Volume 6, Issue 4, December 2018, Page: 175-181
Exercise Changes Oxidative Profile and Purinergic Enzymes Activity in Kidney Disease
Matheus Pelinski da Silveira, Department of Medicine, Federal University of South Frontier, Chapecó, Brazil
Aline Mânica, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, Brazil
João Victor Garcia de Souza, Department of Medicine, Federal University of South Frontier, Chapecó, Brazil
Cíntia Krilow, Department of Medicine, Federal University of South Frontier, Chapecó, Brazil
Pedro Augusto Cavagni Ambrosi, Department of Medicine, Federal University of South Frontier, Chapecó, Brazil
Cristiane Márcia Siepko, Department of Health Sciences, Ibrate College, Curitiba, Brazil
Beatriz Da Silva Rosa Bonadiman, Department of Biochemistry, Federal University of Santa Catarina, Florianópolis, Brazil
Margarete Dulce Bagatini, Academic Coordination, Federal University of South Frontier, Chapecó, Brazil
Débora Tavares Resende e Silva, Academic Coordination, Federal University of South Frontier, Chapecó, Brazil
Received: Oct. 19, 2018;       Accepted: Nov. 12, 2018;       Published: Dec. 20, 2018
DOI: 10.11648/j.ajss.20180604.17      View  42      Downloads  14
Abstract
Chronic Kidney Disease (CKD) patients are inactive and have reduced physical performance. The CKD lead to abnormalities in various systems including the hemostatic and oxidative systems. The platelet activation occurs with the participation of adenine nucleotides such as ATP and ADP. This nucleotides are part of a system calls purinergic signaling, that is a cell-cell communication pathway, present in several physiological mechanisms such as immune responses, pain, inflammation, cell proliferation, oxidative stress and platelet aggregation. In this work we evaluate the physical mobility, functional capacity and changes in oxidative profile and purinergic enzymes activity in patients with CKD during hemodialysis treatment before and after the protocol of resistance exercise (RE) development. Patients during hemodialysis section were recruited (n = 34). All patients underwent a RE three times a week for eight weeks. The data were analyzed in two moments: before the exercises (BE) and after the exercises (AE). Physical training significantly reduced the markers of oxidative stress after RE by increasing enzymatic and non-enzymatic antioxidant defenses. In addition, the activity of the enzymes of the purinergic system was significantly lower by ATP and AMP hydrolysis after RE. We showed, for the first time, that RE decreased significantly the oxidative stress markers after exercise when compared to previous exercise through increased enzymatic and non-enzymatic antioxidant defenses in CDK patients. These results reinforce the main role of RE in patients with chronic disease and future uses to increase the quality of life of CKD patients.
Keywords
Chronic Kidney Disease (CKD), Purinergic Signaling, Oxidative Stress, Platelet Aggregation, Resistance Exercise
To cite this article
Matheus Pelinski da Silveira, Aline Mânica, João Victor Garcia de Souza, Cíntia Krilow, Pedro Augusto Cavagni Ambrosi, Cristiane Márcia Siepko, Beatriz Da Silva Rosa Bonadiman, Margarete Dulce Bagatini, Débora Tavares Resende e Silva, Exercise Changes Oxidative Profile and Purinergic Enzymes Activity in Kidney Disease, American Journal of Sports Science. Vol. 6, No. 4, 2018, pp. 175-181. doi: 10.11648/j.ajss.20180604.17
Copyright
Copyright © 2018 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Reference
[1]
De Nicola L, Zoccali C. Chronic kidney disease prevalence in the general population: heterogeneity and concerns: Table 1. Nephrology Dialysis Transplantation. 2016; 31 (3): 331–5.
[2]
Saheb Sharif-Askari F, Syed Sulaiman SA, Saheb Sharif-Askari N. Anticoagulation Therapy in Patients with Chronic Kidney Disease. Adv Exp Med Biol. 2017; 906: 101–14.
[3]
Bergmeier W, Stefanini L. Platelets at the Vascular Interface. Res Pract Thromb Haemost. 2018; 2 (1): 27–33.
[4]
Evans MD, Dizdaroglu M, Cooke MS. Oxidative DNA damage and disease: induction, repair and significance. Mutation Research/Reviews in Mutation Research. 2004; 567 (1): 1–61.
[5]
Burnstock G. Blood cells: an historical account of the roles of purinergic signalling. Purinergic Signalling. 2015; 11 (4): 411–34.
[6]
Burnstock G. Short- and long-term (trophic) purinergic signalling. Philosophical Transactions of the Royal Society B: Biological Sciences. 2016; 371 (1700): 20150422.
[7]
Yegutkin GG. Nucleotide- and nucleoside-converting ectoenzymes: Important modulators of purinergic signalling cascade. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 2008; 1783 (5): 673–94.
[8]
Najas CS, Pissulin FDM, Pacagnelli FL, Betônico GN, Almeida IC, Neder JA. [Safety and Accuracy of Physical Training in Chronic Renal Insufficiency]. Revista Brasileira de Medicina do Esporte. 2009; 15 (5): 384–8. Portuguese.
[9]
Borg G. [Borg's perceived exertion and pain scales]. São Paulo: Manole; 2000. Portuguese.
[10]
Pilla C, Emanuelli T, Frassetto SS, Battastini AMO, Dias RD, Sarkis JJF. ATP diphosphohydrolase activity (apyrase, EC 3.6.1.5) in human blood platelets. Platelets. January 1996; 7 (4): 225–30.
[11]
Lunkes GI, Lunkes D, Stefanello F, et al. Enzymes that hydrolyze adenine nucleotides in diabetes and associated pathologies. Thrombosis Research. 2003; 109 (4): 189–94.
[12]
Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Analytical Biochemistry. 1976; 72 (1–2): 248–5.
[13]
Araújo CGS de. [Sitting-rising test: introduction of a new procedure for evaluation in Exercise and Sports Medicine]. Revista Brasileira de Medicina do Esporte. 1999; 5 (5): 179–82. Portuguese.
[14]
Olas B, Saluk-Juszczak J, Wachowicz B. d-glucaro 1,4-lactone and resveratrol as antioxidants in blood platelets. Cell Biology and Toxicology. 2008; 24 (2): 189–99.
[15]
Misra HP, Fridovich I. The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase. J Biol Chem. 1972; 247 (10): 3170–5.
[16]
Levine RL, Garland D, Oliver CN, et al. Determination of carbonyl content in oxidatively modified proteins. Meth Enzymol. 1990; 186: 464–78.
[17]
Pimentel VC, Pinheiro FV, Kaefer M, Moresco RN, Moretto MB. Assessment of uric acid and lipid peroxidation in serum and urine after hypoxia–ischemia neonatal in rats. Neurological Sciences. 2011; 32 (1): 59–65.
[18]
Beutler E, Duron O, Kelly BM. Improved method for the determination of blood glutathione. J Lab Clin Med. 1963; 61: 882–8.
[19]
Lowry OH, Lopez JA, Bessey OA. The determination of ascorbic acid in small amounts of blood serum. J Biol Chem. 1945; 160: 609–615.
[20]
Heymann D, Reddington M, Kreutzberg GW. Subcellular Localization of 5’-Nucleotidase in Rat Brain. Journal of Neurochemistry. 1984; 43 (4): 971–8.
[21]
Giusti G, Galanti B. Adenosine deaminase: colorimetric method. In: Bergmeyer HU editors. 3rd ed. Methods of Enzymatic Analysis. vol. 4: Weinheim: Verlag Chemie; 1984; p. 315–323.
[22]
Poulianiti KP, Kaltsatou A, Mitrou GI, et al. Systemic Redox Imbalance in Chronic Kidney Disease: A Systematic Review. Oxidative Medicine and Cellular Longevity. 2016; vol. 2016: 1–19.
[23]
Papavasiliou EC, Gouva C, Siamopoulos KC, Tselepis AD. Erythrocyte PAF-acetylhydrolase activity in various stages of chronic kidney disease: effect of long-term therapy with erythropoietin. Kidney Int. 2005; 68 (1): 246–55.
[24]
Sahni N, Gupta KL, Rana SV, Prasad R, Bhalla AK. Intake of antioxidants and their status in chronic kidney disease patients. J Ren Nutr. 2012; 22 (4): 389–99.
[25]
Bober J, Kedzierska K, Kwiatkowska E, et al. Does oxidative stress affect the activity of the sodium-proton exchanger? Ann Acad Med Stetin. 2010; 56 (3): 5–12.
[26]
Choi J-Y, Yoon YJ, Choi H-J, et al. Dialysis modality-dependent changes in serum metabolites: accumulation of inosine and hypoxanthine in patients on haemodialysis. Nephrol Dial Transplant. 2011; 26 (4): 1304–13.
[27]
da Silva AC, Rocha JBT, Morsch ALB, et al. Oxidative stress and δ-ALA-D activity in chronic renal failure patients. Biomedicine & Pharmacotherapy. 2007; 61 (2–3): 180–5.
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