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Reactive oxygen species and antioxidants

Reactive oxygen species (ROS) are molecules that contain an oxygen atom and that are highly reactive as a result of the presence of a free radical, or a configuration of the oxygen atom whereby there are more electrons than usual. Examples of the first class include the hydroxyl radical (OH), and the superoxide radical (02 ). whereas the peroxide (022-) and hypochlorite [Pg.58]

Because of the reactivity of the hydroxyl radical, and the fact that the ingredients are inexpensive, the Fenton reaction is used on a commercial scale to treat waste water. The Fenton reaction can also occur with copper as the transition metal. Given that Fe2+, Cu+, and H202 are abundantly present in biological systems, hydroxyl radicals can be generated via the Fenton reaction in vivo. Reviews by Schiitzendubel and Polle (2002) and by Valko et al. (2005) describe the impact of ROS in plants and humans, respectively. [Pg.58]

More recently, the impact of excess iron on carcinogenesis has been studied. Toyokuni (2002) reported that in kidney cells of rats an overload of iron can result in carcinogenesis because of Fenton-reaction induced damage to a tumor suppressor gene. This is currently an active area of research. [Pg.60]

O Malley, D. M., Whetten, R., and Sederoff, R.R., 1993, A laccase associated with lignification in loblolly pine xylem. Science 260 672-674. [Pg.61]

Boissy, R. E., Visscher, M., deLong, M. A., 2005, Deoxyarbutin a novel reversible tyrosinase inhibitor with effective in vivo skin lightening potency, Exp. Dermatol. 14 601-608. [Pg.61]


Palmer, H.J. and Paulson, K.E. 1997. Reactive oxygen species and antioxidants in signal transduction and gene expression. Nutr Rev 55 353-361. [Pg.481]

Chappie, L. (1997). Reactive oxygen species and antioxidants in inflammatory diseases. J. Clin. Periodontol. 24(5), 287-296. [Pg.402]

Alscher, R.G., Donahue, J.L., and Cramer, C.L., Reactive oxygen species and antioxidants relationships in green cells. Physiol. Plant., 100, 224, 1997. [Pg.432]

Gill SS., Tuteja N. Reactive oxygen species and antioxidant machinery in abiotic stress tolerance in crop plants. Plant Physiology and Biochemistry 2010 48(12) 909-930. [Pg.213]

Litescu SC, Eremia SAV, Diaconu M, Tache A, l adu G.L (2011) Biosensor applications on Assessment of Reactive Oxygen Species and Antioxidants, in Environmental Biosensors, Ed. Vernon Sommerset, Intech, ISBN 978-953-307-486-3, Riejda Croatia... [Pg.368]

Karihtala, P. and Soini, Y. 2007. Reactive oxygen species and antioxidant mechanisms in human tissues and their relation to malignancies. APMIS acta pathologica, microbiologica, et im-munologica Scandinavica, 115(2), 81-103. [Pg.297]

Jiang, M. and Zhang, J. (2002). Water stress-induced abscisic acid accumulation triggers the increased generation of reactive oxygen species and up-regulates the activities of antioxidant enzymes in maize leaves. Journal of Experimental Botany 53 2401-2410. [Pg.147]

The antioxidant system in humans is a complex network composed by several enzymatic and nonenzymatic antioxidants. In addition to being an antioxidant, lycopene also exerts indirect antioxidant properties by inducing the production of cellular enzymes such as superoxide dismutase, glutathione S-transferase, and quinone reductase that also protect cells from reactive oxygen species and other electrophilic molecules (Goo and others 2007). [Pg.207]

Hassoun, EA Creighton University Assess abilities of endrin to induce the formation of reactive oxygen species and lipid peroxidation and DNA single strand breaks that result in oxidative stress in fetuses of pregnant mice. The protective effects of some antioxidants will also be assessed using this model. [Pg.98]

In the literature, most dmg-induced apoptosis is well known to require intracellular hyper-production of reactive oxygen species and several antioxidants inhibit apoptotic cell death. While it is clear that peroxidation reactions induce apoptosis, the precise molecular mechanism of how reactive oxygen species convey death-signals is unknown. [Pg.21]

Arsenic has been shown to induce oxidative stress (Shi, Shi and Liu, 2004 Hughes and Kitchin, 2006). Oxidative stress is a result of an imbalance between reactive oxygen species and the ability of a cell s antioxidant defense apparatus to respond. Oxidative stress can result in the damage of proteins, lipids, RNA, and deoxyribonucleic acid (DNA). In addition, since oxidant species have a role in cell signaling, a state of oxidative stress could potentially alter signaling within and between cells. [Pg.262]

Dipyridamole has also been shown to have antioxidant effects (19). Antioxidants act to remove harmful reactive-oxygen species and protect low-density lipoproteins (LDL) from oxidation oxidized LDL plays a key role in the development and propagation of atherosclerosis. The antioxidant effects of dipyridamole may be both direct (by scavenging oxygen and hydroxyl radicals, inhibiting lipid peroxidation and oxidative modification of LDL) (20-22) and indirect (via adenosine, which reduces superoxide anion generation). Dipyridamole has been shown to be a more effective anioxidant than ascorbic acid, alpha-tocopherol, or probucol (22). [Pg.72]

The antioxidant properties of vitamin E are well known and documented [5]. In particular, prevention by a-tocopherol of LDL oxidation has been studied [6]. Although the correlation between the level of LDL oxidation and atherosclerosis is not always evident [7], alternative studies have suggested that a-tocopherol protection against LDL oxidation may be secondary to the inhibition of protein kinase C (PKC). This enzyme seems to be responsible for the release of reactive oxygen species and lipid oxidation [8,9]. [Pg.113]


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