Antioxidant System Efficiency in Kidney Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 9042

Special Issue Editors


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Guest Editor
1. Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
2. National Center of Structural Biology and Bioimaging, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
Interests: kidney; acute and chronic kidney disease; vasoactive peptides; renal oxidative stress; cell therapy; extracellular vesicles; biophysics of membrane transport
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Guest Editor
Institute of Biomedical Sciences, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
Interests: kidney; acute and chronic kidney disease

Special Issue Information

Dear Colleagues,

Acute and chronic renal diseases are severe illnesses of significant incidence in which dialysis and transplantation are frequently the only therapeutic options. These options do not avoid fatal outcomes. Chronic renal diseases and their end-stage frequently follow acute episodes. Notably, there are no efficient and specific treatments, which is why dialysis and transplantation are the only therapeutic options at the moment.

Tissue oxidative stress is a critical physiopathological component of renal lesions of many different origins. The intense oxidative metabolism of kidney tissue, especially in the cortex, favors the formation of reactive oxygen species. Due to this critical pathophysiological component, the search for antioxidant agents has recently intensified. At the same time, understanding oxidizing mechanisms and antioxidants has become imperative for a careful search for new agents and products of the most diverse origins.

There are two primary sources of reactive oxygen species capable of causing kidney damage, mitochondrial and extramitochondrial, and there is often crosstalk between them. The central oxidizing species is the superoxide anion, but different cycles can lead to other species, such as oxydryl radical. Thus, antioxidant systems—enzymatic or not—are found within both the mitochondria of the renal cortex and the medulla. They are the target of research to obtain new drugs and products, including natural products and their derivatives, and many forms of medicinal chemistry. Antioxidant products are also encountered in the new field of regenerative medicine.

This Special Issue of Antioxidants aims to stimulate the sharing of new results and ideas in the field of oxidant and antioxidant mechanisms in different segments of kidney tissue, opening up new avenues of knowledge for preventing and treating kidney diseases.

Prof. Dr. Adalberto Vieyra
Dr. Lucienne S. Lara
Guest Editors

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Keywords

  • antioxidants
  • acute renal diseases
  • renal ischemia and reperfusion
  • chronic renal diseases
  • renal oxidative stress
  • mitochondria
  • antioxidant enzymes
  • renal renin–angiotensin–aldosterone and oxidative stress
  • hypertension and renal oxidative stress

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Published Papers (4 papers)

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Research

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15 pages, 1364 KiB  
Article
The DJ-1-Binding Compound Exerts a Protective Effect in Both In Vitro and In Vivo Models of Sepsis-Induced Acute Kidney Injury
by Réka Zrufkó, Csenge Pajtók, Beáta Szebeni, Apor Veres-Székely, Mária Bernáth, Csenge Szász, Péter Bokrossy, Attila J. Szabó, Ádám Vannay and Domonkos Pap
Antioxidants 2025, 14(6), 719; https://doi.org/10.3390/antiox14060719 - 12 Jun 2025
Viewed by 651
Abstract
Although sepsis-induced acute kidney injury (AKI) is associated with significant morbidity and mortality, its treatment remains unresolved. Oxidative stress and inflammation are key elements in the pathomechanism of AKI. Therefore, in the present study, we investigated the role of DJ-1 protein, known for [...] Read more.
Although sepsis-induced acute kidney injury (AKI) is associated with significant morbidity and mortality, its treatment remains unresolved. Oxidative stress and inflammation are key elements in the pathomechanism of AKI. Therefore, in the present study, we investigated the role of DJ-1 protein, known for its antioxidant and anti-inflammatory properties in an animal model of lipopolysaccharide (LPS)-induced AKI. The presence of DJ-1 was detected by immunofluorescence staining in mice kidney samples, human embryonic kidney cells (HEK-293), and peripheral blood mononuclear cells (PBMCs). To investigate DJ-1 functions, Compound-23, a specific DJ-1-binding and preserving compound (CAS: 724737-74-0), was used in vitro and in vivo. Compound-23 reduced the H2O2-induced reactive oxygen species (ROS) production of the HEK-293 cells, and their LPS- or H2O2-induced death, as well. In accordance, Compound-23 decreased the mRNA expression of the oxidative stress markers NAD(P)H quinone dehydrogenase 1 (NQO1) and glutamate-cysteine ligase (GCLC) in the LPS-treated, and NQO1 in the H2O2-treated cells. Moreover, Compound-23 reduced the H2O2- and LPS-induced mRNA expression of inflammatory cytokine interleukin 6 (IL6) in both HEK-293 and PBMCs. Using the mice model of LPS-induced AKI, we demonstrated that Compound-23 treatment improved the renal functions of the mice. In addition, Compound-23 decreased the renal mRNA expression of kidney injury molecule 1 (Kim1), neutrophil gelatinase-associated lipocalin (Ngal), Nqo1, Gclc, and Il6 in the LPS-treated mice. Our study revealed that compounds protecting DJ-1 functions may protect the kidney from LPS-induced damage, suggesting that DJ-1 could be a potential drug target for sepsis-induced AKI therapy. Full article
(This article belongs to the Special Issue Antioxidant System Efficiency in Kidney Diseases)
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18 pages, 2449 KiB  
Article
Corynoxeine Supplementation Ameliorates Colistin-Induced Kidney Oxidative Stress and Inflammation in Mice
by Yue Liu, Ruichen Zhang, Tony Velkov, Jianzhong Shen, Shusheng Tang and Chongshan Dai
Antioxidants 2025, 14(5), 593; https://doi.org/10.3390/antiox14050593 - 15 May 2025
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Abstract
This study investigated the protective effects of corynoxeine, a natural alkaline compound, on colistin-caused nephrotoxicity using a murine model. Forty mice were divided randomly into control, corynoxeine-only (20 mg/kg/day, intraperitoneal injection), colistin-only (20 mg/kg/day, intraperitoneal injection), and colistin (20 mg/kg/day) + corynoxeine (5 [...] Read more.
This study investigated the protective effects of corynoxeine, a natural alkaline compound, on colistin-caused nephrotoxicity using a murine model. Forty mice were divided randomly into control, corynoxeine-only (20 mg/kg/day, intraperitoneal injection), colistin-only (20 mg/kg/day, intraperitoneal injection), and colistin (20 mg/kg/day) + corynoxeine (5 and 20 mg/kg/day) groups (8 mice in each group). All treatments were maintained for seven consecutive days. Results showed that colistin treatment at 20 mg/kg/day for seven days significantly increased serum urea nitrogen and creatinine levels and induced the loss and degeneration of renal tubular epithelial cells, which were markedly ameliorated by corynoxeine co-treatment at 5 or 20 mg/kg/day. Corynoxeine supplementation also markedly attenuated colistin-induced increases in malondialdehyde levels and decreases in reduced glutathione levels and superoxide dismutase and catalase activities in the kidneys. Furthermore, corynoxeine supplementation significantly decreased the expression of transforming growth factor β (TGF-β) and nicotinamide adenine dinucleotide phosphate hydrogen oxidase 4 (NOX4) proteins and nuclear factor kappa B (NF-κB), interleukin-1beta (IL-1β), IL-6, and tumor necrosis factor-α mRNAs, while it significantly increased the expression of erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) proteins in the kidneys. In conclusion, these results reveal that corynoxeine can protect against colistin-induced nephrotoxicity in mice by inhibiting oxidative stress and inflammation, which may partly be attributed to its ability on the activation of the Nrf2/HO-1 pathway and the inhibition of the TGF-β/NOX4 and NF-κB pathways. Full article
(This article belongs to the Special Issue Antioxidant System Efficiency in Kidney Diseases)
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16 pages, 6507 KiB  
Article
Liproxstatin-1 Alleviated Ischemia/Reperfusion-Induced Acute Kidney Injury via Inhibiting Ferroptosis
by Zhiyuan Shi, Yifan Du, Jianzhong Zheng, Wenbin Tang, Qing Liang, Zeyuan Zheng, Bin Liu, Huimin Sun, Kejia Wang and Chen Shao
Antioxidants 2024, 13(2), 182; https://doi.org/10.3390/antiox13020182 - 31 Jan 2024
Cited by 10 | Viewed by 3722
Abstract
Ferroptosis, as a novel regulable cell death, is characterized by iron overload, glutathione depletion, and an accumulation of lipid peroxides. Recently, it has been discovered that ferroptosis is involved in ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) and plays a crucial role in renal [...] Read more.
Ferroptosis, as a novel regulable cell death, is characterized by iron overload, glutathione depletion, and an accumulation of lipid peroxides. Recently, it has been discovered that ferroptosis is involved in ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) and plays a crucial role in renal tubular cell death. In this study, we tried to investigate the effect and mechanism of liproxstatin-1 (Lip-1) in I/R-induced AKI and seek the key regulator of ferroptosis in I/R-induced AKI. Mice were administrated with clamping bilateral renal pedicles for 30 min. We found that early growth response 1 (EGR1) might be a key regulator of ferroptosis, and Lip-1 could suppress ferroptosis via EGR1. Meanwhile, Lip-1 could reduce macrophage recruitment and the release of inflammatory cytokines. These findings indicated that Lip-1 alleviated I/R-induced AKI via regulating EGR1, and it might pave the theoretical basis of a new therapeutic strategy for I/R-induced AKI. Full article
(This article belongs to the Special Issue Antioxidant System Efficiency in Kidney Diseases)
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Review

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33 pages, 1791 KiB  
Review
Oxidative Stress and Nutritional Antioxidants in Renal Diseases: A Narrative Review
by Dorin Dragoș, Iulia I. Enache and Maria M. Manea
Antioxidants 2025, 14(7), 757; https://doi.org/10.3390/antiox14070757 - 20 Jun 2025
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Abstract
Oxidative stress is a key component in the pathogenesis of a broad number of renal disorders, including acute kidney injury, chronic kidney disease, and various types of nephropathies. Moreover, oxidative stress seems to at least partly explain the intricate relationship the kidney has [...] Read more.
Oxidative stress is a key component in the pathogenesis of a broad number of renal disorders, including acute kidney injury, chronic kidney disease, and various types of nephropathies. Moreover, oxidative stress seems to at least partly explain the intricate relationship the kidney has with other pathological entities, for instance with cardiovascular comorbidities. Renal replacement therapies give end-stage renal disease patients a fighting chance; however, even these interventions may carry the risk of enhancing existing oxidative stress. Even if nutritional components are not currently routinely used, many have shown promise in preclinical or even clinical studies and could counter some of the deleterious pathways that oxidative stress sets in place. This narrative review provides an update on how these natural nutrients could be beneficial to renal disease patients, and it also aims to give an incentive to future research in the field. Full article
(This article belongs to the Special Issue Antioxidant System Efficiency in Kidney Diseases)
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