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Biomedical subjects

M Atalay

Publications and source records attributed to M Atalay.

At least 19 recordsLinked to original sources
PubMed2006

Skeletal muscle HSP expression in response to immobilization and remobilization.

Heat shock proteins play an important regulatory role in the cellular defence. Oxidative stress is one of the factors inducing heat shock protein expression. This study tested the effects of 4 weeks of immobilization and subsequent remobilization on heat shock protein expression and oxidative stress in the lateral gastrocnemius and plantaris muscles of the rat. Active mobilization or free mobilization protocols were used for remobilization. In active mobilization, strenuous uphill treadmill running, twice a day, was started immediately after the immobilization and lasted for six days. Rats in the free mobilization group moved freely in their cages immediately after the immobilization. Expression of heat shock proteins was upregulated during the recovery from immobilization, especially in the lateral gastrocnemius muscle in the active mobilization group. However, markers of oxidative stress, such as protein carbonyls and 4-hydroxynonenal protein adducts, or activities of the antioxidant enzymes glutathione peroxidase and glutathione reductase, did not change after the immobilization and subsequent recovery. In summary, following immobilization, both intensive and spontaneous exercise upregulated the heat shock protein expressions in the lateral gastrocnemius muscle and partly in the plantaris muscle, which may contribute to the recovery from immobilization atrophy.

Animals↗
PubMed2004

Anti-angiogenic, antioxidant, and anti-carcinogenic properties of a novel anthocyanin-rich berry extract formula.

Edible berry anthocyanins possess a broad spectrum of therapeutic and anti-carcinogenic properties. Berries are rich in anthocyanins, compounds that provide pigmentation to fruits and serve as natural antioxidants. Anthocyanins repair and protect genomic DNA integrity. Earlier studies have shown that berry anthocyanins are beneficial in reducing age-associated oxidative stress, as well as in improving neuronal and cognitive brain function. Six berry extracts (wild blueberry, bilberry, cranberry, elderberry, raspberry seeds, and strawberry) were studied for antioxidant efficacy, cytotoxic potential, cellular uptake, and anti-angiogenic (the ability to reduce unwanted growth of blood vessels, which can lead to varicose veins and tumor formation) properties. We evaluated various combinations of edible berry extracts and developed a synergistic formula, OptiBerry IH141, which exhibited high ORAC (Oxygen-Radical Absorbing Capacity) value, low cytotoxicity, and superior anti-angiogenic properties compared to the other combinations tested. Anti-angiogenic approaches to treat cancer represent a priority area in vascular tumor biology. OptiBerry significantly inhibited both H2O2- and TNF-alpha-induced VEGF (Vascular Endothelial Growth Factor) expression by human keratinocytes. VEGF is a key regulator of tumor angiogenesis. Matrigel assay using human microvascular endothelial cells showed that OptiBerry impaired angiogenesis. In an in vivo model of angiogenesis, OptiBerry significantly inhibited basal MCP-1 and inducible NF-kappaB transcriptions. Endothelioma cells pretreated with OptiBerry showed a diminished ability to form hemangioma and markedly decreased tumor growth by more than 50%. In essence, these studies highlight the novel anti-angiogenic, antioxidant, and anti-carcinogenic potential of a novel anthocyanin-rich berry extract formula, OptiBerry.

Angiogenesis Inhibitors↗
PubMed2001

Physical exercise induces activation of NF-kappaB in human peripheral blood lymphocytes.

Current understanding of nuclear factor-kappaB (NF-kappaB) activation is derived mostly from in vitro studies, and in vivo human data are limited. This study provides first evidence showing that physical exercise (80% maximal O2 consumption, 1 h) may trigger NF-kappaB activation, as determined by electrophoretic mobility shift assay, in peripheral blood lymphocytes of physically fit young men. Supershift assay showed that the NF-kappaB protein complex contained the transcriptionally active p65 protein. Plasma levels of NF-kappaB-directed gene products such as tumor necrosis factor-alpha and interleukin-2 receptor confirmed that physical exercise caused NF-kappaB transactivation. Exercise-induced NF-kappaB activation in lymphocytes was associated with elevated levels of lipid peroxidation by-products in the plasma.

Adult↗
PubMed2000

Antioxidant enzymes; possible mechanism of gold compound treatment in rheumatoid arthritis.

Reactive oxygen species play a critical role in inflammatory processes including rheumatoid disorders. Antioxidant therapy strategies have been postulated for the treatment of rheumatoid diseases. In this study, we investigated activities and therapeutic implications of antioxidant enzymes in rheumatoid disorders. Activities of antioxidant enzymes glutathione peroxidase, glutathione reductase and catalase were examined in the blood of rheumatic patients and healthy controls. Activity of catalase was decreased significantly, while activities of glutathione peroxidase and glutathione reductase remained unchanged. Thioredoxin reductase is an antioxidant enzyme having an important regulatory task of thiol redox status and intracellular signaling processes coupled with the glutathione system. We also observed that in liver mitochondrial calf thioredoxin reductase was inhibited by antirheumatic drug goldthioglucose in the manner similar to intracellular thioredoxin reductase. Furthermore, during the treatment by goldthioglucose, gold is accumulated in lysosomes of macrophages. Our results suggest that although antioxidant enzyme activities were down-regulated in rheumatoid patients, we can decrease ROS generation by macrophages via inhibition thioredoxin reductase by goldthioglucose.

Journal Article↗
PubMed2000

Light exposure induces antioxidant enzyme activities in eye tissues of frogs.

Retina and pigment epithelium of eyes are prone to increased production of reactive oxygen species and are susceptible to oxidative damage. We studied antioxidant enzyme activities in eye tissues exposed to prolonged low intensity (2000 lx) and short-term high intensity light (50000 lx) of visible range. Both prolonged low intensity and short-term intensive light increased superoxide dismutase, glutathione peroxidase and catalase activities in the pigment epithelium of frogs' eyes, while the activity of these enzymes in the retina remained unchanged. Our results suggest that visible light may increase oxidative stress and cause compensatory up-regulation of antioxidant enzyme activities in frogs' eyes.

Journal Article↗
PubMed2000

Vitamin E regulates changes in tissue antioxidants induced by fish oil and acute exercise.

PURPOSE: Prooxidant effects of fish oil supplementation could unfavorably affect the cardiovascular benefits of fish oil. We tested the effects of 8 wk vitamin E cosupplementation with fish oil on antioxidant defenses at rest and in response to exhaustive exercise in rats. METHODS: Rats (N = 80) were divided into fish oil, fish oil and vitamin E (FOVE), soy oil, and soy oil and vitamin E (SOVE) supplemented groups. For the vitamin E supplemented rats, corresponding groups (FOVE-Ex and SOVE-Ex) performed an acute bout of exhaustive exercise after the supplementation period. RESULTS: Fish oil supplementation increased the activity of catalase, glutathione peroxidase, and glutathione-S-transferase in the liver and red gastrocnemius (RG) muscle. Fish oil decreased liver total glutathione (TGSH) levels. Vitamin E supplementation decreased antioxidant enzyme activities to levels at or near those in SOVE in a tissue specific pattern. Vitamin E increased TGSH in liver, heart, and RG. Regression analysis showed TGSH to be a negative determinant of protein oxidative damage as measured by protein carbonyl levels in both liver and RG. Catalase activity was associated with liver lipid peroxidation as measured by thiobarbituric acid-reacting substances. The exercise-induced decrease in hepatic TGSH tended to be less in FOVE versus SOVE. Exhaustive exercise also modulated tissue antioxidant enzymes. CONCLUSIONS: Vitamin E supplementation markedly decreased fish oil induced antioxidant enzyme activities in all tissues. Sparing of glutathione may be an important mechanism by which vitamin E decreased tissue protein oxidative damage.

Animals↗
PubMed2000

Aerobic exercise and the lipid profile in type 1 diabetic men: a randomized controlled trial.

PURPOSE: Despite the potential importance of favorable changes in the lipid profile produced by aerobic exercise, training-induced lipid profile changes in atherosclerosis-prone type 1 diabetes mellitus (DM) have not heretofore been adequately addressed. METHODS: We assessed the effect of a 12- to 16-wk aerobic exercise program on cardiorespiratory fitness and the lipid profile in young men with type 1 DM. Generally active men aged 20-40 yr with type 1 DM (N = 56) were randomized into training (N = 28) and control (untrained, N = 28) groups after baseline measurements. Training consisted of 30-60 min moderate-intensity running 3-5 times a week for 12-16 wk. RESULTS: For the 42 men finishing the study, peak oxygen consumption (VO2 peak) increased significantly only in the trained group. Total and low-density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B decreased and the high-density lipoprotein (HDL)/apo A-I ratio increased in the trained group. HDL and apo A-I increased in both groups. The exercise program brought about improvements in the HDL/LDL and apo A-I/apo B ratios and apo B and triglyceride levels when comparing the relative (%) changes in the trained versus control group. In the trained group, men with HDL/LDL ratios below the group median at baseline showed even more favorable changes in their lipid profile than those with higher initial HDL/LDL ratios. Body mass index, percent body fat and hemoglobin A1c did not change during the training period in either group. CONCLUSIONS: Endurance training improved the lipid profile in already physically active type 1 diabetic men, independently of effects on body composition or glycemic control. The most favorable changes were in patients with low baseline HDL/LDL ratios, likely the group with the greatest benefit to be gained by such changes.

Adult↗
PubMed1999

Physical exercise and antioxidant defenses in the heart.

Cardiac muscle relies highly on aerobic metabolism. Heart muscle has a high oxygen uptake at resting conditions, which increases many fold during exhaustive physical exercise. Such a high rate of oxidative metabolism is often associated with enhanced production of reactive oxygen metabolites. A single bout of strenuous exercise has been demonstrated to induce oxidative damage in heart. Such oxidant insult may lead to adaptive responses and strengthen antioxidant defenses in the heart tissue. Endurance exercise training has indeed been shown to upregulate heart tissue antioxidant defenses. Recently, we have observed that even predominantly anaerobic sprint training regimens may enhance cardiac antioxidant defenses. Regular physical exercise may beneficially influence cardiac antioxidant defenses and promote overall cardiac function.

Animals↗
PubMed1999

Alpha-lipoic acid supplementation: tissue glutathione homeostasis at rest and after exercise.

Antioxidant nutrients have demonstrated potential in protecting against exercise-induced oxidative stress. alpha-Lipoic acid (LA) is a proglutathione dietary supplement that is known to strengthen the antioxidant network. We studied the effect of intragastric LA supplementation (150 mg/kg, 8 wk) on tissue LA levels, glutathione metabolism, and lipid peroxidation in rats at rest and after exhaustive treadmill exercise. LA supplementation increased the level of free LA in the red gastrocnemius muscle and increased total glutathione levels in the liver and blood. The exercise-induced decrease in heart glutathione S-transferase activity was prevented by LA supplementation. Exhaustive exercise significantly increased thiobarbituric acid-reactive substance levels in the liver and red gastrocnemius muscle. LA supplementation protected against oxidative lipid damage in the heart, liver, and red gastrocnemius muscle. This study reports that orally supplemented LA is able to favorably influence tissue antioxidant defenses and counteract lipid peroxidation at rest and in response to exercise.

Analysis of Variance↗
PubMed1999

Blood glutathione homeostasis as a determinant of resting and exercise-induced oxidative stress in young men.

Although the importance of glutathione in protection against oxidative stress is well recognized, the role of physiological levels of glutathione and other endogenous antioxidants in protecting against exercise-induced oxidative stress is less clear. We evaluated the role of glutathione and selected antioxidant enzymes as determinants of lipid peroxidation at rest and in response to exercise in men (n = 13-14) aged 20-30 years, who cycled for 40 min at 60% of their maximal oxygen consumption (VO2max). Levels of plasma thiobarbituric acid reactive substances (plasma TBARS) and blood oxidised glutathione (GSSG) increased by about 50% in response to exercise. Mean blood reduced glutathione (GSH) decreased by 13% with exercise. Of the measured red blood cell (RBC) antioxidant enzyme activities, only selenium-dependent glutathione peroxidase (Se-GPX) activity rose following exercise. In univariate regression analysis, plasma TBARS levels at rest predicted postexercise plasma TBARS and the exercise-induced change in total glutathione (TGSH). Blood GSSG levels at rest were strongly determinant of postexercise levels. Multiple regression analysis showed blood GSH to be a determinant of plasma TBARS at rest. The relative changes in TGSH were determinant of postexercise plasma TBARS. In summary, higher blood GSH and lower plasma TBARS at rest were associated with lower resting, and exercise-induced, lipid peroxidation. Subjects with a favourable blood glutathione redox status at rest maintained a more favourable redox status in response to exercise-induced oxidative stress. Changes in blood GSH and TGSH in response to exercise were closely associated with both resting and exercise-induced plasma lipid peroxidation. These results underscore the critical role of glutathione homeostasis in modulating exercise-induced oxidative stress and, conversely, the effect of oxidative stress at rest on exercise-induced changes in glutathione redox status.

Adult↗
PubMed1998

Skeletal muscle and liver lipoyllysine content in response to exercise, training and dietary alpha-lipoic acid supplementation.

In human cells, alpha-lipoic acid (LA) is present in a bound lipoyllysine form in mitochondrial proteins that play a central role in oxidative metabolism. The possible effects of oral LA supplementation, a single bout of strenuous exercise and endurance exercise training on the lipoyllysine content in skeletal muscle and liver tissues of rat were examined. Incorporation of lipoyl moiety to tissue protein was not increased by enhanced abundance of LA in the diet. Endurance exercise training markedly increased lipoyllysine content in the liver at rest. A bout of exhaustive exercise also increased hepatic lipoyllysine content. A significant interaction of exhaustive exercise and training to increase tissue lipoyllysine content was evident. In vastus lateralis skeletal muscle, training did not influence tissue lipoyllysine content. A single bout of exhaustive exercise, however, clearly increased the level of lipoyllysine in the muscle. Comparison of tissue lipoyllysine data with that of free or loosely-bound LA results showed a clear lack of association between the two apparently related parameters. Tightly protein-bound lipoyllysine pool in tissues appeared to be independent of the loosely-bound or free LA status in the tissue.

Animals↗
PubMed1997

Altered antioxidant enzyme defences in insulin-dependent diabetic men with increased resting and exercise-induced oxidative stress.

Impaired antioxidant defences may predispose to the increased resting and exercise-induced oxidative stress found in patients with insulin-dependent diabetes mellitus (IDDM). We investigated major erythrocyte antioxidant enzyme activities at rest and in response to sustained, moderate intensity physical exercise in young diabetic men (n = 9) previously reported to have markedly elevated plasma lipid peroxidation and blood glutathione levels compared with control men (n = 13) (Laaksonen et al. 1996). At rest, erythrocyte glutathione reductase activity was 15% higher in the diabetic group (P = 0.049). Se-glutathione peroxidase and glutathione-S-transferase activities were similar in both groups. Red cell Cu, Zn-superoxide dismutase and catalase activities were lower in the IDDM group (P = 0.033 and P = 0.023, respectively). After 40 min of exercise at 60% of the subjects' peak oxygen consumption, Se-glutathione peroxidase activity rose by about 14% in the control group (P = 0.003), but not in the IDDM group (P = 0.47). Exercise did not cause significant changes in other enzyme activities in either group. To conclude, lower erythrocyte Cu, Zn-superoxide dismutase and catalase activity in young men with IDDM at rest may contribute to increased oxidative stress. On the other hand, increased glutathione reductase activity may represent a compensatory upregulation of glutathione homeostasis in response to increased oxidative stress. Upregulation of Se-glutathione peroxidase activity in response to physical activity appeared to be impaired in men with IDDM.

Adult↗
PubMed1997

Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise.

Fish oil supplementation and physical exercise may induce oxidative stress. We tested the effects of 8 wk of alpha-tocopherol (vitamin E) and fish oil (FO) supplementation on resting and exercise-induced oxidative stress. Rats (n = 80) were divided into groups supplemented with FO, FO and vitamin E (FOVE), soy oil (SO), and SO and vitamin E (SOVE), and for FOVE and SOVE they were divided into corresponding exercise groups (FOVE-Ex and SOVE-Ex). Lipid peroxidation [thiobarbituric acid-reacting substances (TBARS)] was 33% higher in FO compared with SO in the liver, but oxidative protein damage (carbonyl levels) remained similar in both liver and red gastrocnemius muscle (RG). Vitamin E supplementation, compared with FO and SO, markedly decreased liver and RG TBARS, but liver TBARS remained 32% higher in FOVE vs. SOVE. Vitamin E also markedly decreased liver and RG protein carbonyl levels, although levels in FOVE and SOVE were similar. Exercise increased liver and RG TBARS and RG protein carbonyl levels markedly, with similar levels in FOVE-Ex and SOVE-Ex. FO increased lipid peroxidation but not protein oxidation in a tissue-specific manner. Vitamin E markedly decreased lipid peroxidation and protein oxidation in both FOVE and SOVE, although liver lipid peroxidation remained higher in FOVE. Despite higher levels of hepatic lipid peroxidation at rest in FOVE compared with SOVE, liver appeared to be relatively less susceptible to exercise-induced oxidative stress in FOVE.

Animals↗
PubMed1996

Glutathione-dependent modulation of exhausting exercise-induced changes in neutrophil function of rats.

Reduced glutathione (GSH) plays a central role in maintaining an effective synergism between various physiological and exogenous antioxidants. We tested the effects of GSH and N-acetylcysteine (NAC, a pro-GSH clinical drug), intraperitoneal (i.p.) supplementation and GSH deficiency on exercise-induced leucocyte margination and neutrophil oxidative burst activity. GSH, NAC (1g.kg-1) or placebo saline was i.p. injected (one or eight times) to male rats (n > or = seven per group). The GSH-deficient rats were prepared by i.p. injections of L-buthionine-[SR]-sulphoximine (BSO, 6 mmol.l-1.kg-1) twice daily for 4 days. Exercised animals were subjected to treadmill run to exhaustion. Exhausting treadmill exercise significantly decreased peripheral blood leucocyte count in the controls (P < 0.001). Such exercise-associated leucocyte margination was prevented by GSH supplementation. Peripheral blood neutrophil counts were significantly higher (P < 0.02) in the GSH-supplemented groups compared to the placebo control groups. Exercise-induced increase in peripheral blood neutrophil oxidative burst activity as measured by luminol-enhanced chemiluminescence per volume of blood tended to be higher in the GSH-supplemented group (P < 0.10), and lower in the GSH-deficient rats (P < 0.02). In these experiments, for the first time we have shown that GSH supplementation can induce neutrophil mobilization and decrease exercise-induced leucocyte margination, and that exogenous and endogenous GSH can regulate exercise-induced stimulation of the neutrophil oxidative burst.

Animals↗
PubMed1996

Skeletal muscle and heart antioxidant defences in response to sprint training.

Although endurance training enhances the antioxidant defence of different tissues, information on the effect of sprint training is scanty. We examined the effect of sprint training on rat skeletal muscle and heart antioxidant defences. Male Wistar rats, 16-17 weeks old, were sprint trained on a treadmill for 6 weeks. Total glutathione levels and activities of glutathione peroxidase, glutathione reductase, glutathione S-transferase and superoxide dismutase in heart and various skeletal muscles were compared in trained and control sedentary animals. Lactate dehydrogenase and citrate synthase enzyme activities were measured in muscle to test the effects of training on glycolytic and oxidative metabolism. Sprint training significantly increased lactate dehydrogenase activity in predominantly fast glycolytic muscles and enhanced total glutathione contents of the superficial white quadriceps femoris, mixed gastrocnemius and fast-glycolytic extensor digitorum longus muscles. Oxidative metabolic capacity increased in plantaris muscle only. Compared with the control group, glutathione peroxidase activities in gastrocnemius, extensor digitorum longus muscles and heart also increased in sprint trained rats. Glutathione reductase activities increased significantly in the extensor digitorum longus muscle and heart. Glutathione S-transferase activity was also higher in the sprint trained extensor digitorum longus muscle. Sprint training did not influence glutathione levels or glutathione-related enzymes in the soleus muscle. Superoxide dismutase activity remained unchanged in skeletal muscle and heart. Sprint training selectively enhanced tissue antioxidant defences by increasing skeletal muscle glutathione content and upregulating glutathione redox cycle enzyme activities in fast and mixed fibre leg muscles and heart.

Animals↗
PubMed1996

Increased resting and exercise-induced oxidative stress in young IDDM men.

OBJECTIVE: To assess the effect of acute physical exercise on oxidative stress and glutathione redox status and the relation to physical fitness in otherwise healthy young men with IDDM. RESEARCH DESIGN AND METHODS: Nine men with IDDM (HbA1 7.3 +/- 1.7%), ages 21-30 years, and 13 matched control subjects exercised on a bicycle ergometer for 40 min at 60% of their maximal oxygen consumption (VO2max). Oxidative stress was assessed with plasma thiobarbituric acid reactive substance (TBARS) levels (an index of lipid peroxidation) and, in response to exercise, also glutathione redox status. For glutathione redox status, blood total glutathione (TGSH) and oxidized glutathione (GSSG) were determined. Blood samples were drawn immediately before and after exercise. RESULTS: Resting plasma TBARS levels were markedly elevated in diabetic patients (2.2 +/- 0.7 vs. 0.9 +/- 0.4 mumol/l; P = 0.0002). Mean blood TGSH was higher in diabetic subjects (1,203 +/- 221 vs. 936 +/- 156 mmol/l; P = 0.002), with no significant difference in GSSG or GSSG/TGSH values. Exercise increased plasma TBARS and blood GSSG by approximately 50% in both groups. Resting plasma TBARS had a strong inverse correlation (r = -0.82; P = 0.006), and the exercise-induced percentage increase in TBARS had a strong positive correlation (r = 0.81, P = 0.008) with VO2max in diabetic subjects only. CONCLUSIONS: Glutathione redox status appears to be adequate in healthy young moderately active diabetic men. On the other hand, they demonstrated increased resting and postexercise oxidative stress as indicated by plasma TBARS. Although exercise acutely induces oxidative stress, in patients with diabetes, physical fitness may have a protective effect against oxidative stress.

Adult↗
PubMed1994

Exercise-induced oxidative stress: glutathione supplementation and deficiency.

Glutathione (GSH) plays a central role in coordinating the synergism between different lipid- and aqueous-phase antioxidants. We documented 1) how exogenous GSH and N-acetylcysteine (NAC) may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], and endurance and 2) the relative role of endogenous GSH in the circumvention of exercise-induced oxidative stress by using GSH-deficient [L-buthionine-(S,R)-sulfoximine (BSO)-treated] rats. Intraperitoneal injection of GSH remarkably increased plasma GSH; exogenous GSH per se was an ineffective delivery agent of GSH to tissues. Repeated administration of GSH (1 time/day for 3 days) increased blood and kidney total GSH [TGSH; GSH+oxidized GSH (GSSG)]. Neither GSH nor NAC influenced endurance to exhaustion. NAC decreased exercise-induced GSH oxidation in the lung and blood. BSO decreased TGSH pools in the liver, lung, blood, and plasma by approximately 50% and in skeletal muscle and heart by 80-90%. Compared with control, resting GSH-deficient rats had lower GSSG in the liver, red gastrocnemius muscle, heart, and blood; similar GSSG/TGSH ratios in the liver, heart, lung, blood, and plasma; higher GSSG/TGSH ratios in the skeletal muscle; and more TBARS in skeletal muscle, heart, and plasma. In contrast to control, exhaustive exercise of GSH-deficient rats did not decrease TGSH in the liver, muscle, or heart or increase TGSH of plasma; GSSG of muscle, blood, or plasma; or TBARS of plasma or muscle. GSH-deficient rats had approximately 50% reduced endurance, which suggests a critical role of endogenous GSH in the circumvention of exercise-induced oxidative stress and as a determinant of exercise performance.

Acetylcysteine↗