Neutrophilic polymorphonuclear leukocytes (neutrophils) are highly specialized for their primary function, the phagocytosis and destruction of microorganisms. When coated with opsonins (generally complement and/or antibody), microorganisms bind to specific receptors on the surface of the phagocyte and invagination of the cell membrane occurs with the incorporation of the microorganism into an intracellular phagosome. There follows a burst of oxygen consumption, and much, if not all, of the extra oxygen consumed is converted to highly reactive oxygen species. In addition, the cytoplasmic granules discharge their contents into the phagosome, and death of the ingested microorganism soon follows. Among the antimicrobial systems formed in the phagosome is one consisting of myeloperoxidase (MPO), released into the phagosome during the degranulation process, hydrogen peroxide (H2O2), formed by the respiratory burst and a halide, particularly chloride. The initial product of the MPO-H2O2-chloride system is hypochlorous acid, and subsequent formation of chlorine, chloramines, hydroxyl radicals, singlet oxygen, and ozone has been proposed. These same toxic agents can be released to the outside of the cell, where they may attack normal tissue and thus contribute to the pathogenesis of disease. This review will consider the potential sources of H2O2 for the MPO-H2O2-halide system; the toxic products of the MPO system; the evidence for MPO involvement in the microbicidal activity of neutrophils; the involvement of MPO-independent antimicrobial systems; and the role of the MPO system in tissue injury. It is concluded that the MPO system plays an important role in the microbicidal activity of phagocytes.

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Myeloperoxidase: friend and foe

Zinc deficiency is one of the most widespread micronutrient deficiencies in plants and causes severe reductions in crop production. There are a number of physiological impairments in Zn-deficient cells causing inhibition of the growth, differentiation and development of plants. Increasing evidence indicates that oxidative damage to critical cell compounds resulting from attack by reactive O2 species (ROS) is the basis of disturbances in plant growth caused by Zn deficiency. Zinc interferes with membrane-bound NADPH oxidase producing ROS. In Zn-deficient plants the iron concentration increases, which potentiates the production of free radicals. The Zn nutritional status of plants influences photooxidative damage to chloroplasts, catalysed by ROS. Zinc-deficient leaves are highly light-sensitive, rapidly becoming chlorotic and necrotic when exposed to high light intensity. Zinc plays critical roles in the defence system of cells against ROS, and thus represents an excellent protective agent against the oxidation of several vital cell components such as membrane lipids and proteins, chlorophyll, SH-containing enzymes and DNA. The cysteine, histidine and glutamate or aspartate residues represent the most critical Zn- binding sites in enzymes, DNA-binding proteins (Zn-finger proteins) and membrane proteins. In addition, animal studies have shown that Zn is involved in inhibition of apoptosis (programmed cell death) which is preceded by DNA and membrane damage through reactions with ROS. contents Summary 185 I. introduction 186 II. effect of zinc on production of reactive oxygen species 186 III. membrane damage by reactive oxygen species 193 III. membrane damage by reactive oxygen species 193 V. involvement of zinc in plant stress tolerance 199 VI. conclusions 199 Acknowledgements 200 References 200.

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Tansley Review No. 111: Possible roles of zinc in protecting plant cells from damage by reactive oxygen species.

This review compiles and evaluates existing scientific information on the use, limitations, and procedural considerations for EROD activity (a catalytic measurement of cytochrome P4501A induction) ...

Ethoxyresorufin-O-deethylase (EROD) activity in fish as a biomarker of chemical exposure.

Cell-permeable Peptide Antioxidants Targeted to Inner Mitochondrial Membrane inhibit Mitochondrial Swelling, Oxidative Cell Death, and Reperfusion Injury

Diana Metodiewa

Papers

Generation of Superoxide and Tyrosine Peroxide as a Result of Tyrosyl Radical Scavenging by Glutathione

Evidence for a peroxidatic oxidation of norepinephrine, a catecholamine, by lactoperoxidase.

The reactions of horseradish peroxidase, lactoperoxidase, and myeloperoxidase with enzymatically generated superoxide.

Horseradish peroxidase-catalyzed aerobic oxidation and peroxidation of indole-3-acetic acid: I. Optical spectra

Oxidation of the substituted catechols dihydroxyphenylalanine methyl ester and trihydroxyphenylalanine by lactoperoxidase and its compounds