Περίληψη:
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. © 2019 Konstantina P. Poulianiti et al.
Συγγραφείς:
Poulianiti, K.P.
Karioti, A.
Kaltsatou, A.
Mitrou, G.I.
Koutedakis, Y.
Tepetes, K.
Christodoulidis, G.
Giakas, G.
Maridaki, M.D.
Stefanidis, I.
Jamurtas, A.Z.
Sakkas, G.K.
Karatzaferi, C.
Λέξεις-κλειδιά:
Blood; Peptides, Blood redox status; Chronic kidney disease; Glutathione reductase; Protein carbonyls; Reduced glutathione; Thiobarbituric acid reactive substances; Tissue specifics; Total antioxidant capacities (TAC), Muscle, carbonyl derivative; catalase; creatinine; glutathione; glutathione disulfide; glutathione reductase; hemoglobin; thiobarbituric acid reactive substance; urea; catalase; glutathione disulfide, animal cell; animal experiment; animal model; animal tissue; antioxidant activity; Article; blood sampling; controlled study; creatinine blood level; enzyme activity; experimental renal failure; female; hemoglobin blood level; New Zealand White (rabbit); nonhuman; protein blood level; psoas muscle; rabbit model; redox stress; skeletal muscle; soleus muscle; urea blood level; uremia; animal; blood; disease model; kidney failure; Leporidae; metabolism; oxidation reduction reaction; protein carbonylation; skeletal muscle, Acids; Blood; Capacity; Control Systems; Organizations; Peptides; Stresses; Tissue, Animals; Catalase; Disease Models, Animal; Female; Glutathione Disulfide; Muscle, Skeletal; Oxidation-Reduction; Protein Carbonylation; Rabbits; Renal Insufficiency; Uremia
