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 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

Hypoxia compounds exercise-induced free radical formation in humans; partitioning contributions from the cerebral and femoral circulation

2018 ◽  
Vol 124 ◽  
pp. 104-113 ◽  
Author(s):  
Damian M. Bailey ◽  
Peter Rasmussen ◽  
Kevin A. Evans ◽  
Aske M. Bohm ◽  
Morten Zaar ◽  
...  
Keyword(s):  
Free Radical ◽  
Radical Formation ◽  
Free Radical Formation ◽  
Exercise Induced

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.

Intermittent hypoxic training: implications for lipid peroxidation induced by acute normoxic exercise in active men

2001 ◽  
Vol 101 (5) ◽  
pp. 465-475 ◽  
Author(s):  
Damian M. BAILEY ◽  
Bruce DAVIES ◽  
Ian S. YOUNG
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Acute Exercise ◽  
Mass Action ◽  
Lipid Hydroperoxides ◽  
Double Blind ◽  
Intermittent Hypoxic Training ◽  
Hypoxic Conditions ◽  
Hypoxic Training ◽  
Exercise Induced

Oxidant generation during regular physical exercise training may influence the adaptive responses that have been shown to confer protection against oxidative stress induced by subsequent acute exercise. To examine this, we randomly assigned 32 males to either a normoxic (n = 14) or a hypoxic (n = 18) group. During the acute phase, subjects in the hypoxic group performed two maximal cycling tests in a randomized double-blind fashion: one under conditions of normoxia and the other under hypoxic conditions (inspired fraction of O2 = 0.21 and 0.16 respectively). During the intermittent phase, the normoxic and hypoxic groups each trained for 4 weeks at the same relative exercise intensity, under conditions of normoxia and hypoxia respectively. During acute exercise under hypoxic conditions, the venous concentrations of lipid hydroperoxides and malondialdehyde were increased, despite a comparatively lower maximal oxygen uptake (o2max) (P < 0.05 compared with normoxia). The increases in lipid hydroperoxides and malondialdehyde were correlated with the exercise-induced decrease in arterial haemoglobin oxygen saturation (r =-0.61 and r =-0.50 respectively; P < 0.05), but not with o2max. Intermittent hypoxic training attenuated the increases in lipid hydroperoxides and malondialdehyde induced by acute normoxic exercise more effectively than did normoxic training, due to a selective mobilization of α-tocopherol (P < 0.05). The latter was related to enhanced exercise-induced mobilization/oxidation of blood lipids due to a selective increase in o2max (P < 0.05 compared with normoxic group). We conclude that lipid peroxidation induced by acute exercise (1) increases during hypoxia; (2) is not regulated exclusively by a mass action effect of o2; and (3) is selectively attenuated by regular hypoxic training. Oxidative stress may thus be considered as a biological prerequisite for adaptation to physical stress in humans.

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 The impact of endogenous intoxication on biochemical indicators of blood of cows with calves

2017 ◽  
Vol 8 (3) ◽  
pp. 438-443 ◽  
Author(s):  
B. Gutyj ◽  
Y. Grymak ◽  
M. Drach ◽  
O. Bilyk ◽  
O. Matsjuk ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Immune System ◽  
Blood Serum ◽  
Antioxidant System ◽  
Total Protein ◽  
Lipid Hydroperoxides ◽  
Glutathione System ◽  
Endogenous Intoxication ◽  
Activity Of Enzymes ◽  
The Impact

The notion “endotoxin” is conditional, for any normal metabolit has a toxic impact of its excessive accumulation in organism. Endotoxins include products of breakdown of tissue proteins, peroxides and other products of free radical oxidation, low molecular weight toxins, toxins of microorganisms. Current knowledge on the mechanism of endotoxin action on the organism of pregnant cows is based on the key role of the immune system: it provides animals with protection against the infections, eliminates extraneous elements of endogenous and exogenous origin. It is defined that under endogenous intoxication, toxic metabolites suppress the activity of immune system of organism, decreases the resistability of an organism to negative effects of environmental factors. Animals under endogenous intoxication had the following clinical symptoms: swelling of mammal gland, edemas of external genitals, anemia of mucous membranes, functional disorders of proventriculuses and intestines, animals were stressed. It was defined that under endogenous intoxication in 8–9 months of pregnancy, blood of highly-productive cows had a tendency of decrease in the number of erythrocytes by 21.0%, in the level of hemoglobin – by 24.3%, increase in the number of leucocytes by 7.6% compared to the value for blood of cows with physiological pregnancy process. The development of endogenous intoxication among pregnant cows causes disorders in protein-synthesizing function of liver, which is indicated by decrease in the level of total protein and its fractions. It was defined that endogenous intoxication decreased the content of total protein in blood by 18.4%. Over the period of study, among pregnant cows under the development of endogenous intoxication, heightened activity of amino transferaces in the blood was observed. In the ninth month of pregnancy, the activity of amino transferaces in blood serum of cows from experimental group increased by 28.6%, and the activity of aspartate aminotransferace increased by 20.1% relatively. The activity of amino transferaces and decrease in the level of total protein and its fractions in blood serum is one of the first biochemical studies on the diagnosing endotoxin manifestations and indicates destructive processes in liver. It was defined that pregnant cows under the development of endogenous intoxication suffer disorders in detoxicating function of liver and disorders in filtrating function of kidneys. The developing endogenous intoxication of pregnant cows suppresses the activity of enzymes in their glutathione system of antioxidant protection, which is indicated by decrease in the activity of glutathione peroxidase by 27.5 %, glutathione reductase by 42.9%, glucose-6-phosphate dehydrogenase by 11.2% in blood serum. The lowest activity of enzymes of glutathione system in blood of highly-productive cows under endogenous intoxication was observed in their ninth month of pregnancy, which is related to increase in activation of processes of lipid peroxidation and misbalance between the activity of antioxidant system and intensity of lipid peroxidation. Reliable increase in the content of lipid hydroperoxides by 70.9% and in concentration of malondialdehide by 54.8% was observed. Misbalance towards generation of active forms of oxygen and their metabolites, exhaustion of antioxidant system and disorders in balance cause oxidative stress. 

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.

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