Alteration of antioxidant enzymes with aging in rat skeletal muscle and liver

1990 ◽  
Vol 258 (4) ◽  
pp. R918-R923 ◽  
Author(s):  
L. L. Ji ◽  
D. Dillon ◽  
E. Wu

Maximal activities of antioxidant enzymes involved in oxygen free radical metabolism in skeletal muscle and liver were investigated in 4-, 26-, and 31-mo-old male Wistar-Furth rat at rest and after a single bout of treadmill exercise. In skeletal muscle, cytosolic (Cu-Zn) and mitochondrial (Mn) superoxide dismutase (SOD) specific activities were significantly higher in the aged rats and at 31 mo reached 135 and 218%, respectively, of those at 4 mo. Resting catalase activity was doubled at 31 mo compared with that at 4 mo. Glutathione peroxidase (GPX) activity increased twofold in muscle cytosol and by 47% in mitochondria of aged rats. Glutathione S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G-6-PDH) activities in muscle were also significantly elevated. Hepatic antioxidant enzymes were altered differentially with aging. Cytosolic SOD and GST activities were decreased, whereas mitochondrial GPX, GR, and G-6-PDH activities were increased. Lipid peroxidation was greater in skeletal muscle homogenate and mitochondria but lower in liver homogenate in the aged rats. An acute exercise bout had little effect on muscle or liver antioxidant enzymes regardless of the animal's age. It is concluded that aging is accompanied with an elevation of antioxidant enzyme activities and lipid peroxidation in skeletal muscle probably due to the increased oxygen free radical production and reaction.

2004 ◽  
Vol 23 (1) ◽  
pp. 29-34 ◽  
Author(s):  
G Kadikoylu ◽  
Z Bolaman ◽  
S Demir ◽  
M Balkaya ◽  
N Akalin ◽  
...  

Cisplatin-induced nephrotoxicity is associated with an increase in lipid peroxidation and oxygen free radicals in rat kidneys. In this study, the effects of desferrioxamine were compared to vitamin C and E on cisplatin-induced lipid peroxidation and antioxidant enzyme activities in rat kidneys. Rats were divided into five groups, with 15 Wistar rats in each group. In the control group, rats received 1 mL/100 g isotonic saline solution intraperitoneally (i.p.). In Group II, 10 mg/kg cisplatin i.p. was injected to rats. Thirty minutes before the same dosage of cisplatin administration, 100 mg/kg i.p. vitamin C or E was given to rats in groups III and IV, respectively. Rats in Group V received 250 mg/kg desferrioxamine i.p., before the same dose of cisplatin administration. All rats were killed by cervical dislocation after 72 hours. The kidneys were immediately removed and washed in cold saline. Spectrophotometric method was used for all analyses. While catalase, glutathione reductase (GR), and super oxide dismutase (SOD) levels were found to be significantly decreased (P B < 0.001), malondialdehyde (MDA) (P < 0.05) and hydrogen peroxide (H2O2) (P < 0.001) levels were significantly increased in the cisplatin group when compared to the controls. MDA levels were decreased by desferrioxamine (P < 0.005) as well as vitamin C and E (P < 0.05 and P < 0.001, respectively). These three compounds induced a significant increase in SOD levels (P B < 0.05), but only in the vitamin C group, were SOD levels not significantly different than the levels of the controls (P > 0.05). In the desferrioxamine (P < 0.05), vitamin C and E groups (P < 0.001 for both), the cisplatin elevated H2O2 levels were decreased. None of these drugs had any effect on GR and catalase levels (P > 0.05). Desferrioxamine is useful to prevent cisplatin-induced lipid peroxidation, however, vitamin C and E are more effective on antioxidant enzymes than desferrioxamine.


1999 ◽  
Vol 87 (1) ◽  
pp. 465-470 ◽  
Author(s):  
J. Bejma ◽  
L. L. Ji

Reactive oxygen species (ROS) are implicated in the mechanism of biological aging and exercise-induced oxidative damage. The present study examined the effect of an acute bout of exercise on intracellular ROS production, lipid and protein peroxidation, and GSH status in the skeletal muscle of young adult (8 mo, n = 24) and old (24 mo, n = 24) female Fischer 344 rats. Young rats ran on a treadmill at 25 m/min and 5% grade until exhaustion (55.4 ± 2.7 min), whereas old rats ran at 15 m/min and 5% grade until exhaustion (58.0 ± 2.7 min). Rate of dichlorofluorescin (DCFH) oxidation, an indication of ROS and other intracellular oxidants production in the homogenate of deep vastus lateralis, was 77% ( P < 0.01) higher in rested old vs. young rats. Exercise increased DCFH oxidation by 38% ( P < 0.09) and 50% ( P < 0.01) in the young and old rats, respectively. DCFH oxidation in isolated deep vastus lateralis mitochondria with site 1 substrates was elevated by 57% ( P < 0.01) in old vs. young rats but was unaltered with exercise. Significantly higher DCFH oxidation rate was also found in aged-muscle mitochondria ( P < 0.01), but not in homogenates, when ADP, NADPH, and Fe3+ were included in the assay medium without substrates. Lipid peroxidation in muscle measured by malondialdehyde content showed no age effect, but was increased by 20% ( P < 0.05) with exercise in both young and old rats. Muscle protein carbonyl formation was unaffected by either age or exercise. Mitochondrial GSH/ GSSG ratio was significantly higher in aged vs. young rats ( P < 0.05), whereas exercise increased GSSG content and decreased GSH/GSSG in both age groups ( P < 0.05). These data provided direct evidence that oxidant production in skeletal muscle is increased in old age and during prolonged exercise, with both mitochondrial respiratory chain and NADPH oxidase as potential sources. The alterations of muscle lipid peroxidation and mitochondrial GSH status were consistent with these conclusions.


1992 ◽  
Vol 262 (3) ◽  
pp. H806-H812 ◽  
Author(s):  
K. Todoki ◽  
E. Okabe ◽  
T. Kiyose ◽  
T. Sekishita ◽  
H. Ito

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.


Author(s):  
Geoffrey Warnier ◽  
Estelle De Groote ◽  
Florian A. Britto ◽  
Ophélie Delcorte ◽  
Joshua P. Nederveen ◽  
...  

Purpose: To investigate exosome-like vesicle (ELV) plasma concentrations and markers of multivesicular body (MVB) biogenesis in skeletal muscle in response to acute exercise. Methods: Seventeen healthy (BMI: 23.5±0.5kg·m-2) and fifteen prediabetic (BMI: 27.3±1.2kg·m-2) men were randomly assigned to two groups performing an acute cycling bout in normoxia or hypoxia (FiO2 14.0%). Venous blood samples were taken before (T0), during (T30) and after (T60) exercise and biopsies from m. vastus lateralis were collected before and after exercise. Plasma ELVs were isolated by size exclusion chromatography, counted by nanoparticle tracking analysis (NTA), and characterized according to international standards, followed by expression analyses of canonical ELV markers in skeletal muscle. Results: In the healthy normoxic group, the total number of particles in the plasma increased during exercise from T0 to T30 (+313%) followed by a decrease from T30 to T60 (-53%). In the same group, an increase in TSG101, CD81 and HSP60 protein expression was measured after exercise in plasma ELVs; however, in the prediabetic group, the total number of particles in the plasma was not affected by exercise. The mRNA content of TSG101, ALIX and CD9 were upregulated in skeletal muscle after exercise in normoxia; whereas, CD9 and CD81 were downregulated in hypoxia. Conclusions: ELV plasma abundance increased in response to acute aerobic exercise in healthy subjects in normoxia, but not in prediabetic subjects, nor in hypoxia. Skeletal muscle analyses suggested that this tissue did not likely play a major role of the exercise-induced increase in circulating ELVs.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ping Wang ◽  
Chun Guang Li ◽  
Zhengtang Qi ◽  
Di Cui ◽  
Shuzhe Ding

Exercise induced skeletal muscle phenotype change involves a complex interplay between signaling pathways and downstream regulators. This study aims to investigate the effect of acute exercise on mitochondrial H2O2production and its association withp66Shc, FOXO3a, and antioxidant enzymes. Male ICR/CD-1 mice were subjected to an acute exercise. Muscle tissues (gastrocnemius and quadriceps femoris) were taken after exercise to measure mitochondrial H2O2content, expression ofp66Shcand FOXO3a, and the activity of antioxidant enzymes. The results showed that acute exercise significantly increased mitochondrial H2O2content and expressions ofp66Shcand FOXO3a in a time-dependent manner, with a linear correlation between the increase in H2O2content andp66Shcor FOXO3a expression. The activity of mitochondrial catalase was slightly reduced in the 90 min exercise group, but it was significantly higher in groups with 120 and 150 min exercise compared to that of 90 min exercise group. The activity of SOD was not significantly affected. The results indicate that acute exercise increases mitochondrial H2O2production in the skeletal muscle, which is associated with the upregulation ofp66Shcand FOXO3a. The association ofp66Shcand FOXO3a signaling with exercise induced H2O2generation may play a role in regulating cellular oxidative stress during acute exercise.


1996 ◽  
Vol 12 (07) ◽  
pp. 447-450 ◽  
Author(s):  
R. Ferrari ◽  
Bruno Battiston ◽  
Giorgio Brunelli ◽  
Adriano Casella ◽  
Luigi Caimi

1997 ◽  
Vol 98 (2) ◽  
pp. 177-180 ◽  
Author(s):  
S Doğru-Abbasoğlu ◽  
S Tamer-Toptani ◽  
B Uğurnal ◽  
N Koçak-Toker ◽  
G Aykaç-Toker ◽  
...  

1995 ◽  
Vol 147 (2) ◽  
pp. 361-365 ◽  
Author(s):  
T Mano ◽  
R Sinohara ◽  
Y Sawai ◽  
N Oda ◽  
Y Nishida ◽  
...  

Abstract To determine how lipid peroxides and free radical scavengers are changed in the brain of hyper- or hypothyroid rats, we examined the behavior of lipid peroxide and free radical scavengers in the cerebral cortex of aged (1·5 years old) rats that had been made hyper- or hypothyroid by the administration of thyroxine or methimazol for 4 weeks. Concentrations of catalase, Mn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were increased in hyperthyroid rats compared with euthyroid rats. Concentrations of total SOD, Cu,Zn-SOD and GSH-PX were increased but that of Mn-SOD was decreased in hypothyroid animals. There were no differences among hyperthyroid, hypothyroid and euthyroid rats in the levels of coenzymes 9 or 10. The concentration of lipid peroxides, determined indirectly by the measurement of thiobarbituric acid reactants, was decreased in hyperthyroid rats but not in hypothyroid rats when compared with euthyroid animals. These findings suggest that free radicals and lipid peroxides are scavenged to compensate for the changes induced by hyper- or hypothyroidism. Journal of Endocrinology (1995) 147, 361–365


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