3
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Un viejo nuevo gas: el mónoxido de carbono (CO): aspectos esenciales en Biología, Patobiología, Bioclínica y Fármaco-Terapeútica Humana Translated title: An old new gas, carbon monoxide (CO): essentials in human Biology, Pathobiology, Bioclinic and human Pharmacotherapeutics

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Ha habido grandes avances en el conocimiento de la producción endógena y de las funciones fisiológicas del monóxido de carbono (CO). La mayor parte del CO endógeno se produce en una reacción que puede ser catalizada por tres enzimas denominadas HEMOoxigenasas (HO). La distribución tisular específica de las isoformas de HO (HO-1, HO-2 y HO-3) está muy relacionada con las acciones biológicas del CO como molécula de señalamiento en diferentes sistemas, a saber: neural, vascular (propiedades vasorrelajantes y cardioprotectoras), inmunológico, respiratorio, reproductivo, gastrointestinal, renal y hepático. El entendimiento de los mecanismos moleculares, celulares, tisulares y sistémicos que regulan la producción y median las acciones fisiológicas del CO provee información sobre los mecanismos patogénicos de muchas enfermedades y estrategias innovadoras para prevenirlas y tratarlas.

          Translated abstract

          Knowledge of the endogenous production and physiological functions of carbon monoxide (CO) has greatly advanced. Most of the endogenous CO is produced in reactions catalyzed by three enzymes named HEMO-oxygenases (HO). The tissue typespecific distribution of these HO isoforms (HO-1, HO-2 y HO-3) is largely linked to the specific biological actions of CO as a signaling molecule in different systems, namely: neural, vascular (vasorelaxant property and cardiac protection), immunological, respiratory, reproductive, gastrointestinal, kidney, and liver. Understanding the molecular, cellular, tisular and systemic mechanisms that regulate the production and mediate the physiological actions of CO may provide an insight into the pathogenic mechanisms of many diseases, and innovative preventive and therapeutic strategies.

          Related collections

          Most cited references89

          • Record: found
          • Abstract: found
          • Article: not found

          Heme oxygenase-1: a provenance for cytoprotective pathways in the kidney and other tissues.

          Rahul Nath (2006)
          Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme, converting heme to biliverdin, during which iron is released and carbon monoxide (CO) is emitted; biliverdin is subsequently converted to bilirubin by biliverdin reductase. At least two isozymes possess HO activity: HO-1 represents the isozyme induced by diverse stressors, including ischemia, nephrotoxins, cytokines, endotoxin, oxidants, and vasoactive substances; HO-2 is the constitutive, glucocorticoid-inducible isozyme. HO-1 is upregulated in the kidney in assorted conditions and diseases. Interest in HO is driven by the capacity of this system to protect the kidney against injury, a capacity likely reflecting, at least in part, the cytoprotective properties of its products: in relatively low concentrations, CO exerts vasorelaxant, antiapoptotic, and anti-inflammatory effects while bile pigments are antioxidant and anti-inflammatory metabolites. This article reviews the HO system and the extent to which it influences the function of the healthy kidney; it summarizes conditions and stimuli that elicit HO-1 in the kidney; and it explores the significance of renal expression of HO-1 as induced by ischemia, nephrotoxins, nephritides, transplantation, angiotensin II, and experimental diabetes. This review also points out the tissue specificity of the HO system, and the capacity of HO-1 to induce renal injury in certain settings. Studies of HO in other tissues are discussed insofar as they aid in elucidating the physiologic and pathophysiologic significance of the HO system in the kidney.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            The molecule of the year.

            D Koshland (1992)
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Heme oxygenase expression in human central nervous system disorders.

              In the normal mammalian CNS, heme oxygenase-2 (HO-2) is constitutively, abundantly, and fairly ubiquitously expressed, whereas heme oxygenase-1 (HO-1) mRNA and protein are confined to small populations of scattered neurons and neuroglia. Unlike ho-2, the ho-1 gene in neural (and many systemic) tissues is exquisitely sensitive to upregulation by a host of pro-oxidant and other noxious stimuli. In Alzheimer disease, HO-1 immunoreactivity is significantly augmented in neurons and astrocytes of the hippocampus and cerebral cortex relative to age-matched, nondemented controls and colocalizes to senile plaques, neurofibrillary tangles, and corpora amylacea. In Parkinson disease, HO-1 decorates Lewy bodies of affected dopaminergic neurons and is highly overexpressed in astrocytes residing within the substantia nigra. The ho-1 gene is also upregulated in glial cells within multiple sclerosis plaques; in the vicinity of human cerebral infarcts, hemorrhages, and contusions; and in various other degenerative and nondegenerative human CNS disorders. The products of the heme oxygenase reaction, free ferrous iron, carbon monoxide, and biliverdin/bilirubin, are all biologically active molecules that may profoundly influence tissue redox homeostasis under a wide range of pathophysiological conditions. Evidence adduced from whole animal and in vitro studies indicates that enhanced HO-1 activity may either ameliorate or exacerbate neural injury, effects likely contingent upon the specific model employed, the duration and intensity of HO-1 induction, and the chemistry of the local redox microenvironment. HO-1 hyperactivity also promotes mitochondrial sequestration of nontransferrin iron in oxidatively challenged astroglia and may thereby contribute to the pathological iron deposition and bioenergetic failure amply documented in aging and degenerating human neural tissues.
                Bookmark

                Author and article information

                Contributors
                Role: ND
                Role: ND
                Journal
                iat
                Iatreia
                Iatreia
                Universidad de Antioquia (Medellín )
                0121-0793
                September 2008
                : 21
                : 3
                : 307-320
                Affiliations
                [1 ] Pontificia Universidad Javeriana Colombia
                [2 ] Universidad Colegio Mayor de Nuestra Señora del Rosario Colombia
                Article
                S0121-07932008000300009
                639fd2b8-bd04-4986-b291-be46880677b7

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Colombia

                Self URI (journal page): http://www.scielo.org.co/scielo.php?script=sci_serial&pid=0121-0793&lng=en
                Categories
                MEDICINE, GENERAL & INTERNAL

                Internal medicine
                Carbon monoxide (CO),HEMO-oxigenasas (HO),Monóxido de carbono (CO)
                Internal medicine
                Carbon monoxide (CO), HEMO-oxigenasas (HO), Monóxido de carbono (CO)

                Comments

                Comment on this article