DOXORUBICIN FREE RADICAL FORMATION AND LIPID PEROXIDATION IN RAT HEPATOCYTES

1985 ◽  
Vol 37 (S12) ◽  
pp. 20P-20P
Author(s):  
T.J. Lavelle ◽  
J. Basra ◽  
J.R. Brown ◽  
L.H. Patterson
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Rat Hepatocytes ◽  
Radical Formation ◽  
Free Radical Formation

scholarly journals Free radical formation in DNA by lipid peroxidation.

1984 ◽  
Vol 48 (2) ◽  
pp. 571-572 ◽  
Author(s):  
Tsutomu NAKAYAMA ◽  
Masahiko KODAMA ◽  
CHIKAYOSHI NAGATA
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Radical Formation ◽  
Free Radical Formation

scholarly journals Sedentary aging increases resting and exercise-induced intramuscular free radical formation

2010 ◽  
Vol 109 (2) ◽  
pp. 449-456 ◽  
Author(s):  
Damian M. Bailey ◽  
Jane McEneny ◽  
Odile Mathieu-Costello ◽  
Robert R. Henry ◽  
Philip E. James ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Total Protein ◽  
Acute Exercise ◽  
Young Group ◽  
Radical Formation ◽  
Lipid Hydroperoxides ◽  
Free Radical Formation ◽  
Exercise Induced ◽  
The Impact

Mitochondrial free radical formation has been implicated as a potential mechanism underlying degenerative senescence, although human data are lacking. Therefore, the present study was designed to examine if resting and exercise-induced intramuscular free radical-mediated lipid peroxidation is indeed increased across the spectrum of sedentary aging. Biopsies were obtained from the vastus lateralis in six young (26 ± 6 yr) and six aged (71 ± 6 yr) sedentary males at rest and after maximal knee extensor exercise. Aged tissue exhibited greater ( P < 0.05 vs. the young group) electron paramagnetic resonance signal intensity of the mitochondrial ubisemiquinone radical both at rest (+138 ± 62%) and during exercise (+143 ± 40%), and this was further complemented by a greater increase in α-phenyl-tert-butylnitrone adducts identified as a combination of lipid-derived alkoxyl-alkyl radicals (+295 ± 96% and +298 ± 120%). Lipid hydroperoxides were also elevated at rest (0.190 ± 0.169 vs. 0.148 ± 0.071 nmol/mg total protein) and during exercise (0.567 ± 0.259 vs. 0.320 ± 0.263 nmol/mg total protein) despite a more marked depletion of ascorbate and uptake of α/β-carotene, retinol, and lycopene ( P < 0.05 vs. the young group). The impact of senescence was especially apparent when oxidative stress biomarkers were expressed relative to the age-related decline in mitochondrial volume density and absolute power output at maximal exercise. In conclusion, these findings confirm that intramuscular free radical-mediated lipid peroxidation is elevated at rest and during acute exercise in aged humans.

scholarly journals Influence of Acidosis on Lipid Peroxidation in Brain Tissues in vitro

1985 ◽  
Vol 5 (2) ◽  
pp. 253-258 ◽  
Author(s):  
Bo K. Siesjö ◽  
George Bendek ◽  
Tohru Koide ◽  
Eva Westerberg ◽  
Tadeusz Wieloch
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Thiobarbituric Acid ◽  
Protonated Form ◽  
Radical Formation ◽  
Ferrous Ions ◽  
Ph Optimum ◽  
Free Radical Formation ◽  
Brain Tissues

To study the influence of acidosis on free radical formation and lipid peroxidation in brain tissues, homogenates fortified with ferrous ions and, in some experiments, with ascorbic acid were equilibrated with 5–15% O2 at pH values of 7.0, 6.5, 6.0, and 5.0, with subsequent measurements of thiobarbituric acid-reactive (TBAR) material, as well as of water- and lipid-soluble antioxidants (glutathione, ascorbate, and α-tocopherol) and phospholipid-bound fatty acids (FAs). Moderate to marked acidosis (pH 6.5–6.0) was found to grossly exaggerate the formation of TBAR material and the decrease in α-tocopherol content and to enhance degradation of phospholipid-bound, polyenoic FAs. These effects were reversed at pH 5.0, suggesting a pH optimum at pH 6.0–6.5. It is concluded that acidosis of a degree encountered in ischemic brain tissues has the potential of triggering increased free radical formation. This effect may involve increased formation of the protonated form of superoxide radicals, which is strongly prooxidant and lipid soluble, and/or the decompartmentalization of iron bound to cellular macromolecules like ferritin.

Free Radical Formation in DNA by Lipid Peroxidation

1984 ◽  
Vol 48 (2) ◽  
pp. 571-572
Author(s):  
Tsutomu Nakayama, ◽  
Masahiko Kodama ◽  
Chikayoshi Nagata
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Radical Formation ◽  
Free Radical Formation

scholarly journals Effects of creatine supplementation on homocysteine levels and lipid peroxidation in rats

2008 ◽  
Vol 102 (1) ◽  
pp. 110-116 ◽  
Author(s):  
Rafael Deminice ◽  
Guilherme Vannucchi Portari ◽  
Helio Vannucchi ◽  
Alceu Afonso Jordao
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Creatine Supplementation ◽  
Thiobarbituric Acid ◽  
Significant Negative Correlation ◽  
Protective Role ◽  
Radical Formation ◽  
Control Group ◽  
Free Radical Formation ◽  
Plasma Tbars

Hyperhomocysteinaemia is an independent risk factor for CVD. Recent data show a relationship between homocysteine (Hcy) and free radical formation. Since creatine synthesis is responsible for most of the methyl group transfers that result in Hcy formation, creatine supplementation might inhibit Hcy production and reduce free radical formation. The present study investigated the effects of creatine supplementation on Hcy levels and lipid peroxidation biomarkers. Thirty rats were divided into three groups: control group; diet with creatine group (DCr; 2 % creatine in the diet for 28 d); creatine overload plus diet with creatine group (CrO+D; 5 g creatine/kg by oral administration for 5 d+2 % in the diet for 23 d). Plasma Hcy was significantly lower (P < 0·05) in DCr (7·5 (sd1·2) μmol/l) and CrO+D (7·2 (sd1·7) μmol/l) groups compared with the control group (12·4 (sd2·2) μmol/l). Both plasma thiobarbituric acid-reactive species (TBARS) (control, 10 (sd3·4); DCr, 4·9 (sd0·7); CrO+D, 2·4 (sd1) μmol/l) and plasma total glutathione (control, 4·3 (sd1·9); DCr, 2·5 (sd0·8); CrO+D, 1·8 (sd0·5) μmol/l) were lower in the groups that received creatine (P < 0·05). In addition, Hcy showed significant negative correlation (P < 0·05) with plasma creatine (r− 0·61) and positive correlation with plasma TBARS (r0·74). Plasma creatine was negatively correlated with plasma TBARS (r− 0·75) and total peroxide (r− 0·40). We conclude that creatine supplementation reduces plasma Hcy levels and lipid peroxidation biomarkers, suggesting a protective role against oxidative damage. Modulating Hcy formation may, however, influence glutathione synthesis and thereby affect the redox state of the cells.

Pyruvate reduces anoxic injury and free radical formation in perfused rat hepatocytes

1996 ◽  
Vol 270 (3) ◽  
pp. G535-G540 ◽  
Author(s):  
A. B. Borle ◽  
R. T. Stanko
Keyword(s):  
Free Radical ◽  
Protective Action ◽  
Rat Hepatocytes ◽  
Radical Formation ◽  
Antimycin A ◽  
Anoxic Injury ◽  
H2o2 Generation ◽  
H2o2 Formation ◽  
Free Radical Formation ◽  
Ldh Release

The effects of 5 mM pyruvate on anoxic injury, superoxide (O2-.) and hydrogen peroxide (H2O2) generation, and lactate dehydrogenase (LDH) release during reoxygenation after 2.5 h anoxia were studied in perfused rat hepatocytes. When pyruvate was present during anoxia and reoxygenation, there was little anoxic injury, and the generation of free radicals and LDH release during reoxygenation were reduced 50-60%. When Pyruvate was added during reoxygenation, there was no decrease in O2-. or LDH release, although H2O2 formation was depressed. Free radical formation and anoxic/reperfusion injury were significantly reduced when pyruvate was added during the anoxic period only. Pyruvate reduced the deleterious effects of 10 microM antimycin A by preventing the increase in O2-. formation and LDH release evoked by the inhibitor. These results indicate that pyruvate protected hepatocytes against anoxic injury and that its protective action occurred principally during anoxia and not during reoxygenation. Pyruvate appeared to act at a mitochondrial site, since it reduced the deleterious effects of antimycin A.

Oxygen free radical formation by rat hepatocytes during postanoxic reoxygenation: scavenging effect of albumin

1994 ◽  
Vol 266 (3) ◽  
pp. G451-G458 ◽  
Author(s):  
P. Caraceni ◽  
A. Gasbarrini ◽  
D. H. Van Thiel ◽  
A. B. Borle
Keyword(s):  
Free Radical ◽  
Trypan Blue ◽  
Cell Injury ◽  
Rat Hepatocytes ◽  
Radical Formation ◽  
Low Level ◽  
Short Period ◽  
Reoxygenation Injury ◽  
Free Radical Formation ◽  
Ldh Release

Free radical formation and reoxygenation injury were studied in rat hepatocytes perfused with Krebs-Henseleit bicarbonate buffer containing 1% or no albumin. After 2, 2.5, or 3 h of anoxia followed by 1 h reoxygenation in the absence of albumin, free radical formation assessed by low-level chemiluminescence and cell injury measured by lactate dehydrogenase (LDH) release and by trypan blue uptake increased proportionately. Chemiluminescence increased 4- to 7-fold, LDH release and trypan blue uptake increased 1.5- to 2-fold, compared with the end of anoxia. With 1% albumin, there was no increase in free radical formation during reoxygenation, and LDH release returned to control levels. There was a linear relation between the increase in chemiluminescence and the rise in LDH release (r2 = 0.83) and the increase in trypan blue uptake (r2 = 0.80), suggesting that free radical formation during reoxygenation is responsible for the cell injury. These experiments demonstrate that freshly isolated hepatocytes produce oxygen free radicals detectable by low-level chemiluminescence and that reoxygenation injury occurs after a relatively short period of anoxia (2-3 h). Albumin acts as a free radical scavenger, suppresses the release of reactive oxygen species, and significantly reduces reoxygenation injury.

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