Carnosine, homocarnosine and anserine have been proposed to act as antioxidants in vivo. Our studies show that all three compounds are good scavengers of the hydroxyl radical (.OH) but that none of them can react with superoxide radical, hydrogen peroxide or hypochlorous acid at biologically significant rates. None of them can bind iron ions in ways that interfere with ‘site-specific’ iron-dependent radical damage to the sugar deoxyribose, nor can they restrict the availability of Cu2+ to phenanthroline. Homocarnosine has no effect on iron ion-dependent lipid peroxidation; carnosine and anserine have weak inhibitory effects when used at high concentrations in some (but not all) assay systems. However, the ability of these compounds to interfere with a commonly used version of the thiobarbituric acid (TBA) test may have led to an overestimate of their ability to inhibit lipid peroxidation in some previous studies. By contrast, histidine stimulated iron ion-dependent lipid peroxidation. It is concluded that, because of the high concentrations present in vivo, carnosine and anserine could conceivably act as physiological antioxidants by scavenging .OH, but that they do not have a broad spectrum of antioxidant activity, and their ability to inhibit lipid peroxidation is not well established. It may be that they have a function other than antioxidant protection (e.g. buffering), but that they are safer to accumulate than histidine, which has a marked pro-oxidant action upon iron ion-dependent lipid peroxidation. The inability of homocarnosine to react with HOCl, interfere with the TBA test or affect lipid peroxidation systems in the same way as carnosine is surprising in view of the apparent structural similarity between these two molecules.
conclude that at present no causal relation has been established.Results from the large case-control studies of child- hood cancer currently in progress will be awaited with great interest.
No abstract is provided for this article.
Correspondence| March 15 1986 Effect of oxidized glutathione on the inhibition of glucose-6-phosphate dehydrogenase by NADPH Barry Halliwell Barry Halliwell 1Department of Biochemistry, King's College (KQC), Strand Campus, London WC2R 2LS, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1986) 234 (3): 741. https://doi.org/10.1042/bj2340741 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation Barry Halliwell; Effect of oxidized glutathione on the inhibition of glucose-6-phosphate dehydrogenase by NADPH. Biochem J 15 March 1986; 234 (3): 741. doi: https://doi.org/10.1042/bj2340741 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 Journal Search Advanced Search This content is only available as a PDF. © 1986 London: The Biochemical Society1986 Article PDF first page preview Close Modal You do not currently have access to this content.
A cquired immunodeficiency syndrome (AIDS) results from A infection with a human immunodeficiency virus (HIV-1 or HIV-2) that eventually destroys a specific subset (CD4+) of helper T lymphocytes, so that the patient ultimately succumbs to opportunistic infections and/or certain neoplasms.<sup>1</sup>A high proportion of, and perhaps all, HIV-seropositive patients will show disease progression. Thus, of a cohort of HIV-1—positive subjects who were followed up for 3 years, 19% developed AIDS-related complex (ARC) and 26% developed AIDS.<sup>2</sup>Also, 41% of those who remained asymptomatic showed laboratory evidence of decline of immunologic status.<sup>2</sup>The only drug currently approved for the treatment of AIDS is 3'-azido-3'-deoxythymidine (azidothymidine, or AZT, now called zidovudine), which is therapeutically effective but has significant time- and dose-related toxicity.<sup>3,4</sup> Recent reports have implicated<i>reactive oxygen species</i>both in the pathogenesis of HIV infection and in some of the side effects of drugs such as zidovudine.
Flavonoids have powerful antioxidant activities in vitro, but the evidence that they act as antioxidants in vivo in humans is equivocal at best. However, they may be able to help protect the gastro-intestinal tract against reactive oxygen species.
1. A mixture of NADH and phenazine methosulphate hydroxylates aromatic compounds at acidic pH values. 2. Hydroxylation is inhibited by catalase and by scavengers of the hydroxyl radical (-OH) but not by superoxide dismutase. 3. It is concluded that neither O2 leads to nor HO2- is sufficiently reactive to hydroxylate aromatic rings.
AbstractStress-Inducible Cellular Responses Eds. U. Feige, R. I. Morimoto, I. Yahara and 8. S. Polla Birkhauser Verlag, Basel, 1996
Diets rich in polyphenols are epidemiologically associated with lower risk of developing some age-related diseases in humans. This apparent disease-protective effect of polyphenols is often attributed to their powerful antioxidant activities, as established in vitro. However, polyphenols can also exert pro-oxidant activities under certain experimental conditions. Neither pro-oxidant nor anti-oxidant activities have yet been clearly established to occur in vivo in humans, nor are they likely given the limited levels of polyphenols that are achievable in vivo after consumption of foods and beverages rich in them. Other actions of polyphenols may be more important in vivo. Many studies of the biological effects of polyphenols in cell culture have been affected by their ability to oxidise in culture media, and awareness of this problem can avoid erroneous claims.
The stroma of spinach chloroplasts contains ascorbic acid and glutathione at millimolar concentrations. [Reduced glutathione]/[oxidized glutathione] and [ascorbate]/[dehydroascorbate] ratios are high under both light and dark conditions and no evidence for a role of oxidized glutathione or dehydroascorbate in the dark-deactivation of fructose bisphosphatase could be obtained. Addition of H2O2 to chloroplasts in the dark decreases the above ratios, an effect that is reversed on illumination. Addition of Paraquat to illuminated chloroplasts caused a rapid oxidation of reduced glutathione and ascorbate, and apparent loss of dehydroascorbate. Paraquat rapidly inactivated fructose bisphosphatase activity, as assayed under physiological conditions.
