Enzyme-Generated Free Radicals as Initiators of Lipid Peroxidation in Biological Membranes

1976 ◽  
pp. 239-256 ◽  
Author(s):  
Paul B. McCay ◽  
J. Lee Poyer
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Biological Membranes

Phenolic constituents and inhibitory effects of the leaf of Rauvolfia vomitoria Afzel on free radicals, cholinergic and monoaminergic enzymes in rat’s brain in vitro

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Olubukola H. Oyeniran ◽  
Adedayo O. Ademiluyi ◽  
Ganiyu Oboh
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Methanolic Extract ◽  
Array Detector ◽  
Oh Radicals ◽  
Inhibitory Effects ◽  
Methanolic Extracts ◽  
Phenolic Constituents ◽  
Rauvolfia Vomitoria

AbstractObjectivesRauvolfia vomitoria is a medicinal plant used traditionally in Africa in the management of several human diseases including psychosis. However, there is inadequate scientific information on the potency of the phenolic constituents of R. vomitoria leaf in the management of neurodegeneration. Therefore, this study characterized the phenolic constituents and investigated the effects of aqueous and methanolic extracts of R. vomitoria leaf on free radicals, Fe2+-induced lipid peroxidation, and critical enzymes linked to neurodegeneration in rat’s brain in vitro.MethodsThe polyphenols were evaluated by characterizing phenolic constituents using high-performance liquid chromatography coupled with diode array detector (HPLC-DAD). The antioxidant properties were assessed through the extracts ability to reduce Fe3+ to Fe2+; inhibit ABTS, DPPH, and OH radicals and Fe2+-induced lipid peroxidation. The effects of the extracts on AChE and MAO were also evaluated.ResultsThe phenolic characterization of R. vomitoria leaf revealed that there were more flavonoids present. Both aqueous and methanolic extracts of R. vomitoria leaf had inhibitory effects with the methanolic extract having higher significant (p≤0.05) free radicals scavenging ability coupled with inhibition of monoamine oxidases. However, there was no significant (p≤0.05) difference obtained in the inhibition of lipid peroxidation and cholinesterases.ConclusionThis study suggests that the rich phenolic constituents of R. vomitoria leaf might contribute to the observed antioxidative and neuroprotective effects. The methanolic extract was more potent than the aqueous extract; therefore, extraction of R. vomitoria leaf with methanol could offer better health-promoting effects in neurodegenerative condition.

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 Malondialdehyde levels can be measured in serum and saliva by using a fast HPLC method with visible detection / Determinarea printr-o metodă HPLC-VIS rapidă a concentraţiilor serice şi salivare ale malondialdehidei

2016 ◽  
Vol 24 (3) ◽  
pp. 319-326 ◽  
Author(s):  
Erzsébet Fogarasi ◽  
Mircea Dumitru Croitoru ◽  
Ibolya Fülöp ◽  
Enikő Nemes-Nagy ◽  
Robert Gabriel Tripon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Unsaturated Fatty Acids ◽  
Pearson Correlation ◽  
Living Organism ◽  
Hplc Method ◽  
Limit Of Quantification ◽  
Pearson Correlation Test ◽  
Repeated Sample

Abstract Oxidative stress appears when the amount of free radicals that are formed in a living organism exceed its spin-trapping ability. One of the most dangerous free radicals that are formed in the human body is the hydroxyl radical. It can alter several biomolecules, including the unsaturated fatty acids; this process is known as lipid peroxidation and can lead to cell necrosis and generation of several harmful byproducts including malondialdehyde, which serves also as a biomarker of oxidative stress. A new HPLC method with visible detection was developed for the detection of malondialdehyde in human serum and saliva samples. The method was verified in terms of specificity, linearity, limits of detection (0.35 ng/ml), limit of quantification (1.19 ng/ml), recovery (90.13±10.25 – 107.29±14.33) and precision (3.84±1.49% – 6.66±1.76%). An analysis time of only 1 minute was obtained and no interferences from the matrices were observed. Statistical analysis (Pearson correlation test) showed a moderate correlation (R = 0.5061, p = 0.0099) between serum and saliva concentrations (N = 25). The possibility of measuring salivary concentrations of malondialdehyde extents the applications of oxidative stress/lipid peroxidation estimations to categories of population unreachable before (pregnant women, small children, etc); repeated sample studies are also easier to make.

Manganese neurotoxicity: a model for free radical mediated neurodegeneration?

1982 ◽  
Vol 60 (11) ◽  
pp. 1398-1405 ◽  
Author(s):  
John Donaldson ◽  
Duncan McGregor ◽  
Frank LaBella
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Neuropsychiatric Symptoms ◽  
Brain Regions ◽  
Neonatal Rats ◽  
Manganese Neurotoxicity ◽  
Neuronal Homeostasis ◽  
Significant Depression ◽  
Disease Study ◽  
Bizarre Behavior

In man, manganese neurointoxication is characterised in the early phase by bizarre behavior reminiscent of that observed in schizophrenia. During chronic manganese intoxication the neuropsychiatric symptoms manifested earlier disappear and are followed by a permanent neurological phase typified by extrapyramidal symptoms similar to those of Parkinson's disease. Study of manganese intoxication in animals may provide important clues towards elucidation of the biochemical defect underlying neuropsychiatric as well as extrapyramidal diseases. Investigations in our laboratory suggest that neurotoxicity of manganese is an exaggeration of function in normal neuronal homeostasis. Manganese neurointoxication in neonatal rats resulted in significant depression of lipid peroxidation in several rat brain regions examined. In the striatum, lipid peroxidative activity was abolished, an effect which may be related to alteration in neurotransmitters often observed in the striatum of manganese-treated rats. The chronic, extrapyramidal stage of manganism, may ensue when excess Mn2+ is oxidised to higher valency forms where it can potentiate the autoxidation of catecholamines, like dopamine, resulting in concomitant formation of free radicals and cytotoxic quinones. This latter effect may arise preferentially in the substantia nigra, where neuromelanin is formed nonenzymatically by autoxidation of dopamine.

Role of Free Radicals and Lipid Peroxidation in Gastric Mucosal Injury Induced by Ischemia-Reperfusion in Rats

1989 ◽  
Vol 24 (sup162) ◽  
pp. 55-58 ◽  
Author(s):  
S. Ueda ◽  
T. Yoshikawa ◽  
S. Takahashi ◽  
H. Ichikawa ◽  
M. Yasuda ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury

Free Radicals and Lipid Peroxidation in Liver of Rats Kept on a Diet Devoid of Choline

1989 ◽  
Vol 7 (3-6) ◽  
pp. 233-240 ◽  
Author(s):  
S. Banni ◽  
F. P. Corongiu ◽  
M. A. Dessi ◽  
A. Iannone ◽  
B. Lombardi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals

Oxygen free radical-mediated selective endothelial dysfunction in isolated coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. H806-H812 ◽  
Author(s):  
K. Todoki ◽  
E. Okabe ◽  
T. Kiyose ◽  
T. Sekishita ◽  
H. Ito
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Free Radical ◽  
Coronary Artery ◽  
Iron Chelator ◽  
Oxygen Free Radical ◽  
Alpha Tocopherol ◽  
Endothelium Dependent Relaxation ◽  
Iron Chelator Deferoxamine

To understand the direct involvement of free radicals causing reduction in endothelium-dependent relaxation of isolated canine coronary ring preparations, this study was undertaken to examine the effect of free radicals generated from dihydroxy fumarate (DHF) plus Fe(3+)-ADP or from H2O2 plus FeSO4. The vasodilators (acetylcholine, bradykinin, A23187, and nitroglycerin) were given after DHF/Fe(3+)-ADP or H2O2/FeSO4 was removed from the organ chamber. The earlier DHF/Fe(3+)-ADP exposure produced an attenuation of the relaxation of the rings induced by acetylcholine, bradykinin, or A23187 but not of the relaxation induced by nitroglycerin. The observed effect of previous DHF/Fe(3+)-ADP exposure was significantly protected in the vessels isolated from the dogs treated with alpha-tocopherol. In the experiments for assessing the effect of various scavengers, 1O2 scavenger histidine or iron chelator deferoxamine effectively protected the attenuation induced by DHF/Fe(3+)-ADP exposure of the relaxation elicited by acetylcholine; superoxide dismutase (SOD), catalase, or dimethyl sulfoxide (DMSO) had no effect on this system. Furthermore, the relaxation elicited by acetylcholine, but not nitroglycerin, was significantly attenuated by the earlier exposure to .OH generated by Fenton's reagent (H2O2+FeSO4); the attenuation was significantly protected by DMSO. These results are consistent with the view that .OH, 1O2, and/or iron-dependent reactive species selectively damage endothelium-dependent relaxation as opposed to endothelium-independent relaxation in endothelium-intact coronary ring preparations. It is also postulated that lipid peroxidation may be responsible for this effect.

scholarly journals Oxidative stress in ageing

2017 ◽  
Vol 5 (11) ◽  
pp. 4826 ◽  
Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Free Radical ◽  
Age Groups ◽  
The Body ◽  
Antioxidant Systems ◽  
Lipid Peroxidation Product ◽  
Free Radical Theory ◽  
Radical Theory

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.

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