At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, how...

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Free Radicals in the Physiological Control of Cell Function

Publisher Summary This chapter discusses the role of free radicals and catalytic metal ions in human disease. The importance of transition metal ions in mediating oxidant damage naturally leads to the question as to what forms of such ions might be available to catalyze radical reactions in vivo . The chapter discusses the metabolism of transition metals, such as iron and copper. It also discusses the chelation therapy that is an approach to site-specific antioxidant protection. The detection and measurement of lipid peroxidation is the evidence most frequently cited to support the involvement of free radical reactions in toxicology and in human disease. A wide range of techniques is available to measure the rate of this process, but none is applicable to all circumstances. The two most popular are the measurement of diene conjugation and the thiobarbituric acid (TBA) test, but they are both subject to pitfalls, especially when applied to human samples. The chapter also discusses the essential principles of the peroxidation process. When discussing lipid peroxidation, it is essential to use clear terminology for the sequence of events involved; an imprecise use of terms such as initiation has caused considerable confusion in the literature. In a completely peroxide-free lipid system, first chain initiation of a peroxidation sequence in a membrane or polyunsaturated fatty acid refers to the attack of any species that has sufficient reactivity to abstract a hydrogen atom from a methylene group.

Role of free radicals and catalytic metal ions in human disease: an overview.

ROS Function in Redox Signaling and Oxidative Stress

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

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Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

https://link.springer.com/content/pdf/10.1097%2FWOX.0b013e3182439613.pdf

Oxidative Stress and Antioxidant Defense

Protein thiol oxidation and formation of S-glutathionylated cyclophilin A in cells exposed to chloramines and hypochlorous acid.

Neutrophil granule proteins generate bactericidal ammonia chloramine on reaction with hydrogen peroxide

Living organisms are continually exposed to free radicals and other reactive oxygen species as a result of metabolizing oxygen and other redox-active compounds. Excessive production can result in biological damage, whereas in other situation, specific oxidants are generated as a host defense mechanism or as a cell signal that activates gene expression and metabolic responses. This article provides an overview of the specific reactive oxygen species that are generated biologically, how and where they arise, and their chemical reactivity with biological molecules.


Keywords:

biological generation of reactive oxygen species;
biological reactivity of reactive oxygen species;
oxygen radicals;
superoxide;
hydrogen peroxide;
oxidative stress;
redox regulation

Biological Chemistry of Reactive Oxygen Species

Objectives. To find out whether plasma concentrations of protein carbonyl (a specific marker of oxidative damage of proteins) are increased during intestinal ischaemia-reperfusion and whether they are correlated with von Willebrand's factor (vWF, a marker of endothelial injury) or myeloperoxidase (a marker of neutrophil activation).Design. Randomised experimental study.Setting. University department of surgery, New Zealand.Animals. Thirty anaesthetised adult Wistar rats.Interventions. The sham operated group (n ≥ 10) had laparotomy and isolation of the superior mesenteric artery without clamping. The ischaemia-reperfusion group (IR, n ≥ 10) had the superior mesenteric artery clamped for 1 hour and reperfusion for 15 minutes. The control group (n ≥ 10) had direct puncture of the heart to sample blood.Main outcome measures. Plasma concentrations of protein carbonyl, vWF, and myeloperoxidase.Results. Plasma protein carbonyl concentrations were significantly higher in the IR group than in the sham group (p < ...

Christine C. Winterbourn

Papers

Protein thiol oxidation and formation of S-glutathionylated cyclophilin A in cells exposed to chloramines and hypochlorous acid.

Neutrophil granule proteins generate bactericidal ammonia chloramine on reaction with hydrogen peroxide

Biological Chemistry of Reactive Oxygen Species

Small Bowel Ischaemia-Reperfusion Increases Plasma Concentrations of Oxidised Proteins in Rats

Interactions of staphyloxanthin and enterobactin with myeloperoxidase and reactive chlorine species.