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| View Larger Image | Increased DNA damage and oxidative stress in patients with cutaneous leishmaniasis [An article from: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis] | Digitalby A. Kocyigit (Author), H. Keles (Author), S. Selek (Author), S. Guzel (Author), Celik (Author)
| List Price: | $8.95 | | | Available: | Available for download now |
| | Binding: | Digital | | Publisher: | Elsevier |
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EDITORIAL REVIEWS | Product Description This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: Cutaneous leishmaniasis (CL) is a chronic infectious and granulomatous disease caused by the Leishmania parasite that invades the skin. Reactive oxygen and nitrogen species (ROS and RNS) produced during an inflammatory response are an important part of host-defense strategies of organisms to kill the parasite. However, it is not well known whether these intermediates cause DNA damage in CL patients. We investigated the effect of Leishmania infection on basal levels of DNA strand breaks and on the oxidative/anti-oxidative status of patients with CL, and compared the data with those of healthy subjects. Twenty-five CL patients and 19 age- and sex-matched control subjects were enrolled in the study. We used the single-cell gel electrophoresis (also called comet assay) to measure DNA strand breaks in peripheral blood mononuclear leukocytes. Plasma protein carbonyl (PC), malondialdehyde (MDA) and total peroxide (TP) concentrations were measured to determine oxidative status and total anti-oxidative response (TAR) in plasma was measured to determine anti-oxidative status. The mean values of DNA damage and MDA and TP concentrations were significantly higher in CL patients than in the control group (p |
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