Chronic inflammation results in increased nitrogen monoxide (⋅NO) formation and the accumulation of nitrite (NO \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}_{2}^{-}\end{equation*}\end{document} ). Neutrophils stimulated by various inflammatory mediators release myeloperoxidase to produce the cytotoxic agent hypochlorous acid (HOCl). Exposure of chondrocytic SW1353 cells to HOCl resulted in a concentration- and time-dependent loss in viability, ATP, and glutathione levels. Treatment of cells with NO \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}_{2}^{-}\end{equation*}\end{document} but not nitrate (NO \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}_{3}^{-}\end{equation*}\end{document} ) substantially decreased HOCl-dependent cellular toxicity even when NO \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}_{2}^{-}\end{equation*}\end{document} was added at low (μM) concentrations. In contrast, NO \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}_{2}^{-}\end{equation*}\end{document} alone (even at 1 mM concentrations) did not affect cell viability or ATP and glutathione levels. These data suggest that NO \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}_{2}^{-}\end{equation*}\end{document} accumulation at chronic inflammatory sites, where both HOCl and ⋅NO are overproduced, may be cytoprotective against damage caused by HOCl. We propose that this is because HOCl is removed by reacting with NO \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} \begin{equation*}_{2}^{-}\end{equation*}\end{document} to give nitryl chloride (NO 2 Cl), which is less damaging in our cell system.
The synthetic oestrogens diethylstilboestrol, hexoestrol and 17 α‐ethynyloestradiol are known to be carcinogenic, yet they all exert antioxidant properties in vitro in that they are good inhibitors of iron ion‐dependent lipid peroxidation. In rat liver microsomes incubated with Fe(III)‐ascorbate or Fe(III)‐ADP/NADPH and also in ox‐brain phospholipid liposomes incubated with Fe(III)‐ascorbate; the overall order of effectiveness of the compounds tested as inhibitors of lipid peroxidation was diethylstilboestrol ⪢ hexoestrol ⪢ 17 α‐ethynyloestradiol ⪢ 4‐hydroxytamoxifen ⪢ 17 β‐oestradiol ⪢ tamoxifen. Compounds acting as antioxidants towards lipids may also exert pro‐oxidant effects towards other molecules such as DNA and thus must never be assumed to be safe for human use.
Superoxide dismutases are enzymes which catalyse the breakdown of the superoxide radical, a -, to Hz O2 and triplet O2 _ They are present in all aerobic organisms and play an important role in protection against 0; -. generated in vivo [l-3] .Superoxide dismutases are metalloproteins, containing either copper and zinc.manganese or iron as the prosthetic
No abstract is provided for this article.
Peroxynitrite, formed by combination of superoxide radical with nitric oxide, is a reactive tissue‐damaging species apparently involved in the pathology of several human diseases. Peroxynitrite nitrates tyrosine residues and inactivates α 1 ‐antiprotinase. We show that both lipoic acid and dihydrolipoic acid efficiently protect against damage by peroxynitrite. By contrast, other disulphides tested did not. The biological antioxidant effects of lipoate/dihydrolipoate may involve scavenging of reactive nitrogen species as well as reactive oxygen species.
Hydrogen peroxide (H(2)O(2)) can be detected in freshly-voided human urine from healthy subjects and has been proposed as a "biomarker" of oxidative stress. This paper summarizes our studies to examine the extent to which urinary H(2)O(2) measurement fulfils the criteria for the "ideal biomarker". Levels of H(2)O(2), standardised for creatinine, varied widely between subjects. In most subjects, levels also varied considerably when measurements were made at different times and on different days. A reproducible increase in urinary H(2)O(2) was detected in all subjects examined after drinking coffee, a beverage rich in H(2)O(2). By contrast, green tea decreased urinary H(2)O(2) levels. We conclude that the H(2)O(2) in coffee is not excreted into urine. Instead, hydroxyhydroquinone from coffee is absorbed, excreted and oxidises in urine to produce H(2)O(2). No other confounders of urinary H(2)O(2) have been identified to date. Work is underway to compare H(2)O(2) levels with variations in other biomarkers of oxidative damage, to test the possibility that there are daily or other periodic variations in oxidative damage rates.
