Ethane production as a measure of lipid peroxidation after renal ischemia

1986 ◽  
Vol 251 (5) ◽  
pp. F839-F843 ◽  
Author(s):  
M. S. Paller ◽  
R. P. Hebbel
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Superoxide Radical ◽  
Oxygen Free Radicals ◽  
Tissue Injury ◽  
Renal Ischemia ◽  
Radical Scavenger ◽  
Base Line ◽  
Ethane Production

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.

scholarly journals Pharmacological Effects of Salvianolic Acid B Against Oxidative Damage

2020 ◽  
Vol 11 ◽  
Author(s):  
Zhun Xiao ◽  
Wei Liu ◽  
Yong-ping Mu ◽  
Hua Zhang ◽  
Xiao-ning Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Free Radicals ◽  
Clinical Application ◽  
Oxygen Free Radicals ◽  
Salvianolic Acid B ◽  
Related Factor ◽  
Pharmacological Effects ◽  
Hydrogen Atoms ◽  
Salvianolic Acid

Salvianolic acid B (Sal B) is one of the main active ingredients of Salvia miltiorrhiza, with strong antioxidant effects. Recent findings have shown that Sal B has anti-inflammatory, anti-apoptotic, anti-fibrotic effects and can promote stem cell proliferation and differentiation, and has a beneficial effect on cardiovascular and cerebrovascular diseases, aging, and liver fibrosis. Reactive oxygen species (ROS) include oxygen free radicals and oxygen-containing non-free radicals. ROS can regulate cell proliferation, survival, death and differentiation to regulate inflammation, and immunity, while Sal B can scavenge oxygen free radicals by providing hydrogen atoms and reduce the production of oxygen free radicals and oxygen-containing non-radicals by regulating the expression of antioxidant enzymes. The many pharmacological effects of Sal B may be closely related to its elimination and inhibition of ROS generation, and Nuclear factor E2-related factor 2/Kelch-like ECH-related protein 1 may be the core link in its regulation of the expression of antioxidant enzyme to exert its antioxidant effect. What is confusing and interesting is that Sal B exhibits the opposite mechanisms in tumors. To clarify the specific target of Sal B and the correlation between its regulation of oxidative stress and energy metabolism homeostasis will help to further understand its role in different pathological conditions, and provide a scientific basis for its further clinical application and new drug development. Although Sal B has broad prospects in clinical application due to its extensive pharmacological effects, the low bioavailability is a serious obstacle to further improving its efficacy in vivo and promoting clinical application. Therefore, how to improve the availability of Sal B in vivo requires the joint efforts of many interdisciplinary subjects.

Effect of Hyperbaric Oxygen Treatment on Nitric Oxide and Oxygen Free Radicals in Rat Brain

2000 ◽  
Vol 83 (4) ◽  
pp. 2022-2029 ◽  
Author(s):  
Ikram M. Elayan ◽  
Milton J. Axley ◽  
Paruchuri V. Prasad ◽  
Stephen T. Ahlers ◽  
Charles R. Auker
Keyword(s):  
Nitric Oxide ◽  
Free Radicals ◽  
Rat Brain ◽  
Hyperbaric Oxygen ◽  
High Pressures ◽  
Oxygen Free Radicals ◽  
In Vivo Microdialysis ◽  
Sprague Dawley ◽  
Fourfold Increase

Oxygen (O2) at high pressures acts as a neurotoxic agent leading to convulsions. The mechanism of this neurotoxicity is not known; however, oxygen free radicals and nitric oxide (NO) have been suggested as contributors. This study was designed to follow the formation of oxygen free radicals and NO in the rat brain under hyperbaric oxygen (HBO) conditions using in vivo microdialysis. Male Sprague-Dawley rats were exposed to 100% O2 at a pressure of 3 atm absolute for 2 h. The formation of 2,3-dihydroxybenzoic acid (2,3-DHBA) as a result of perfusing sodium salicylate was followed as an indicator for the formation of hydroxyl radicals. 2,3-DHBA levels in hippocampal and striatal dialysates of animals exposed to HBO conditions were not significantly different from controls. However, rats treated under the same conditions showed a six- and fourfold increase in nitrite/nitrate, break down products of NO decomposition, in hippocampal and striatal dialysates, respectively. This increase was completely blocked by the nitric oxide synthase (NOS) inhibitor l-nitroarginine methyl ester (l-NAME). Using neuronal NOS, we determined the NOS O2 K m to be 158 ± 28 (SD) mmHg, a value which suggests that production of NO by NOS would increase approximately four- to fivefold under hyperbaric O2 conditions, closely matching the measured increase in vivo. The increase in NO levels may be partially responsible for some of the detrimental effects of HBO conditions.

scholarly journals Activation of BNIP3-mediated mitophagy protects against renal ischemia–reperfusion injury

2019 ◽  
Vol 10 (9) ◽  
Author(s):  
Chengyuan Tang ◽  
Hailong Han ◽  
Zhiwen Liu ◽  
Yuxue Liu ◽  
Lijun Yin ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Glucose Deprivation ◽  
Renal Ischemia ◽  
Renal Tubules ◽  
Renal Tubular Cells

Abstract Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its pathophysiological role in AKI remains unclear. Here, we demonstrated an increase of BNIP3 expression in cultured renal proximal tubular epithelial cells following oxygen-glucose deprivation-reperfusion (OGD-R) and in renal tubules after renal ischemia–reperfusion (IR)-induced injury in mice. Functionally, silencing Bnip3 by specific short hairpin RNAs in cultured renal tubular cells reduced OGD-R-induced mitophagy, and potentiated OGD-R-induced cell death. In vivo, Bnip3 knockout worsened renal IR injury, as manifested by more severe renal dysfunction and tissue injury. We further showed that Bnip3 knockout reduced mitophagy, which resulted in the accumulation of damaged mitochondria, increased production of reactive oxygen species, and enhanced cell death and inflammatory response in kidneys following renal IR. Taken together, these findings suggest that BNIP3-mediated mitophagy has a critical role in mitochondrial quality control and tubular cell survival during AKI.

Depression of heart sarcolemmal Ca2+-pump activity by oxygen free radicals

1989 ◽  
Vol 256 (2) ◽  
pp. H368-H374 ◽  
Author(s):  
M. Kaneko ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Protective Effect ◽  
Oxygen Free Radicals ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Exact Nature ◽  
Dependent Manner ◽  
Membrane Phospholipids ◽  
Generating System

Although oxygen free radicals have been implicated as mediators of cellular injury in myocardial ischemia-reperfusion, the exact nature of defects produced by these radicals is not clear. Because sarcolemmal Ca2+-pump is involved in the efflux of Ca2+ from the cell, this study was undertaken to examine the effects of oxygen free radicals on sarcolemmal ATP-dependent Ca2+ accumulation and Ca2+-stimulated Mg2+-dependent adenosinetriphosphatase (ATPase) activities as well as lipid peroxidation of membrane phospholipids. Isolated rat heart sarcolemmal membranes were incubated with xanthine + xanthine oxidase [a superoxide anion radical (O2-)-generating system], H2O2, or H2O2 + Fe2+ [a hydroxyl radical (HO.)-generating system] and assayed for Ca2+-pump activities. O2- inhibited the Ca2+-pump activities in a time-dependent manner; a significant inhibition of Ca2+-stimulated ATPase activity was seen after 1 min of incubation. Superoxide dismutase showed a protective effect on depression in Ca2+-pump activities caused by O2-.H2O2 inhibited Ca2+-pump activities in a dose-dependent manner; this inhibition was protected by the addition of catalase. HO. depressed the Ca2+-pump activities to a greater extent in comparison with H2O2. Mannitol showed a protective effect on HO.-induced inhibition of Ca2+-pump activities. The promotion of lipid peroxidation by free radicals was evident from increased formation of malondialdehyde. These results indicate that the sarcolemmal membrane is altered on exposure to oxygen free radicals, and this may result in depressing the Ca2+-pump mechanism for Ca2+ efflux from the myocardial cell.

scholarly journals Oxygen free-radicals and lipid peroxidation: inhibition by the protein caeruloplasmin

FEBS Letters ◽  
1980 ◽  
Vol 112 (2) ◽  
pp. 269-272 ◽  
Author(s):  
John M.C. Gutteridge ◽  
Ramsay Richmond ◽  
Barry Halliwell
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Lipid Peroxidation Inhibition
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