Different glutathione redox status and lipid peroxidation in the cortex and the medulla of the rat kidney subjected to ischemia-reperfusion stress

1993 ◽  
Vol 105 (1) ◽  
pp. 157-163 ◽  
Author(s):  
Rolando Campos ◽  
Francisco Maureira ◽  
Argelia Garrido ◽  
Alfonso Valenzuela
Keyword(s):  
Lipid Peroxidation ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Redox Status ◽  
Glutathione Redox

scholarly journals Diazoxide and Exercise Enhance Muscle Contraction during Obesity by Decreasing ROS Levels, Lipid Peroxidation, and Improving Glutathione Redox Status

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1232
Author(s):  
Mariana Gómez-Barroso ◽  
Koré M. Moreno-Calderón ◽  
Elizabeth Sánchez-Duarte ◽  
Christian Cortés-Rojo ◽  
Alfredo Saavedra-Molina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Muscle Contraction ◽  
Katp Channel ◽  
Metabolic Stress ◽  
Muscular Contraction ◽  
Redox Status ◽  
Glutathione Redox ◽  
Katp Channel Openers

Obesity causes insulin resistance and hyperinsulinemia which causes skeletal muscle dysfunction resulting in a decrease in contraction force and a reduced capacity to avoid fatigue, which overall, causes an increase in oxidative stress. KATP channel openers such as diazoxide and the implementation of exercise protocols have been reported to be actively involved in protecting skeletal muscle against metabolic stress; however, the effects of diazoxide and exercise on muscle contraction and oxidative stress during obesity have not been explored. This study aimed to determine the effect of diazoxide in the contraction of skeletal muscle of obese male Wistar rats (35 mg/kg), and with an exercise protocol (five weeks) and the combination from both. Results showed that the treatment with diazoxide and exercise improved muscular contraction, showing an increase in maximum tension and total tension due to decreased ROS and lipid peroxidation levels and improved glutathione redox state. Therefore, these results suggest that diazoxide and exercise improve muscle function during obesity, possibly through its effects as KATP channel openers.

Lipid Peroxidation and the Expressional Regulation of the Heat-Shock Response during Ischemia-Reperfusion of Rat Kidney

2000 ◽  
Vol 65 (1) ◽  
pp. 32-39 ◽  
Author(s):  
Ziya Akçetin ◽  
Reinhard Pregla ◽  
Alexander Busch ◽  
Guido Kessler ◽  
Hans Heynemann ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Shock Response

scholarly journals Effects of cisplatin on lipid peroxidation and the glutathione redox status in the liver of male rats: The protective role of selenium

2010 ◽  
Vol 62 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Ivana Trbojevic ◽  
Branka Ognjanovic ◽  
Natasa Djordjevic ◽  
Snezana Markovic ◽  
A.S. Stajn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Membrane Lipids ◽  
Redox Status ◽  
Protective Role ◽  
Male Rats ◽  
Albino Rats ◽  
Wistar Albino Rats ◽  
Glutathione Redox

The role of oxidative stress in cisplatin (CP) toxicity and its prevention by pretreatment with selenium (Se) was investigated. Male Wistar albino rats were injected with a single dose of cisplatin (7.5 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.) alone or in combination. The results suggest that CP intoxication induces oxidative stress and alters the glutathione redox status: reduced glutathione (GSH), oxidized glutathione (GSSG) and the GSH/GSSG ratio (GSH RI), resulting in increased lipid peroxidation (LPO) in rat liver. The pretreatment with selenium prior to CP treatment showed a protective effect against the toxic influence of CP on peroxidation of the membrane lipids and an altering of the glutathione redox status in the liver of rats. From our results we conclude that selenium functions as a potent antioxidant and suggest that it can control CP-induced hepatotoxicity in rats.

scholarly journals Mechanisms of Fasting-Mediated Protection against Renal Injury and Fibrosis Development after Ischemic Acute Kidney Injury

Biomolecules ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 404 ◽  
Author(s):  
Pedro Rojas-Morales ◽  
Edilia Tapia ◽  
Juan Carlos León-Contreras ◽  
Susana González-Reyes ◽  
Angélica Saraí Jiménez-Osorio ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Reperfusion Injury ◽  
Renal Fibrosis ◽  
Ischemia Reperfusion Injury ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Chronic Phase ◽  
Kidney Injury ◽  
Redox Status ◽  
Extracellular Signal

Ischemia-reperfusion injury of the kidney may lead to renal fibrosis through a combination of several mechanisms. We recently demonstrated that fasting protects the rat kidney against oxidative stress and mitochondrial dysfunction in early acute kidney injury, and also against fibrosis development. Here we show that preoperative fasting preserves redox status and mitochondrial homeostasis at the chronic phase of damage after severe ischemia. Also, the protective effect of fasting coincides with the suppression of inflammation and endoplasmic reticulum stress, as well as the down-regulation of the mechanistic target of rapamycin (mTOR) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways in the fibrotic kidney. Our results demonstrate that fasting targets multiple pathophysiological mechanisms to prevent renal fibrosis and damage that results after renal ischemia-reperfusion injury.

Evidence for only a moderate lipid peroxidation during ischemia-reperfusion of rat kidney due to its high antioxidative capacity

1999 ◽  
Vol 27 (4) ◽  
pp. 280-284 ◽  
Author(s):  
Ziya Akçetin ◽  
Alexander Busch ◽  
Guido Kessler ◽  
Hans Heynemann ◽  
Jürgen Holtz ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Antioxidative Capacity

scholarly journals Dynamics of hyaluronan, CD44, and inflammatory cells in the rat kidney after ischemia/reperfusion injury

2006 ◽  
Author(s):  
Anne-Emilie Declèves ◽  
Nathalie Caron ◽  
Denis Nonclercq ◽  
Alexandre Legrand ◽  
Gérard Toubeau ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Inflammatory Cells

scholarly journals Antioxidant Synergy of Mitochondrial Phospholipase PNPLA8/iPLA2γ with Fatty Acid–Conducting SLC25 Gene Family Transporters

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 678
Author(s):  
Martin Jabůrek ◽  
Pavla Průchová ◽  
Blanka Holendová ◽  
Alexander Galkin ◽  
Petr Ježek
Keyword(s):  
Lipid Peroxidation ◽  
Unsaturated Fatty Acids ◽  
Second Messengers ◽  
Redox Status ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Carrier ◽  
Mitochondrial Superoxide ◽  
Redox Activation ◽  
Mitochondrial Carrier Family ◽  
Alternatively Activated

Patatin-like phospholipase domain-containing protein PNPLA8, also termed Ca2+-independent phospholipase A2γ (iPLA2γ), is addressed to the mitochondrial matrix (or peroxisomes), where it may manifest its unique activity to cleave phospholipid side-chains from both sn-1 and sn-2 positions, consequently releasing either saturated or unsaturated fatty acids (FAs), including oxidized FAs. Moreover, iPLA2γ is directly stimulated by H2O2 and, hence, is activated by redox signaling or oxidative stress. This redox activation permits the antioxidant synergy with mitochondrial uncoupling proteins (UCPs) or other SLC25 mitochondrial carrier family members by FA-mediated protonophoretic activity, termed mild uncoupling, that leads to diminishing of mitochondrial superoxide formation. This mechanism allows for the maintenance of the steady-state redox status of the cell. Besides the antioxidant role, we review the relations of iPLA2γ to lipid peroxidation since iPLA2γ is alternatively activated by cardiolipin hydroperoxides and hypothetically by structural alterations of lipid bilayer due to lipid peroxidation. Other iPLA2γ roles include the remodeling of mitochondrial (or peroxisomal) membranes and the generation of specific lipid second messengers. Thus, for example, during FA β-oxidation in pancreatic β-cells, H2O2-activated iPLA2γ supplies the GPR40 metabotropic FA receptor to amplify FA-stimulated insulin secretion. Cytoprotective roles of iPLA2γ in the heart and brain are also discussed.

scholarly journals Kaempferol Ameliorates Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Ferroptosis by Activating Nrf2/SLC7A11/GPX4 Axis

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 923
Author(s):  
Yuan Yuan ◽  
Yanyu Zhai ◽  
Jingjiong Chen ◽  
Xiaofeng Xu ◽  
Hongmei Wang
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Antioxidant Capacity ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Related Factor ◽  
Protective Effects

Kaempferol has been shown to protect cells against cerebral ischemia/reperfusion injury through inhibition of apoptosis. In the present study, we sought to investigate whether ferroptosis is involved in the oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal injury and the effects of kaempferol on ferroptosis in OGD/R-treated neurons. Western blot, immunofluorescence, and transmission electron microscopy were used to analyze ferroptosis, whereas cell death was detected using lactate dehydrogenase (LDH) release. We found that OGD/R attenuated SLC7A11 and glutathione peroxidase 4 (GPX4) levels as well as decreased endogenous antioxidants including nicotinamide adenine dinucleotide phosphate (NADPH), glutathione (GSH), and superoxide dismutase (SOD) in neurons. Notably, OGD/R enhanced the accumulation of lipid peroxidation, leading to the induction of ferroptosis in neurons. However, kaempferol activated nuclear factor-E2-related factor 2 (Nrf2)/SLC7A11/GPX4 signaling, augmented antioxidant capacity, and suppressed the accumulation of lipid peroxidation in OGD/R-treated neurons. Furthermore, kaempferol significantly reversed OGD/R-induced ferroptosis. Nevertheless, inhibition of Nrf2 by ML385 blocked the protective effects of kaempferol on antioxidant capacity, lipid peroxidation, and ferroptosis in OGD/R-treated neurons. These results suggest that ferroptosis may be a significant cause of cell death associated with OGD/R. Kaempferol provides protection from OGD/R-induced ferroptosis partly by activating Nrf2/SLC7A11/GPX4 signaling pathway.

Sign in / Sign up

Export Citation Format

Share Document