Thymoquinone attenuates oxidative stress of kidney mitochondria and exerts nephroprotective effects in oxonic acid‐induced hyperuricemia rats

BioFactors ◽  
2020 ◽  
Vol 46 (2) ◽  
pp. 292-300 ◽  
Author(s):  
Ayed A. Dera ◽  
Prasanna Rajagopalan ◽  
Mohammad A. Alfhili ◽  
Irfan Ahmed ◽  
Harish C Chandramoorthy
Keyword(s):  
Oxidative Stress ◽  
Kidney Mitochondria ◽  
Oxonic Acid

Carvedilol protects against cisplatin-induced oxidative stress, redox state unbalance and apoptosis in rat kidney mitochondria

2011 ◽  
Vol 189 (1-2) ◽  
pp. 45-51 ◽  
Author(s):  
M.A. Carvalho Rodrigues ◽  
J.L. Rodrigues ◽  
N.M. Martins ◽  
F. Barbosa ◽  
C. Curti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox State ◽  
Rat Kidney ◽  
Kidney Mitochondria

scholarly journals Role of oxidative stress in the renal abnormalities induced by experimental hyperuricemia

2008 ◽  
Vol 295 (4) ◽  
pp. F1134-F1141 ◽  
Author(s):  
Laura G. Sánchez-Lozada ◽  
Virgilia Soto ◽  
Edilia Tapia ◽  
Carmen Avila-Casado ◽  
Yuri Y. Sautin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Uric Acid ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Systemic Hypertension ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Renal Abnormalities ◽  
Oxonic Acid

Endothelial dysfunction is a characteristic feature during the renal damage induced by mild hyperuricemia. The mechanism by which uric acid reduces the bioavailability of intrarenal nitric oxide is not known. We tested the hypothesis that oxidative stress might contribute to the endothelial dysfunction and glomerular hemodynamic changes that occur with hyperuricemia. Hyperuricemia was induced in Sprague-Dawley rats by administration of the uricase inhibitor, oxonic acid (750 mg/kg per day). The superoxide scavenger, tempol (15 mg/kg per day), or placebo was administered simultaneously with the oxonic acid. All groups were evaluated throughout a 5-wk period. Kidneys were fixed by perfusion and afferent arteriole morphology, and tubulointerstitial 3-nitrotyrosine, 4-hydroxynonenal, NOX-4 subunit of renal NADPH-oxidase, and angiotensin II were quantified. Hyperuricemia induced intrarenal oxidative stress, increased expression of NOX-4 and angiotensin II, and decreased nitric oxide bioavailability, systemic hypertension, renal vasoconstriction, and afferent arteriolopathy. Tempol treatment reversed the systemic and renal alterations induced by hyperuricemia despite equivalent hyperuricemia. Moreover, because tempol prevented the development of preglomerular damage and decreased blood pressure, glomerular pressure was maintained at normal values as well. Mild hyperuricemia induced by uricase inhibition causes intrarenal oxidative stress, which contributes to the development of the systemic hypertension and the renal abnormalities induced by increased uric acid. Scavenging of the superoxide anion in this setting attenuates the adverse effects induced by hyperuricemia.

Effects of dietary iron restriction on kidney mitochondria function and oxidative stress in streptozotocin-diabetic rats

Mitochondrion ◽  
2020 ◽  
Vol 54 ◽  
pp. 41-48
Author(s):  
Donovan J. Peña-Montes ◽  
Maribel Huerta-Cervantes ◽  
Mónica Ríos-Silva ◽  
Xóchitl Trujillo ◽  
Christian Cortés-Rojo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats ◽  
Dietary Iron ◽  
Kidney Mitochondria ◽  
Iron Restriction ◽  
Streptozotocin Diabetic Rats ◽  
And Oxidative Stress

scholarly journals Damaging Effects of Bisphenol A on the Kidney and the Protection by Melatonin: Emerging Evidences from In Vivo and In Vitro Studies

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Anongporn Kobroob ◽  
Wachirasek Peerapanyasut ◽  
Nipon Chattipakorn ◽  
Orawan Wongmekiat
Keyword(s):  
Oxidative Stress ◽  
Bisphenol A ◽  
Mitochondrial Function ◽  
Dependent Manner ◽  
Redox Equilibrium ◽  
Membrane Potential Change ◽  
Kidney Mitochondria ◽  
Dose Dependent

This study investigates the effects of bisphenol A (BPA) contamination on the kidney and the possible protection by melatonin in experimental rats and isolated mitochondrial models. Rats exposed to BPA (50, 100, and 150 mg/kg, i.p.) for 5 weeks demonstrated renal damages as evident by increased serum urea and creatinine and decreased creatinine clearance, together with the presence of proteinuria and glomerular injuries in a dose-dependent manner. These changes were associated with increased lipid peroxidation and decreased antioxidant glutathione and superoxide dismutase. Mitochondrial dysfunction was also evident as indicated by increased reactive oxygen species production, decreased membrane potential change, and mitochondrial swelling. Coadministration of melatonin resulted in the reversal of all the changes caused by BPA. Studies using isolated mitochondria showed that BPA incubation produced dose-dependent impairment in mitochondrial function. Preincubation with melatonin was able to sustain mitochondrial function and architecture and decreases oxidative stress upon exposure to BPA. The findings indicated that BPA is capable of acting directly on the kidney mitochondria, causing mitochondrial oxidative stress, dysfunction, and subsequently, leading to whole organ damage. Emerging evidence further suggests the protective benefits of melatonin against BPA nephrotoxicity, which may be mediated, in part, by its ability to diminish oxidative stress and maintain redox equilibrium within the mitochondria.

Dietary avocado oil supplementation attenuates the alterations induced by type I diabetes and oxidative stress in electron transfer at the complex II-complex III segment of the electron transport chain in rat kidney mitochondria

2013 ◽  
Vol 45 (3) ◽  
pp. 271-287 ◽  
Author(s):  
Omar Ortiz-Avila ◽  
Carlos Alberto Sámano-García ◽  
Elizabeth Calderón-Cortés ◽  
Ismael H. Pérez-Hernández ◽  
Ricardo Mejía-Zepeda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Electron Transport Chain ◽  
Type I Diabetes ◽  
Rat Kidney ◽  
Complex Iii ◽  
Type I ◽  
Kidney Mitochondria ◽  
Avocado Oil ◽  
Transport Chain ◽  
And Oxidative Stress

The Nephroprotective Role of Carnosine Against Ifosfamide-Induced Renal Injury and Electrolytes Imbalance is Mediated Via the Regulation of Mitochondrial Function and Alleviation of Oxidative Stress

Drug Research ◽  
2019 ◽  
Vol 70 (01) ◽  
pp. 49-56 ◽  
Author(s):  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Vahid Ghanbarinejad ◽  
Hamid Reza Mohammadi ◽  
Mousavi Khadijeh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Renal Injury ◽  
Elevated Serum ◽  
Renal Tissue ◽  
Experimental Models ◽  
Kidney Mitochondria ◽  
Urine Biomarkers ◽  
Markers Of Oxidative Stress

Abstract Background Ifosfamide (IFO) is an alkylating agent administered against different types of malignancies. Several cases of renal injury and serum electrolytes disturbances have been reported in IFO-treated patients. Oxidative stress and mitochondrial dysfunction are suspected of being involved in the mechanism of IFO nephrotoxicity. Carnosine is a dipeptide which its antioxidant and mitochondria protecting properties have been mentioned in different experimental models. The current study aimed to evaluate the nephroprotective properties of carnosine against IFO-induced renal injury. Methods Rats were treated with IFO (50 mg/kg, i.p) alone or in combination with carnosine. Serum and urine biomarkers of renal injury in addition to kidney markers of oxidative stress were evaluated. Moreover, kidney mitochondria were isolated, and some mitochondrial indices were assessed. Results Elevated serum creatinine and BUN, hypokalemia, and hypophosphatemia, in addition, to an increase in urine glucose, protein, γ-GT, and alkaline phosphatase (ALP), were evident in IFO-treated animals. IFO also caused an increase in kidney reactive oxygen species (ROS) and lipid peroxidation (LPO). Renal GSH levels and antioxidant capacity were also depleted with IFO therapy. Mitochondrial dehydrogenase activity, GSH level, membrane potential, and ATP content were decreased while mitochondrial LPO and permeabilization were increased in IFO group. Carnosine (250 and 500 mg/kg, i.p) mitigated IFO-induced oxidative stress and mitochondrial impairment in renal tissue. Conclusion Our data suggest mitochondrial dysfunction and oxidative stress as fundamental mechanisms of renal injury induced by IFO. On the other hand, carnosine supplementation protected kidneys against IFO-induced injury through regulating mitochondrial function and mitigating oxidative stress.

Cisplatin-induced nephrotoxicity is associated with oxidative stress, redox state unbalance, impairment of energetic metabolism and apoptosis in rat kidney mitochondria

2007 ◽  
Vol 81 (7) ◽  
pp. 495-504 ◽  
Author(s):  
N. A. G. Santos ◽  
C. S. Catão ◽  
N. M. Martins ◽  
C. Curti ◽  
M. L. P. Bianchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox State ◽  
Rat Kidney ◽  
Energetic Metabolism ◽  
Kidney Mitochondria

Apigenin ameliorates oxidative stress and mitochondrial damage induced by multiwall carbon nanotubes in rat kidney mitochondria

2021 ◽  
Author(s):  
Fatemeh Zamani ◽  
Fatemeh Samiei ◽  
Zahra Mousavi ◽  
Mansour Rezazadeh Azari ◽  
Enayatollah Seydi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Nanotubes ◽  
Rat Kidney ◽  
Multiwall Carbon Nanotubes ◽  
Mitochondrial Damage ◽  
Kidney Mitochondria ◽  
Multiwall Carbon

Studies on Hg(II)-induced H2O2 formation and oxidative stress in vivo and in vitro in rat kidney mitochondria

1993 ◽  
Vol 45 (10) ◽  
pp. 2017-2024 ◽  
Author(s):  
Bert-Ove Lund ◽  
Dennis M. Miller ◽  
James S. Woods
Keyword(s):  
Oxidative Stress ◽  
Rat Kidney ◽  
Kidney Mitochondria ◽  
H2o2 Formation ◽  
And Oxidative Stress
Sign in / Sign up

Export Citation Format

Share Document