Heterogenous effect of flavonoids on K+ loss and lipid peroxidation induced by oxygen-free radicals in human red cells

1986 ◽  
Vol 18 (1) ◽  
pp. 61-72 ◽  
Author(s):  
I. Maridonneau-Parini ◽  
P. Braquet ◽  
R.P. Garay
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Red Cells ◽  
Human Red Cells

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.

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

scholarly journals Neutrophils mediate lipid peroxidation in human red cells

Blood ◽  
1984 ◽  
Vol 64 (5) ◽  
pp. 1079-1084 ◽  
Author(s):  
S Claster ◽  
DT Chiu ◽  
A Quintanilha ◽  
B Lubin
Keyword(s):  
Lipid Peroxidation ◽  
Red Cells ◽  
Red Cell ◽  
Normal Cells ◽  
Sickle Cells ◽  
Induce Lipid Peroxidation ◽  
Activated Neutrophils ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Human Red Cells

Abstract Activated neutrophils (ANs) are known to release reactive oxygen species that may cause oxidative damage to surrounding tissues. We determined if ANs could induce lipid peroxidation (LP) in human red cells and investigated the mechanism involved in this interaction. We studied neonatal glucose-6-phosphate dehydrogenase (G6PD) deficient, and sickle red cells, since each of these are known to be susceptible to oxidant injury. Neutrophils were isolated from whole blood and activated by incubation with opsonized zymosan. Mixtures of such neutrophils and red cells at a ratio of 1:100 were incubated for two hours at 37 degrees C, after which the malonyldialdehyde content in red cells was measured as an index of LP. All red cells underwent LP after AN treatment, and the degree of LP was proportional to the amount of AN in the mixture. Superoxide dismutase and catalase partially inhibited LP. When compared to normal red cells, only sickle cells demonstrated a significant increase in AN-mediated LP. Conversion of hemoglobin to carboxy-hemoglobin increased AN-mediated LP, whereas conversion to met- hemoglobin decreased AN-mediated LP. The protective effect of met- hemoglobin on LP was less in sickle cells than in normal cells. We conclude that AN can induce LP in red cells in vitro and that sickle cells are more susceptible to this process than normal cells. Hemoglobin can serve as an electron trap and protect the cell against peroxidative damage, but this mechanism is impaired in sickle cells. We speculate that the pathogenesis of hemolysis associated with infectious disease may include AN-induced red cell LP.

Effect of reactive oxygen species on the erythrocyte calcium-pump function in protein-energy malnutrition

1992 ◽  
Vol 12 (6) ◽  
pp. 433-443 ◽  
Author(s):  
W. G. Okunade ◽  
O. O. Olorunsogo
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Reactive Oxygen ◽  
Heme Iron ◽  
Calcium Pump ◽  
Oxygen Species ◽  
Non Heme Iron ◽  
Normal Individuals

The presence of detectagle amounts of non-heme iron in erythrocyte ghost membranes have been postulated to lead to the initiation of membrane lipid peroxidation and the attendant perturbation of membrane functions. We have investigated the presence of non-heme iron and endogenous products of lipid peroxidation in erythrocyte membranes of normal and kwashiorkor (KWA) subjects and assessed the susceptibility of the membranes to exogenously generated reactive oxygen species. The modulation of the basal and calmodulin-stimulated calcium-pumping activity of these membranes by reactive oxygen species was also assessed. The results show the presence of significant amounts of non-heme iron and endogenous free radical reaction products in the red cell membranes of KWA subjects compared with that of normal children. Estimation of the extent of lipid peroxidation in the presence of exogenously generated reactive oxygen species further revealed that erythrocyte ghost membranes of KWA subjects are more susceptible to oxidative stress than those of normal individuals. Although both the basal and calmodulin-stimulated activities of the membrane-bound Ca2+-pump enzyme in normal and KWA subjects were inhibited by oxygen-free radicals, the erythrocyte enzyme in KWA subjects showed higher susceptibility to inhibition by oxygen free radicals than that of normal individuals. We propose that the reduced erythrocyte calcium-pump function in KWA is not unconnected with excessive generation of reactive oxygen species.

Biochemical evidence for free radicalinduced lipid peroxidation as a mechanism for subchronic toxicity of malathion in blood and liver of rats

2003 ◽  
Vol 22 (4) ◽  
pp. 205-211 ◽  
Author(s):  
Maryam Akhgari ◽  
Mohammad Abdollahi ◽  
Abbas Kebryaeezadeh ◽  
Ruhollah Hosseini ◽  
Omid Sabzevari
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Organophosphorus Compounds ◽  
Liver Lipid ◽  
Subchronic Toxicity ◽  
Male Wistar Rats ◽  
Liver Lipid Peroxidation ◽  
Different Doses

Organophosphorus compounds may induce oxidative stress leading to generation of free radicals and alterations in antioxidant and scavengers of oxygen free radicals (OFRs). The effect of subchronic exposure to malathion in the production of oxidative stress was evaluated in male Wistar rats. Administration of malathion (100, 316, 1000, 1500 ppm) for 4 weeks increased catalase (CAT), superoxide dismutase (SOD) activities as well as malondialdehyde (MDA) concentration in red blood cells (RBC) and liver. However, acetylcholinesterase (AChE) and cholinesterase (ChE) activities were decreased in these samples. The increase in RBC and liver lipid peroxidation correlated well with the inhibition in RBC AChE and liver ChE activities. Elevation of MDA concentrations and increased activities of CAT and SOD showed significant correlations in both RBC and liver samples when different doses of malathion were used. The results of the present study suggest the usefulness of RBC AChE measurement as a good biomarker in the estimation of malathion-induced oxidative stress affecting blood and liver.

scholarly journals Na+,K(+)-ATPase activity of rabbit kidney cortex membranes in ischemia and reperfusion.

1993 ◽  
Vol 40 (4) ◽  
pp. 545-547 ◽  
Author(s):  
S Aydin ◽  
A Aricioglu ◽  
N Turkozkan ◽  
F Bingol ◽  
C Aydin
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Atpase Activity ◽  
Microsomal Fraction ◽  
Oxygen Free Radicals ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Ischemia And Reperfusion ◽  
Enzymatic Function ◽  
Irreversible Impairment

The activity of Na+,K(+)-ATPase in the microsomal fraction of rabbit kidney cortex was strongly decreased by ischemia and increased slightly, but not significantly, after reperfusion. These changes were correlated with a dramatic increase in lipid peroxidation in microsomes isolated from both ischemic and reperfused kidneys. This correlation may point to irreversible impairment of the enzymatic function under the influence of either oxygen free radicals or lipid peroxidation.

scholarly journals 385 Honey Dew Fruit Senescence is Regulated by Polyamine Inhibition of Lipid Peroxidation

HortScience ◽  
1999 ◽  
Vol 34 (3) ◽  
pp. 510C-510
Author(s):  
Gene Lester
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Phospholipase D ◽  
Cucumis Melo ◽  
Oxygen Free Radicals ◽  
Phospholipid Content ◽  
Total Chlorophyll ◽  
Direct Inhibition ◽  
Activated Oxygen ◽  
Membrane Peroxidation

Polyamines are effective scavengers of activated oxygen free radicals produced by lipoxygenase (LOX) and phospholipase-D (PL-D). Activated oxygen free radicals cause peroxidative damage to membranes and hasten senescence. Exogenous polyamine spermidine (SPD) compared to spermine (SPM) at 1 mM or no polyamine was an effective inhibitor of honey dew (Cucumis melo L. var. inodorus) membrane peroxidation, as determined by malondialdehyde (MDA), following dark incubation for 6 or 48 hours of fully abscised fruit hypodermal mesocarp tissue. MDA levels in SPD-treated tissue was lowest in both 6 and 48 hours compared to SPM or no polyamine. SPD was effective in slowing lipid peroxidation as MDA was highly negatively correlated with the loss in total chlorophyll, plasma membrane H+ pumping ATPase activity, and microsomal phospholipid content (r = -0.89, -0.64 and -0.57, respectively). Both LOX and PL-D enzyme activities were not correlated with the total chlorophyll and microsomal membrane phospholipid losses or MDA levels, demonstrating that these enzymes act indirectly in the degradation of membranes through the production of lipid peroxidating free radicals. The results also demonstrate that the effect of polyamines as anti-senescence compounds is through direct inhibition of lipid peroxidation and not by affecting LOX or PL-D free radicle production.

Sign in / Sign up

Export Citation Format

Share Document