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      Effects of folic acid on rat kidney exposed to 900 MHz electromagnetic radiation

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          Abstract

          Because of increased use of cell phones, the purpose of this study was to investigation of the oxidative damage caused by electromagnetic radiation (EMR) emitted by cell phones and histological and morphometrical determination of the possible protective role of folic acid (FA) in preventing the detrimental effects of EMR on the kidney. Twenty-four adult male Wistar albino rats were divided into control (Cont), EMR, EMR + FA and FA groups, each containing six rats. The EMR and EMR + FA groups were exposed to EMR for 60 min a day over a period of 21 days, while no EMR exposure was applied to the Cont and FA groups. The source of the EMR was an EMR device which emits a digital signal producing 900-MHz frequency radiation. The generator connected to a one-monopole antenna was used in this study and the rats were placed in the plexiglass restrainer at an equal distance from the monopole antenna. Following the experimental period, and after tissue processing, a physical disector-Cavalieri method combination was applied to the sections. The mean volume of the cortex, medulla, proximal and distal tubules increased significantly in the EMR groups compared to the Cont group (p < 0.01). Contrarily, the total number of glomeruli in the EMR group decreased compared to the Cont group (p < 0.01). The protective effects of FA was observed in the kidney (p < 0.05).

          In conclusion, the 900-MHz EMR leads to kidney damage. FA may exhibit a protective effect against the adverse effects of EMR exposure in terms of the total number of glomeruli.

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          Antioxidant enzymes and human diseases.

          J. M. Mates, C Pérez-Gómez, I Núñez de Castro (1999)
          To describe the importance of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase working together in human cells against toxic reactive oxygen species, their relationship with several pathophysiologic processes and their possible therapeutic implications. Reactive oxygen species (ROS) are involved in the cell growth, differentiation, progression, and death. Low concentrations of ROS may be beneficial or even indispensable in processes such as intracellular signaling and defense against micro-organisms. Nevertheless, higher amounts of ROS play a role in the aging process as well as in a number of human disease states, including cancer, ischemia, and failures in immunity and endocrine functions. As a safeguard against the accumulation of ROS, several nonenzymatic and enzymatic antioxidant activities exist. Therefore, when oxidative stress arises as a consequence of a pathologic event, a defense system promotes the regulation and expression of these enzymes.
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            Oxyl radicals, redox-sensitive signalling cascades and antioxidants.

            Marcelo Genestra (2007)
            Oxidative stress is an increase in the reduction potential or a large decrease in the reducing capacity of the cellular redox couples. A particularly destructive aspect of oxidative stress is the production of reactive oxygen species (ROS), which include free radicals and peroxides. Some of the less reactive of these species can be converted by oxidoreduction reactions with transition metals into more aggressive radical species that can cause extensive cellular damage. In animals, ROS may influence cell proliferation, cell death (either apoptosis or necrosis) and the expression of genes, and may be involved in the activation of several signalling pathways, activating cell signalling cascades, such as those involving mitogen-activated protein kinases. Most of these oxygen-derived species are produced at a low level by normal aerobic metabolism and the damage they cause to cells is constantly repaired. The cellular redox environment is preserved by enzymes and antioxidants that maintain the reduced state through a constant input of metabolic energy. This review summarizes current studies that have been regarding the production of ROS and the general redox-sensitive targets of cell signalling cascades.
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              Oxidative Stress and Nucleic Acid Oxidation in Patients with Chronic Kidney Disease

              Chih-Chien Sung, Yu-Chuan Hsu, Chun-Chi Chen … (2013)
              Patients with chronic kidney disease (CKD) have high cardiovascular mortality and morbidity and a high risk for developing malignancy. Excessive oxidative stress is thought to play a major role in elevating these risks by increasing oxidative nucleic acid damage. Oxidative stress results from an imbalance between reactive oxygen/nitrogen species (RONS) production and antioxidant defense mechanisms and can cause vascular and tissue injuries as well as nucleic acid damage in CKD patients. The increased production of RONS, impaired nonenzymatic or enzymatic antioxidant defense mechanisms, and other risk factors including gene polymorphisms, uremic toxins (indoxyl sulfate), deficiency of arylesterase/paraoxonase, hyperhomocysteinemia, dialysis-associated membrane bioincompatibility, and endotoxin in patients with CKD can inhibit normal cell function by damaging cell lipids, arachidonic acid derivatives, carbohydrates, proteins, amino acids, and nucleic acids. Several clinical biomarkers and techniques have been used to detect the antioxidant status and oxidative stress/oxidative nucleic acid damage associated with long-term complications such as inflammation, atherosclerosis, amyloidosis, and malignancy in CKD patients. Antioxidant therapies have been studied to reduce the oxidative stress and nucleic acid oxidation in patients with CKD, including alpha-tocopherol, N-acetylcysteine, ascorbic acid, glutathione, folic acid, bardoxolone methyl, angiotensin-converting enzyme inhibitor, and providing better dialysis strategies. This paper provides an overview of radical production, antioxidant defence, pathogenesis and biomarkers of oxidative stress in patients with CKD, and possible antioxidant therapies.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Microsc Ultrastruct
                Journal ID (iso-abbrev): J Microsc Ultrastruct
                Journal ID (publisher-id): JMAU
                Title: Journal of Microscopy and Ultrastructure
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2213-879X
                ISSN (Electronic): 2213-8803
                Publication date (Print): Oct-Dec 2017
                Publication date (Electronic): 17 June 2017
                Volume: 5
                Issue: 4
                Pages: 198-205
                Affiliations
                [1] Department of Histology and Embryology, Medical Faculty, Ondokuz Mayıs University, Samsun, 55139, Turkey
                Author notes
                [* ] Corresponding author. E-mail address: omur.denizomu@ 123456gmail.com (Ö.G. Deniz).
                Article
                Publisher ID: JMAU-5-198
                DOI: 10.1016/j.jmau.2017.06.001
                PMC ID: 6025785
                PubMed ID: 30023255
                SO-VID: a11eb76f-34d2-4f1f-a9bb-bfc1b251d819
                Copyright © Copyright: © 2017 Saudi Society of Microscopes
                License:

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 26 March 2017
                Date revision received : 29 May 2017
                Date accepted : 15 June 2017
                Categories
                Subject: Original Article

                Keywords: electromagnetic radiation,folic acid,stereology,histopathology,rat
                Data availability:
                Keywords: electromagnetic radiation, folic acid, stereology, histopathology, rat

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