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The NuGOwiki Metabolite Database is a joint initiative of NuGO and HMDB
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| Oxygen | |
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| Chemical Name | oxygen |
| Chemical Formula | O2 |
| CAS Number | 7782-44-7 |
| Chemical Information | HMDB01377 |
| Biochemical Taxonomy |
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| Functional Taxonomy | Not Available |
| Nutritional Taxonomy | Not Available |
| Metabolic Pathways | Not Available |
| Biofluid Location |
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| Tissue Location |
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| Normal Biofluid Concentrations |
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| Normal Tissue Concentrations | Not Available |
| Diseases / Conditions Related to Nutrition | Not Available |
| Other (Monogenic Disorders) |
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| Abnormal Biofluid Concentrations | Not Available |
| Abnormal Tissue Concentrations | Not Available |
| Physiological Processes | Not Available |
| Authors: | |
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Contents |
Introduction
guidelines
Oxygen is the most abundant element on earth and essential for respiration. A constant supply of oxygen is indispensable for cardiac viability and function. However, the role of oxygen and oxygen-associated processes in the heart is complex, and they and can be either beneficial or contribute to cardiac dysfunction and death. As oxygen is a major determinant of cardiac gene expression, and a critical participant in the formation of Reactive oxygen species (ROS) and numerous other cellular processes, consideration of its role in the heart is essential in understanding the pathogenesis of cardiac dysfunction. The mammalian heart is an obligate aerobic organ. At a resting pulse rate, the heart consumes approximately 8-15 ml O2/min/100 g tissue. This is significantly more than that consumed by the brain (approximately 3 ml O2/min/100 g tissue) and can increase to more than 70 ml O2/min/100 g myocardial tissue during vigorous exercise. Mammalian heart muscle cannot produce enough energy under anaerobic conditions to maintain essential cellular processes; thus, a constant supply of oxygen is indispensable to sustain cardiac function and viability. The story of oxygen in the heart is complex, however, and goes well beyond its role in energy metabolism.
ROS are a family of oxygen-derived free radicals that are produced in mammalian cells under normal and pathologic conditions. Many ROS, such as the superoxide anion (O2-)and hydrogen peroxide (H2O2), act within blood vessels, altering mechanisms mediating mechanical signal transduction and autoregulation of cerebral blood flow. Reactive oxygen species are believed to be involved in cellular signaling in blood vessels in both normal and pathologic states. The major pathway for the production of ROS is by way of the one-electron reduction of molecular oxygen to form an oxygen radical, the superoxide anion (O2-). Within the vasculature there are several enzymatic sources of O2-, including xanthine oxidase, the mitochondrial electron transport chain, and nitric oxide (NO) synthases. Studies in recent years, however, suggest that the major contributor to O2- levels in vascular cells is the membrane-bound enzyme NADPH-oxidase. Produced O2- can react with other radicals, such as NO, or spontaneously dismutate to produce hydrogen peroxide (H2O2). In cells, the latter reaction is an important pathway for normal O2- breakdown and is usually catalyzed by the enzyme superoxide dismutase (SOD). Once formed, H2O2 can undergo various reactions, both enzymatic and nonenzymatic. The antioxidant enzymes catalase and glutathione peroxidase act to limit ROS accumulation within cells by breaking down H2O2 to H2O. Metabolism of H2O2 can also produce other, more damaging ROS. For example, the endogenous enzyme myeloperoxidase uses H2O2 as a substrate to form the highly reactive compound hypochlorous acid. Alternatively, H2O2 can undergo Fenton or Haber-Weiss chemistry, reacting with Fe2+/Fe3+ ions to form toxic hydroxyl radicals (-.OH). (PMID: 17027622, 15765131)
Biological Function
Catabolism
Diseases / Conditions Related to Nutrition
Other (Monogenic) Disorders
- Amyotrophic lateral sclerosis 1 OMIM: 105400
- Ataxia-telangiectasia OMIM: 208900
- Chediak-higashi syndrome OMIM: 214500
- Coenzyme Q10 deficiency OMIM: 607426
- Congenital disorder of glycosylation, type IA OMIM: 212065
- Dystrophia myotonica 1 OMIM: 160900
- Fabry disease OMIM: 301500
- Fanconi anemia OMIM: 227650
- Friedreich ataxia 1 OMIM: 229300
- Glycogen storage disease vII OMIM: 232800
- Granulomatous disease, chronic, autosomal recessive, cytochrome b-positi ve, OMIM: 233700
- Granulomatous disease, chronic, x-linked OMIM: 306400
- Hemoglobin--variants for which the chain carrying the mutation is OMIM: 142309
- Hypophosphatemic rickets, x-linked dominant OMIM: 307800
- Laron syndrome, type II OMIM: 245590
- Leber optic atrophy OMIM: 535000
- Macular degeneration, age-related, 1 OMIM: 603075
- Mitochondrial complex i deficiency OMIM: 252010
- Myopathy with deficiency of succinate dehydrogenase and aconitase OMIM: 255125
- Parkinson disease, mitochondrial OMIM: 556500
- Pearson marrow-pancreas syndrome OMIM: 557000
- Porphyria variegata OMIM: 176200
- Pulmonary alveolar proteinosis OMIM: 265120
- Werner syndrome OMIM: 277700
- Wilson disease OMIM: 277900