Dose—response effects of malachite green on free radical formation, lipid peroxidation and DNA damage in Syrian embryo cells and their modulation by antioxidants

1994 ◽  
Vol 15 (11) ◽  
pp. 2445-2448 ◽  
Author(s):  
A. Panandiker ◽  
G.B. Maru ◽  
K.V.K. Rao
Keyword(s):  
Lipid Peroxidation ◽  
Dna Damage ◽  
Free Radical ◽  
Malachite Green ◽  
Dose Response ◽  
Radical Formation ◽  
Embryo Cells ◽  
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.

Role of chromium(IV) in the chromium(VI)-related free radical formation, dG hydroxylation, and DNA damage

1996 ◽  
Vol 64 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Hai Luo ◽  
Yongde Lu ◽  
Yan Mao ◽  
Xianglin Shi ◽  
Nar S Dalal
Keyword(s):  
Dna Damage ◽  
Free Radical ◽  
Radical Formation ◽  
Chromium Vi ◽  
Free Radical Formation

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.

Sign in / Sign up

Export Citation Format

Share Document