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      Evaluation of local trace element status and 8-Iso-prostaglandin F concentrations in patients with Tinea pedis

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          Abstract

          Background

          Tinea pedis (TP) is an infection of the feet caused by fungi. The infectious diseases caused by dermatophytes are mainly related to the enzymes produced by these fungi. Up to the now, the local 8-iso-prostaglandin F (8-iso-PGF ), concentration as oxidative stress biomarker and trace elements status have not been published in patients with TP. The aim of this study is to evaluate the relationship between oxidative stress and trace elements (Cu, Zn, Se), and to evaluate the ratios of Cu/Zn and Cu/Se in this disorder.

          Methods

          Forty-three consecutive patients with a diagnosis of unilateral interdigital TP were enrolled in this study. The samples were obtained by scraping the skin surface. 8-iso-PGF concentrations in scraping samples were determined by ELISA. In addition, the levels of Se, Zn and Cu in scraping samples were determined on flame and furnace atomic absorption spectrophotometer using Zeeman background correction.

          Results

          Oxidative stress was confirmed by the significant elevation in 8-iso-PGF concentrations ( p < 0.05). When compared to non-lesional area, Zn and Se levels were significantly lower on lesional area, whereas Cu levels was higher on the lesional area than the non-lesional area ( p < 0.05). In addition, the correlation results of this study were firstly shown that there were significant and positive correlations between Cu and 8-iso-PGF parameters, but negative correlations between Se-Cu; Se-8-iso-PGF parameters in lesional area. Furthermore, the ratios of Cu/Zn and Cu/Se were significantly higher on the lesional area than the non-lesional area ( p < 0.05). According to sex and fungal subtypes, there was no significant difference in the concentrations of 8-iso-PGF and trace elements in patients with TP ( p > 0.05).

          Conclusions

          Our results showed that there is a possible link between oxidative stress (increased 8-iso-PGF concentrations) and imbalanced of trace elements status in lesional area of TP patients. The use of antifungal agents together with both Zn and Se drugs could be helpful in the both regression of disease and in shortening the duration of disease.

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          Most cited references34

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          The biochemical basis of zinc physiology.

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            Zinc deficiency, DNA damage and cancer risk.

            Emily Ho (2004)
            A large body of evidence suggests that a significant percentage of deaths resulting from cancer in the United States could be avoided through greater attention to proper and adequate nutrition. Although many dietary compounds have been suggested to contribute to the prevention of cancer, there is strong evidence to support the fact that zinc, a key constituent or cofactor of over 300 mammalian proteins, may be of particular importance in host defense against the initiation and progression of cancer. Remarkably, 10% of the U.S. population consumes less than half the recommended dietary allowance for zinc and are at increased risk for zinc deficiency. Zinc is known to be an essential component of DNA-binding proteins with zinc fingers, as well as copper/zinc superoxide dismutase and several proteins involved in DNA repair. Thus, zinc plays an important role in transcription factor function, antioxidant defense and DNA repair. Dietary deficiencies in zinc can contribute to single- and double-strand DNA breaks and oxidative modifications to DNA that increase risk for cancer development. This review will focus on potential mechanisms by which zinc deficiency impairs host protective mechanisms designed to protect against DNA damage, enhances susceptibility to DNA-damaging agents and ultimately increases risk for cancer.
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              A series of prostaglandin F2-like compounds are produced in vivo in humans by a non-cyclooxygenase, free radical-catalyzed mechanism.

              Increasing attention has focused on the role of free radicals derived from oxygen in the pathophysiology of a wide variety of disorders. One of the well-recognized targets of free radical-induced injury is peroxidation of lipids. Using a variety of approaches, we have found that a series of prostaglandin F2-like compounds are produced in vivo in humans by a non-cyclooxygenase mechanism involving free radical-catalyzed peroxidation of arachidonic acid. Levels of these compounds in normal human plasma and urine range from 5 to 40 pg/ml and 500 to 4000 pg/mg of creatinine, respectively. In rats, their formation was found to increase as much as 200-fold in association with marked free radical-catalyzed lipid peroxidation induced by administration of CCl4 and diquat. To explore whether these prostanoids can exert biological activity, the effects of one of the compounds formed by this mechanism, 8-epi-prostaglandin F2 alpha, was examined in the kidney in the rat. Infusion of 8-epi-prostaglandin F2 alpha into a peripheral vein (5 micrograms/kg per min) or intrarenally (0.5-2.0 micrograms/kg per min) resulted in marked parallel reductions in renal blood flow and glomerular filtration rate. That the formation of these prostanoids is catalyzed by free radicals and that they can exert potent biological activity suggest that these prostanoids may participate as pathophysiological mediators in oxidant injury. Quantification of these compounds may also provide a noninvasive approach to assess oxidant status in humans. That the formation of these prostanoids occurs independent of the catalytic activity of the cyclooxygenase enzyme suggests that there may be limitations at times regarding the reliability of the use of cyclooxygenase inhibitors to assess the role of prostaglandins in certain pathophysiological processes.
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                Author and article information

                Contributors
                +90 322 3386060 , miray70@gmail.com
                ergulkurutas@gmail.com
                drperihanozturk@hotmail.com
                ozerari@gmail.com
                Journal
                Biol Proced Online
                Biol Proced Online
                Biological Procedures Online
                BioMed Central (London )
                1480-9222
                1480-9222
                5 January 2016
                5 January 2016
                2016
                : 18
                : 1
                Affiliations
                [ ]Department of Microbiology, Faculty of Medicine, Cukurova University, 01330 Adana, Turkey
                [ ]Department of Biochemistry, Sutcu Imam University, Faculty of Medicine, Kahramanmaras, Turkey
                [ ]Department of Dermatology, Sutcu Imam University, Faculty of Medicine, Kahramanmaras, Turkey
                [ ]Department of Dermatology, Fatih University, Faculty of Medicine, Istanbul, Turkey
                Article
                30
                10.1186/s12575-015-0030-x
                4702401
                26740800
                26353911-90ab-4b93-b2c1-45d39e48f027
                © Miraloglu et al. 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 4 October 2015
                : 23 December 2015
                Categories
                Research
                Custom metadata
                © The Author(s) 2016

                Life sciences
                8-iso-pgf2α,oxidative stress,trace elements,tinea pedis
                Life sciences
                8-iso-pgf2α, oxidative stress, trace elements, tinea pedis

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