Research Article Evidence of Blood and Muscle Redox Status Imbalance in Experimentally Induced Renal Insufficiency in a Rabbit Model Konstantina P. Poulianiti, 1,2 Aggeliki Karioti, 1 Antonia Kaltsatou, 1 Georgia I. Mitrou, 1,3 Yiannis Koutedakis, 2,4,5 Konstantinos Tepetes , 6 Grigoris Christodoulidis , 6 Giannis Giakas, 2,4 Maria D. Maridaki , 7 Ioannis Stefanidis, 8 Athanasios Z. Jamurtas , 2,4 Giorgos K. Sakkas, 1,3,4 and Christina Karatzaferi 1,3,4 1 Muscle Physiology & Mechanics Group, CREHP, DPESS, University of Thessaly, Trikala 42100, Greece 2 Human Performance Group, CREHP, DPESS, University of Thessaly, Trikala 42100, Greece 3 EMIP/EmPOWER, School of Health Sciences, Plymouth Marjon University, Plymouth PL6 8BH, UK 4 Institute for Research and Technology-CERTH, Thessaly, Trikala 42100, Greece 5 School of Sports, Performing Arts & Leisure, University of Wolverhampton, Wolverhampton WV1 1LY, UK 6 Department of Surgery, School of Medicine, University of Thessaly, Larissa 41110, Greece 7 DPESS, National and Kapodistrian University of Athens, Athens 17237, Daphne, Greece 8 Department of Nephrology, School of Medicine, University of Thessaly, Larissa 41110, Greece Correspondence should be addressed to Christina Karatzaferi; karatzaferi.c@gmail.com Received 19 October 2018; Revised 20 February 2019; Accepted 28 February 2019; Published 4 April 2019 Academic Editor: Fernanda Amicarelli Copyright © 2019 Konstantina P. Poulianiti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Chronic kidney disease (CKD) is accompanied by a disturbed redox homeostasis, especially in end-stage patients, which is associated with pathological complications such as anemia, atherosclerosis, and muscle atrophy. However, limited evidence exists about redox disturbances before the end stage of CKD. Moreover, the available redox literature has not yet provided clear associations between circulating and tissue-specific (muscle) oxidative stress levels. The aim of the study was to evaluate commonly used redox status indices in the blood and in two different types of skeletal muscle (psoas, soleus) in the predialysis stages of CKD, using an animal model of renal insufficiency, and to investigate whether blood redox status indices could be reflecting the skeletal muscle redox status. Indices evaluated included reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), catalase (CAT), total antioxidant capacity (TAC), protein carbonyls (PC), and thiobarbituric acid reactive substances (TBARS). Results showed that blood GSH was higher in the uremic group compared to the control (17 50 ± 1 73 vs. 12 43 ± 1 01, p =0 033). In both muscle types, PC levels were higher in the uremic group compared to the control (psoas: 1 086 ± 0 294 vs. 0 596 ± 0 372, soleus: 2 52 ± 0 29 vs. 0 929 ± 0 41, p <0 05). The soleus had higher levels of TBARS, PC, GSH, CAT, and GR and lower TAC compared to the psoas in both groups. No significant correlations in redox status indices between the blood and skeletal muscles were found. However, in the uremic group, significant correlations between the psoas and soleus muscles in PC, GSSG, and CAT levels emerged, not present in the control. Even in the early stages of CKD, a disturbance in redox homeostasis was observed, which seemed to be muscle type-specific, while blood levels of redox indices did not seem to reflect the intramuscular condition. The above results highlight the need for further research in order to identify the key mechanisms driving the onset and progression of oxidative stress and its detrimental effects on CKD patients. 1. Introduction Redox homeostasis encompasses the balance between oxi- dants (or prooxidants) and antioxidants and is maintained by several complex mechanisms. Redox homeostasis can be disrupted due to a dysfunction of any of these mechanisms, resulting in reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) levels and/or a decreased scavenging Hindawi Oxidative Medicine and Cellular Longevity Volume 2019, Article ID 8219283, 14 pages https://doi.org/10.1155/2019/8219283