Nitrogen dioxide (NO* 2 ) is often present in inhaled air and may be generated in vivo from nitric oxide. Exposure of human blood plasma to NO* 2 caused rapid losses of ascorbic acid, uric acid and protein thiol groups, as well as lipid peroxidation and depletions of α‐tocopherol, bilirubin and ubiquinol‐10. No increase in protein carbonyls was detected. Supplementation of plasma with ascorbate decreased the rates of lipid peroxidation. α‐tocopherol depletion and loss of uric acid. Uric acid supplementation decreased rates of lipid peroxidation but not the loss of α‐tecopherol. We conclude that ascorbic acid, protein ‐SH groups, uric acid and α‐tocopherol may be important agents protecting against NO* 2 in vivo. If these antioxidants are depleted, peroxidation of lipids occurs and might contribute to the toxicity of NO* 2 .
No abstract is provided for this article.
Book Review| April 01 1985 Oxygen Radicals in Chemistry and Biology Oxygen Radicals in Chemistry and Biology. W. BORS, M. SARAN, D. TAIT. de GruyterBerlin 1984 pp. 1029, £72 BARRY HALLIWELL BARRY HALLIWELL Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1985) 13 (2): 536. https://doi.org/10.1042/bst0130536 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation BARRY HALLIWELL; Oxygen Radicals in Chemistry and Biology. Biochem Soc Trans 1 April 1985; 13 (2): 536. doi: https://doi.org/10.1042/bst0130536 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1985 Biochemical Society1985 Article PDF first page preview Close Modal You do not currently have access to this content.
Oxidation of low-density lipoproteins (LDLs) plays a role in the development of atherosclerosis, but many questions remain unanswered. This paper aims to evaluate critically the available data pertinent to the following questions: 1) How is LDL oxidation initiated, especially in early atherosclerotic lesions? 2) Is nitric oxide good or bad in lesions? and 3) Which antioxidants are really important in protecting LDLs against oxidation in the human body?
Ascorbate is an essential enzyme cofactor but is often also regarded as an important antioxidant in vivo, protecting against cancer by scavenging DNA-damaging reactive oxygen species. Recent studies suggest that ascorbate sometimes increases DNA damage in humans. Although there is no evidence that any of these effects are deleterious to humans, we might need to change our thinking about the mechanisms of the antioxidant action of ascorbate in vivo.
Neutrophils contain the enzyme myeloperoxidase, which oxidizes Cl− ions into the powerful oxidant hypochlorous acid (HOCl). HOCl inactivates α1antiprotease, permitting uncontrolled protease activities. Most anti-inflammatory drugs tested are capable of reacting with HOCl, but the reactions seem insufficiently rapid under physiological conditions to protect α1-antiprotease against inactivation by HOCl. However, rapid scavenging of HOC1 might contribute to the anti-inflammatory effects of penicillamine, gold sodium thiomalate, phenylbutazone and primaquine.
Reactive oxygen species in rheumatoid arthritis It is now generally accepted that oxygen free radicals and other reactive oxygen species play some part in the pathology of inflammatory joint disease, though whether this is a major or minor part remains to be established.'A radical is any species containing one or more unpaired electrons (denoted by a superscript dot, ).Examples are the superoxide radical (Q2-) and hydroxyl radical (OH,).The term reactive oxygen species is a broader term that includes not only Q°and OH-but also certain non- radical oxygen derived species, such as hydro- gen peroxide (H202) and hypochlorous acid (HOCI), which are potentially, damaging.)Increased formation of reactive oxygen species is probably a generalised response to tissue injury, as may be the increased synthesis of other 'injury mediators' such as prostaglandins, leukotrienes, interleukins, and tumour necrosis factors. 1 2 There is therefore nothing special in showing increased activity of reactive oxygen species in any human disease: it is almost to be expected.1 2 What needs to be done (as for any putatively important injury mediator) is to show that reactive oxygen species are important contributors to disease activity (table 1).This has been exceptionally difficult because reactive oxygen species are hard to measure, but fortunately new methods are becoming avail- able.' Sources of reactive oxygen species in rheumatoid arthritis Synovial fluid neutrophils, and macrophages in the pannus, probably generate some 02and H202 in the inflamed rheumatoid joint.
No abstract is provided for this article.
Flavonoids and other polyphenolic compounds have powerful antioxidant effects in vitro in many test systems, but can act as pro-oxidants in some others. Whether pro-oxidant, antioxidant, or any of the many other biological effects potentially exerted by flavonoids account for or contribute to the health benefits of diets rich in plant-derived foods and beverages is uncertain. Phenolic compounds may help to protect the gastrointestinal tract against damage by reactive species present in foods or generated within the stomach and intestines. The overall health benefit of flavonoids is uncertain, and consumption of large quantities of them in fortified foods or supplements should not yet be encouraged.
Ergothioneine is a thiol/thione molecule synthesised only by some fungi and bacteria. Nonetheless, it is avidly taken up from the diet by humans and other animals through a transporter, OCTN 1, and accumulates to high levels in certain tissues. Ergothioneine is not rapidly metabolised, or excreted in urine and is present in many, if not all, human tissues and body fluids. Ergothioneine has powerful antioxidant and cytoprotective properties in vitro and there is evidence that the body may concentrate it at sites of tissue injury by raising OCTN 1 levels. Decreased blood and/or plasma levels of ergothioneine have been observed in some diseases, suggesting that a deficiency could be relevant to the disease onset or progression. This brief Review explores the possible roles of ergothioneine in human health and disease.
