Journal Article

Characterization of the Oxidative Stress in Renal Ischemia/Reperfusion-Induced Cardiorenal Syndrome Type 3

De Angelis, Kátia, Pieretti, Joana Claudio, Neres-Santos, Raquel Silva, Seabra, Amedea Barozzi, Pelegrino, Milena Trevisan, Caio-Silva, Wellington, Carneiro-Ramos, Marcela Sorelli, Panico, Karine, Junho, Carolina Victoria Cruz, da Silva Dias, Danielle

2020

Overview

In kidney disease (KD), several factors released into the bloodstream can induce a series of changes in the heart, leading to a wide variety of clinical situations called cardiorenal syndrome (CRS). Reactive oxygen species (ROS) play an important role in the signaling and progression of systemic inflammatory conditions, as observed in KD. The aim of the present study was to characterize the redox balance in renal ischemia/reperfusion-induced cardiac remodeling. C57BL/6 male mice were subjected to occlusion of the left renal pedicle, unilateral, for 60 min, followed by reperfusion for 8 and 15 days, respectively. The following redox balance components were evaluated: catalase (CAT), superoxide dismutase (SOD), total antioxidant capacity (FRAP), NADPH oxidase (NOX), nitric oxide synthase (NOS), hydrogen peroxide (H2O2), and the tissue bioavailability of nitric oxide (NO) such as S-nitrosothiol (RSNO) and nitrite (NO2−). The results indicated a process of renoprotection in both kidneys, indicated by the reduction of cellular damage and some oxidant agents. We also observed an increase in the activity of antioxidant enzymes, such as SOD, and an increase in NO bioavailability. In the heart, we noticed an increase in the activity of NOX and NOS, together with increased cell damage on day 8, followed by a reduction in protein damage on day 15. The present study concludes that the kidneys and heart undergo distinct processes of damage and repair at the analyzed times, since the heart is a secondary target of ischemic kidney injury. These results are important for a better understanding of the cellular mechanisms involved in CRS.

• Publisher: Hindawi Publishing Corporation,Hindawi,John Wiley & Sons, Inc
• Subject: Analysis / Animals / Antioxidants / Antioxidants - metabolism / Aqueous solutions / Bioavailability / Cardio-Renal Syndrome - metabolism / Care and treatment / Catalase / Catalase - metabolism / Damage / Diagnosis / Enzymes / Gene expression / Health aspects / Heart / Heart failure / Hydrogen peroxide / Hydrogen Peroxide - metabolism / Inflammation / Ischemia / Kidney - metabolism / Kidney diseases / Kidneys / Male / Mice / Mice, Inbred C57BL / NAD(P)H oxidase / NADPH Oxidases - metabolism / Nitric oxide / Nitric Oxide - metabolism / Nitric Oxide Synthase - metabolism / Nitric-oxide synthase / Nitrogen dioxide / Occlusion / Oxidants / Oxidants - metabolism / Oxidation / Oxidation-Reduction / Oxidative stress / Oxidative Stress - physiology / Oxidizing agents / Potassium / Proteins / Reactive oxygen species / Reactive Oxygen Species - metabolism / Reduction / Reperfusion / Reperfusion injury / Reperfusion Injury - metabolism / Risk factors / Superoxide dismutase / Superoxide Dismutase - metabolism / Tumor necrosis factor-TNF / Variance analysis