et al.  Quantitation of nitrotyrosine levels in lung sections of patients and animals with acute lung injury. , 1994, The Journal of clinical investigation.

[33]  T. Higenbottam,et al.  Mixed expired nitric oxide in primary pulmonary hypertension in relation to lung diffusion capacity. , 1994, QJM : monthly journal of the Association of Physicians.

[34]  K. Schulze-Osthoff,et al.  Distinct effects of thioredoxin and antioxidants on the activation of transcription factors NF-kappa B and AP-1. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[35]  J S Beckman,et al.  Pathological implications of nitric oxide, superoxide and peroxynitrite formation. , 1993, Biochemical Society transactions.

[36]  A. Wendel,et al.  Selenoenzymes regulate the activity of leukocyte 5-lipoxygenase via the peroxide tone. , 1993, The Journal of biological chemistry.

[37]  W. Leonard,et al.  Modulation of transcription factor NF-kappa B binding activity by oxidation-reduction in vitro. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[38]  J. Morrow,et al.  A series of prostaglandin F2-like compounds are produced in vivo in humans by a non-cyclooxygenase, free radical-catalyzed mechanism. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[39]  B. Freeman,et al.  Apparent hydroxyl radical production by peroxynitrite: implications for endothelial injury from nitric oxide and superoxide. , 1990, Proceedings of the National Academy of Sciences of the United States of America.