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DNA damage by oxygen-derived species Its mechanism and measurement in mammalian systems

TLDR
Observation of the role of different oxygen‐derived species in DNA cleavage reactions has been used to determine the extent of oxidative damage to DNA in vivo and to investigate the mechanism of DNA damage by ionizing radiation and chemical carcinogens.
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This article is published in FEBS Letters.The article was published on 1991-04-09 and is currently open access. It has received 1555 citations till now. The article focuses on the topics: DNA damage & Free radical damage to DNA.

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Reactive Oxygen Species, Oxidative Damage, and Antioxidative Defense Mechanism in Plants under Stressful Conditions

TL;DR: The generation, sites of production and role of ROS as messenger molecules as well as inducers of oxidative damage are described and the antioxidative defense mechanisms operating in the cells for scavenging of ROS overproduced under various stressful conditions of the environment are described.
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Reactive Oxygen Species and the Central Nervous System

TL;DR: The nature of antioxidants is discussed, it being suggested that antioxidant enzymes and chelators of transition metal ions may be more generally useful protective agents than chain‐breaking antioxidants.
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Development and validation of an improved oxygen radical absorbance capacity assay using fluorescein as the fluorescent probe.

TL;DR: The improved ORAC(FL) assay provides a direct measure of hydrophilic chain-breaking antioxidant capacity against peroxyl radical and demonstrates that fluorescein (FL) is superior to B-phycoerythrin.
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Damage to DNA by reactive oxygen and nitrogen species: role in inflammatory disease and progression to cancer.

TL;DR: ROS and RNS could contribute to the initiation of cancer, in addition to being important in the promotion and progression phases, as evidence is growing that antioxidants may prevent or delay the onset of some types of cancer.
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Lipid peroxidation: its mechanism, measurement, and significance.

TL;DR: An increased concentration of end products of lipid peroxidation is the evidence most frequently quoted for the involvement of free radicals in human disease, but it is likely that increased oxidative damage occurs in most, if not all, human diseases and plays a significant pathological role in only some of them.
References
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Journal ArticleDOI

Oxidative stress: oxidants and antioxidants

TL;DR: These low molecular mass antioxidant molecules add significantly to the defense provided by the enzymes superoxide dismutase, catalase and glutathione peroxidases, which are termed ‘oxidative stress’.
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Tissue Destruction by Neutrophils

TL;DR: With increasing frequency, the human neutrophil is being implicated as a mediator of tissue-destructive events in inflammatory diseases ranging from rheumatoid arthritis and myocardial reperfusion injury to respiratory distress syndromes, blistering skin disorders, and ulcerative colitis.
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Dietary carcinogens and anticarcinogens Oxygen radicals and degenerative diseases

TL;DR: Dietary intake of natural antioxidants could be an important aspect of the body's defense mechanism against these agents of cancer and other age-related diseases.
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Prooxidant states and tumor promotion.

Peter A. Cerutti
- 25 Jan 1985 - 
TL;DR: Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents.
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