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1.
Chronobiol Int ; 41(5): 599-608, 2024 May.
Article in English | MEDLINE | ID: mdl-38689400

ABSTRACT

Professional athletes competing in the NBA are frequently exposed to time-zone-shifting travels. These time zone changes may cause circadian rhythm (CR) phase shifts and these shifts affect sportive performance. The aim of this study was to investigate the effects of CR phase shifts on the performance of NBA teams. 25016 regular season games across 21 consecutive seasons were included in the CR phase shift calculations. To examine the CR phase shift effect on team performance, teams were divided into three groups regarding Coordinated Universal Time (UTC): the same internal UTC as the local UTC (LS); the internal UTC ahead of the local UTC (LA); and the internal UTC behind the local UTC (LB). With a different approach, teams were divided into another three categories: the same internal UTC as its opponent's internal UTC (OS); the internal UTC ahead of its opponent's internal UTC (OA); and the internal UTC behind its opponent's internal UTC (OB). 24985 game data were used to compare these groups in terms of 25 variables. Statistical analyses were conducted separately for home and away teams. For home games, it was found that LA and OA are the most and LB is the least successful group in winning and scoring performances. For away games, it was determined that LS is the most advantageous group with the best winning percentage. These results revealed that teams from more west may have a CR advantage in regular season home games. However, it is thought that the performance of away teams depends more on travel fatigue than CR phase shifts.


Subject(s)
Athletic Performance , Circadian Rhythm , Humans , Circadian Rhythm/physiology , Athletic Performance/physiology , Athletes , Seasons , Sports/physiology , Time Factors
2.
Turk J Med Sci ; 49(3): 914-921, 2022 Feb.
Article in English | MEDLINE | ID: mdl-36441146

ABSTRACT

BACKGROUND: Mesenchymal stem cells (MSCs) are a type of adult stem cell consisting of a heterogeneous subset of stromal stem cells that can be isolated from adult tissues. Folic acid is another important contributor to tissue regeneration and repair, which affects the synthesis of some building block molecules used for wound healing. In this study, we examine the effect of folic acid and MSCderived soluble factors in the wound healing model. METHODS: Human umbilical vein endothelial cells (HUVECs) and bone marrow-derived MSCs (BMSCs) were cultured for this study. Cell proliferation analysis was done with xCELLigence RTCA. After 48 h of cultivation, the cell culture medium was collected as MSC conditional medium containing mesenchymal stem cell-derived soluble factors (MDFs). Different concentrations of MDFs (12%, 25%, 50%, 75%, and 100%) were applied to the HUVEC cell line. Folic acid (25, 30, 50, 60, 75, 90, and 100 µM) was tested by application of three different groups (control, 25 µM folic acid, 625 µM folic acid inhibitors) for proliferation on the HUVEC cell line. The combined effects of folic acid and MDFs were tested on the HUVEC cell line with 25 µM folic acid and 50 µM MDFs. All data were statistically analyzed using SPSS 15.0 for Windows. RESULTS: Significant differences were observed between controls and cells treated with folic acid, as well as between controls and both folic acid and MDFs (P < 0.05). Among the treated groups, the fastest wound closure rate was seen in cells treated with both folic acid and MDFs. DISCUSSION: The results show that both folic acid and MDFs increased the wound healing rate in HUVECs when they were used separately. The strongest benefits were seen in treatment using folic acid and MDFs together.


Subject(s)
Mesenchymal Stem Cells , Stem Cell Factor , Adult , Humans , Folic Acid/pharmacology , Endothelial Cells , Cell Line
3.
Biol Futur ; 73(2): 237-244, 2022 Jun.
Article in English | MEDLINE | ID: mdl-35291017

ABSTRACT

Oxidative damage and proinflammatory cytokines are involved in exhaustive exercise-induced fatigue. This study aimed to investigate the effects of bee venom, a natural toxin, on fatigue and tissue damage in rats that underwent forced swimming exercise. Rats were divided into four groups: control, swimming exercise (SE), bee venom (BV) and swimming exercise + bee venom (SE + BV). SE and SE + BV groups were subjected to forced swimming (load of 7% body weight) for 5 days. BV and SE + BV groups were injected with 1 mg/kg BV subcutaneously. Swimming time, blood lactate and TNF-α levels, MDA and GSH levels in liver and gastrocnemius muscle were evaluated. Swimming time was shorter in SE + BV group than SE group. There was no difference in lactate levels between SE and SE + BV groups. MDA and GSH levels were increased in SE, BV and SE + BV groups. TNF-α levels were increased in BV group compared to control and SE groups. Our study demonstrated that BV administration before exhaustive exercise in rats did not provide anti-fatigue effect. Additionally, BV did not show anti-inflammatory activity and had different effects on antioxidant capacity at tissue level. Further research might explore the effects of different doses and durations of BV on exhaustive exercise.


Subject(s)
Bee Venoms , Physical Conditioning, Animal , Animals , Bee Venoms/pharmacology , Lactates , Liver , Muscle, Skeletal , Rats , Swimming/physiology , Tumor Necrosis Factor-alpha
4.
PeerJ ; 10: e12876, 2022.
Article in English | MEDLINE | ID: mdl-35178305

ABSTRACT

Background: Sleep quality plays a principal role in the protection of health. There is an increasing number of studies in the literature demonstrating that internet addiction and smartphone addiction impair sleep quality. However, the number of studies on Turkish adolescents is very limited. Therefore, this study examined the effects of internet addiction and smartphone addiction on sleep quality among Turkish adolescents. Methods: Participants in this cross-sectional study were 910 adolescents aged 13-18 years. Data were collected with the Short Internet Addiction Test, Smartphone Addiction Scale, and Pittsburgh Sleep Quality Index. In addition, a questionnaire was used to gather information about the demographic, socioeconomic, and health-related characteristics. Pearson's Chi-square test, Chi-square test for trend, Mann-Whitney U test, logistic regression analysis, and Spearman's correlation analysis were used in the analysis. Results: The sleep quality of 58.7% of the adolescents was poor. Additionally, girls and adolescents ≥16 years old had poor sleep quality. Sleep quality deteriorated as perceived health status and perceived economic status of family deteriorated. Compared to participants with normal internet addiction scores, poor sleep quality was 1.83 (95% CI [1.22-2.74]) times higher in those with problematic internet addiction and 1.99 (95% CI [1.23-3.87]) times higher in those with pathological internet addiction. One point increase in Smartphone Addiction Scale total score increased poor sleep quality 1.01 (95% CI [1.00-1.02]) times. Sleep quality scale were positively correlated with the smartphone addiction and internet addiction. However, there was no positive correlation between habitual sleep efficiency subcomponent of sleep quality and smartphone addiction and internet addiction. Conclusions: Internet addiction and smartphone addiction were associated with poor sleep quality in adolescents. Older adolescents (≥16 years), gender (female), poor health perception, and perception of moderate economic status of the family were other factors associated with poor sleep quality.


Subject(s)
Behavior, Addictive , Sleep Quality , Humans , Adolescent , Female , Internet Addiction Disorder , Cross-Sectional Studies , Behavior, Addictive/epidemiology , Smartphone
5.
Turk J Med Sci ; 49(3)2019 May 09.
Article in English | MEDLINE | ID: mdl-31070342

ABSTRACT

Background/aim: Mesenchymal stem cells (MSCs) are a type of adult stem cell consisting of a heterogeneous subset of stromal stem cells that can be isolated from adult tissues. Folic acid is another important contributor to tissue regeneration and repair, which affects the synthesis of some building block molecules used for wound healing. In this study, we examine the effect of folic acid and MSCderived soluble factors in the wound healing model. Materials and methods: Human umbilical vein endothelial cells (HUVECs) and bone marrow-derived MSCs (BMSCs) were cultured for this study. Cell proliferation analysis was done with xCELLigence RTCA. After 48 h of cultivation, the cell culture medium was collected as MSC conditional medium containing mesenchymal stem cell-derived soluble factors (MDFs). Different concentrations of MDFs (12%, 25%, 50%, 75%, and 100%) were applied to the HUVEC cell line. Folic acid (25, 30, 50, 60, 75, 90, and 100 µM) was tested by application of three different groups (control, 25 µM folic acid, 625 µM folic acid inhibitors) for proliferation on the HUVEC cell line. The combined effects of folic acid and MDFs were tested on the HUVEC cell line with 25 µM folic acid and 50 µM MDFs. All data were statistically analyzed using SPSS 15.0 for Windows. Results: Significant differences were observed between controls and cells treated with folic acid, as well as between controls and both folic acid and MDFs (P < 0.05). Among the treated groups, the fastest wound closure rate was seen in cells treated with both folic acid and MDFs. Conclusion: The results show that both folic acid and MDFs increased the wound healing rate in HUVECs when they were used separately. The strongest benefits were seen in treatment using folic acid and MDFs together.

6.
Neurosci Lett ; 452(3): 281-5, 2009 Mar 20.
Article in English | MEDLINE | ID: mdl-18817845

ABSTRACT

Although regular physical exercise is beneficial to the body, it is well known that exhaustive exercise causes oxidative stress in muscle. Recent studies suggest that regular moderate physical exercise has the beneficial effects on brain. There is a little information regarding whether or not exercise could generate oxidative stress in the brain and the findings are conflicting. The aim of this study was to investigate the effects of acute and chronic exercise on thiobarbituric acid reactive substances, as an indicator of lipid peroxidation, in the hippocampus, which has a high concentration of glucocorticoid receptors, and prefrontal cortex and striatum, which have high dopamine content. Additionally we examined antioxidant enzyme activities, superoxide dismutase and glutathione peroxidase and nitrite-nitrate levels to assess the effects of reactive oxygen and nitrogen species. In this study it was shown that acute treadmill exercise at different strengths did not cause oxidative stress in prefrontal cortex, striatum and hypocampus regions of the brain. Regular treadmill exercise performed at different strengths was shown not to cause oxidative stress in prefrontal cortex, striatum and hippocampus regions of brain. As a result, we propose that acute and chronic exercise do not cause oxidant stress in prefrontal cortex, striatum and hippocampus and chronic exercise has a favorable effect on hippocampus, possibly by decreasing superoxide radical formation.


Subject(s)
Antioxidants/metabolism , Corpus Striatum/physiology , Hippocampus/physiology , Oxidants/metabolism , Physical Conditioning, Animal/physiology , Prefrontal Cortex/physiology , Animals , Glutathione Peroxidase/metabolism , Lipid Peroxidation/physiology , Male , Nitrates/metabolism , Nitrites/metabolism , Oxidative Stress/physiology , Rats , Rats, Sprague-Dawley , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/metabolism
7.
Environ Monit Assess ; 141(1-3): 339-45, 2008 Jun.
Article in English | MEDLINE | ID: mdl-17849228

ABSTRACT

The aim of this study was to identify possible relationships between biochemical- superoxide dismutase (SOD), glutathione peroxidase (GPx), thiobarbituric acid reactive substances (TBARS) of mussels (Mytilus galloprovincialis) and chemical (Hg, Cd, Pb, Cr, Cu, Zn, Mn and Fe) contaminants from relatively clean area (Middle Bay) and heavily polluted area (Inner Bay) of the Izmir Bay. Sampling of mussels was performed in the beginning of May 2004. Mussel digestive glands have been used for biochemical assays. Trace metal content was determined by atomic absorption spectrophotometer using standard procedures. Metal contents in mussels collected at polluted site increased compared to the middle part of the bay. While there was a positive correlation between metals and SOD enzyme activity, there was a negative correlation between metals and GPx enzyme activity. An increase was observed in SOD enzyme activity and a decrease of GPx enzyme activity at the inner part of the bay.


Subject(s)
Biomarkers/analysis , Metals, Heavy/analysis , Trace Elements/analysis , Water Pollutants, Chemical/analysis , Animals , Bivalvia/enzymology , Glutathione Peroxidase/metabolism , Sensitivity and Specificity , Superoxide Dismutase/metabolism , Turkey
8.
Intensive Care Med ; 33(3): 511-6, 2007 Mar.
Article in English | MEDLINE | ID: mdl-17186286

ABSTRACT

OBJECTIVE: To evaluate the effect of melatonin on the intestinal apoptosis along with oxidative damage in endotoxemic infant rats. DESIGN AND SETTING: Prospective animal study in a university-based experimental research laboratory. SUBJECTS AND INTERVENTIONS: Wistar albino 7-day-old rat pups (n=21). The animals were randomized into three experimental groups: (1) controls; (2) endotoxemia; (3) endotoxemia treated with melatonin (10mg/kg). Endotoxemia was induced in rats by intraperitoneal injection of lipopolysaccharide (Escherichia coli serotype 0111:B4; 3 mg/kg). MEASUREMENTS AND RESULTS: Four hours after LPS injection, the antioxidant enzyme activities, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and thiobarbituric acid reactive substance (TBARS) levels as an indicator of lipid peroxidation, were determined. Intestinal apoptosis was assessed by hematoxylin-eosin staining and terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling. The administration of melatonin into endotoxemic rats prevented the increase in the TBARS levels, and increased the activities of antioxidant enzymes and attenuated apoptotic cell death in both intestinal epithelium and lamina propria. CONCLUSIONS: Melatonin diminished the intestinal oxidative stress and apoptotic damage induced by endotoxemia in infant rats.


Subject(s)
Antioxidants/pharmacology , Apoptosis/drug effects , Intestinal Mucosa/metabolism , Melatonin/pharmacology , Oxidative Stress/drug effects , Sepsis/drug therapy , Animals , Animals, Newborn , Antioxidants/therapeutic use , Endotoxemia/drug therapy , Endotoxemia/physiopathology , Intestinal Mucosa/drug effects , Intestinal Mucosa/enzymology , Lipid Peroxidation , Lipopolysaccharides , Melatonin/therapeutic use , Oxidoreductases/metabolism , Prospective Studies , Random Allocation , Rats , Rats, Wistar , Sepsis/physiopathology
9.
Neurosci Lett ; 406(1-2): 148-51, 2006 Oct 02.
Article in English | MEDLINE | ID: mdl-16905254

ABSTRACT

Although regular physical exercise is beneficial to the body, it is well known that exhaustive exercise causes oxidative stress in muscle. Recent studies suggest that regular moderate physical exercise has the beneficial effects on brain. However, there is little information regarding whether or not exhaustive exercise could generate oxidative stress in brain and the findings are conflicting. The aim of this study was to investigate the effects of exhaustive exercise on thiobarbituric acid reactive substances, as an indicator of lipid peroxidation, in the hippocampus, prefrontal cortex and striatum. Additionally we examined antioxidant enzymes activities, superoxide dismutase and glutathione peroxidase, to assess the effects of reactive oxygen species. Exhaustive exercise did not change superoxide dismutase and glutathione peroxidase enzyme activities and thiobarbituric acid reactive substances levels neither immediately (0 min) nor at 3, 6, 12, 24 and 48 h after the cessation of exercise in the brain. These results indicate that acute exhaustive exercise may not cause significant lipid peroxidation in the hippocampus, prefrontal cortex and striatum during the post-exercise period.


Subject(s)
Brain/metabolism , Exercise Tolerance/physiology , Muscle Fatigue/physiology , Oxidative Stress/physiology , Physical Conditioning, Animal/physiology , Physical Exertion/physiology , Animals , Antioxidants/metabolism , Brain/physiology , Corpus Striatum/metabolism , Corpus Striatum/physiology , Glutathione Peroxidase/metabolism , Hippocampus/metabolism , Hippocampus/physiology , Lipid Peroxidation/physiology , Male , Prefrontal Cortex/metabolism , Prefrontal Cortex/physiology , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/metabolism , Time Factors
10.
Int J Vitam Nutr Res ; 75(4): 243-50, 2005 Jul.
Article in English | MEDLINE | ID: mdl-16229340

ABSTRACT

This study aimed to determine whether high-dose antioxidant supplementation had an impact on the acute exercise effects related to erythrocyte membrane mechanics. Experimental animals (n=32) were divided into four groups as control, exercised, supplemented, and supplemented + exercise. Four-week antioxidant supplementation (vitamin C, vitamin E, and zinc) was applied to experimental animals. Following acute exercise on a motor-driven rodent treadmill, erythrocyte aggregation and deformability, erythrocyte adhesion to endothelial cells, superoxide dismutase (SOD), and glutathione peroxidase activities of the erythrocytes were analyzed. In both supplemented and non-supplemented exercised groups, there was a significant decrease in SOD activities and erythrocyte aggregation, and an increase in adhesion to endothelial cell although there was no change on erythrocyte deformability. There were no differences in the responses to the exercise of supplemented and nonsupplemented rats. The data suggested that high-dose antioxidant supplementation did not alter the effects of acute exercise on erythrocyte membrane mechanics.


Subject(s)
Antioxidants/administration & dosage , Dietary Supplements , Endothelium, Vascular/enzymology , Erythrocyte Membrane/metabolism , Physical Conditioning, Animal , Animals , Cell Adhesion/drug effects , Cells, Cultured , Coculture Techniques , Endothelium, Vascular/cytology , Erythrocyte Aggregation/drug effects , Male , Rats , Rats, Wistar , Superoxide Dismutase/metabolism
11.
Neuro Endocrinol Lett ; 26(4): 419-22, 2005 Aug.
Article in English | MEDLINE | ID: mdl-16135998

ABSTRACT

OBJECTIVES: L-carnitine is a naturally compound widely distributed in the body. It has an antiradical effect and decreases lipid peroxidation. In acute or chronic streptozotocin (STZ)-induced diabetic rats, the pancreatic content of carnitine was found to be significantly lower than nondiabetic group. We investigated the effects of L-carnitine on the development of STZ-induced diabetes in rats, to determine if L-carnitine can prevent the onset of diabetes or reduce the severity of hyperglycemia and this prevention/reduction is associated with the reduction in oxidative stress. SETTING AND DESIGN: The rats were divided into 3 groups: Control, STZ-treated (65 mg/kg intraperitoneally) and L-carnitine (500 mg/kg) and STZ-treated. METHODS: Oxidative stress was assessed by measuring pancreatic thiobarbituric acid reactive substance (TBARS) formation levels using the method of Rehncrona et al, pancreatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities using a Randox test combination (RANSOD and RANDOX). RESULTS: L-carnitine did not prevent the onset of diabetes at this dose. Development of diabetes was associated with an increase in pancreatic TBARS (0.028 +/- 0.008 and 0.046 +/- 0.017 nmol/mg Protein, respectively), and GPx activity (0.067 +/- 0.011 and 0.098 +/- 0.016 U/mg Protein, respectively). MAIN FINDINGS: L-carnitine prevented this increase induced by diabetes; TBARS (0.039 +/- 0.006 nmol/mg Protein) and GPx activity (0.053 +/- 0.011 U/mg Protein). CONCLUSION: These results suggest that L-carnitine exerts anti-oxidative effect in experimental diabetes.


Subject(s)
Antibiotics, Antineoplastic/pharmacology , Carnitine/pharmacology , Diabetes Mellitus, Experimental/metabolism , Streptozocin/pharmacology , Vitamin B Complex/pharmacology , Animals , Antioxidants/pharmacology , Blood Glucose , Drug Interactions , Glutathione Peroxidase/metabolism , Male , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/metabolism
12.
Neurosci Lett ; 385(3): 234-9, 2005 Sep 16.
Article in English | MEDLINE | ID: mdl-15970378

ABSTRACT

It is well known that head trauma induces the cognitive dysfunction resulted from hippocampal damage. In the present study, we aimed to demonstrate the effect of melatonin on hippocampal damage and spatial memory deficits in 7-day-old rat pups subjected to contusion injury. Melatonin was injected intraperitoneally at the doses of 5 or 20 mg/kg of body weight immediately after induction of traumatic injury. Hippocampal damage was examined by cresyl violet staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Spatial memory performance was assessed in the Morris water maze. Melatonin significantly attenuated trauma-induced neuronal death in hippocampal CA1, CA3 regions and dentate gyrus, and improved spatial memory deficits, which was equally effective at doses of 5-20 mg/kg. The present results suggest that melatonin is a highly promising agent for preventing the unfavorable outcomes of traumatic brain injury in young children.


Subject(s)
Brain Injuries/drug therapy , Hippocampus/drug effects , Melatonin/pharmacology , Memory Disorders/prevention & control , Neuroprotective Agents/pharmacology , Animals , Apoptosis/drug effects , Brain Injuries/complications , In Situ Nick-End Labeling , Maze Learning/drug effects , Memory Disorders/etiology , Neurons/drug effects , Neurons/pathology , Rats , Rats, Wistar
13.
Neurosci Lett ; 384(1-2): 98-101, 2005.
Article in English | MEDLINE | ID: mdl-15885903

ABSTRACT

Developing brain is much more sensitive to all kind of stressors than the developed brain. Early maternal deprivation causes some behavioural and physiological effects on rats. After the birth, there is no endocrinological response to stressors between post-natal 4 and 14th days, which is called stress-hyporesponsive period (SHRP) in rats. This hypo-responsiveness is time- and stressor-specific, as some more severe stressors have been shown to induce a stress response. The present study examined the effects of maternal deprivation on oxidative stress in the hippocampus, prefrontal cortex (PFC) and striatum regions of the brain both during and after SHRP of the infant rats. The results showed that maternal deprivation in SHRP increased antioxidant enzyme activities and reduced lipid peroxidation in infant rat brain. However, by the termination of SHRP, maternal deprivation reduced enzyme activities and increased lipid peroxidation. The results indicated that infant brain might be protected in SHRP from maternal deprivation-induced oxidative stress.


Subject(s)
Aging/physiology , Brain/metabolism , Maternal Deprivation , Oxidative Stress/physiology , Animals , Animals, Newborn , Brain/anatomy & histology , Brain/growth & development , Female , Male , Pregnancy , Rats , Rats, Wistar
14.
Neurosci Lett ; 383(3): 241-5, 2005 Aug 05.
Article in English | MEDLINE | ID: mdl-15878799

ABSTRACT

It is known that positive effects of regular aerobic exercise on cognitive functions in humans and also animals; but how to the effects of aerobic exercise in adolescent period is unknown. The present study examined the effects of regular aerobic exercise on spatial memory using the Morris water maze, cell density and apoptosis of hippocampus in adolescent rats. Twenty-two days of age male rats were run on a treadmill for 30 min/session at a speed of 8m/min and 0 degrees slope, five times a week for 8 weeks. The present study showed that exercise induced significant cognitive improvement throughout brain maturation in rats. The number of hippocampal CA1 and CA3 neurons, and gyrus dentatus neurons were significantly increased in the exercised rats. There was no significant difference of CA2 neuron density between exercise and control groups. There was no significantly differences in any groups according to the results of apoptosis that account of TUNEL positive cells. The present results suggest that regular moderate aerobic treadmill exercise benefit in cognitive functions. This result may derive from treadmill exercise-induced increase cell density without altering of apoptosis in the hippocampus and dentate gyrus of adolescent rats.


Subject(s)
Apoptosis/physiology , Hippocampus/cytology , Memory/physiology , Neurons/physiology , Physical Conditioning, Animal/physiology , Space Perception/physiology , Animals , Behavior, Animal , Cell Count/methods , Hippocampus/physiology , In Situ Nick-End Labeling/methods , Male , Maze Learning/physiology , Rats , Rats, Wistar , Reaction Time/physiology , Time Factors
15.
Biol Neonate ; 87(1): 15-8, 2005.
Article in English | MEDLINE | ID: mdl-15334031

ABSTRACT

BACKGROUND: We have previously shown that erythropoietin (Epo) exerts neuroprotective effects in the Rice-Vannucci model of neonatal hypoxic-ischemic brain injury. However, the mechanisms of Epo protection in this model are still unclear. OBJECTIVES: In the present study, we studied the effects of systemically administered Epo on lipid peroxidation levels and antioxidant enzyme (superoxide dismutase and glutathione peroxidase) activities following hypoxic-ischemic brain injury in neonatal rats. METHODS: Seven-day-old Wistar rat pups were subjected to left carotid artery occlusion followed by 2.5 h of hypoxic exposure. Brain lipid peroxidation levels and antioxidant enzyme activities were measured in the injured hemispheres 24 h after the hypoxic-ischemic insult. RESULTS: Hypoxic-ischemic injury significantly increased the thiobarbituric acid-reactive substance levels in the injured hemispheres as compared to the control group. In addition, glutathione peroxidase activity was significantly elevated in Epo-treated animals compared to saline-treated animals and the control group. CONCLUSIONS: These results suggest that Epo exerts neuroprotective effects against hypoxic-ischemic brain injury at least partially via the modulation of antioxidant enzyme activity.


Subject(s)
Animals, Newborn , Erythropoietin/administration & dosage , Glutathione Peroxidase/metabolism , Hypoxia-Ischemia, Brain/drug therapy , Lipid Peroxidation/drug effects , Animals , Brain/enzymology , Brain/metabolism , Hypoxia-Ischemia, Brain/enzymology , Hypoxia-Ischemia, Brain/metabolism , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/analysis
16.
Neurosci Lett ; 354(3): 225-8, 2004 Jan 16.
Article in English | MEDLINE | ID: mdl-14700737

ABSTRACT

Increasing age decreases spatial learning and memory. Spatial learning is coordinated with different brain regions. Since the oxidative damage may play a role in the aging process, including the associated cognitive decline, age-related impairment in spatial learning and memory may be alleviated by antioxidant treatment. The present study examined the effects of the monoamine oxidase B inhibitor L-deprenyl, alone and in combination with estradiol, on spatial memory using the Morris water maze and oxidant stress in aged female rat brains. We demonstrated that co-administration of deprenyl and estradiol caused a synergistic effect on spatial memory. However, use of either deprenyl or estradiol alone increased antioxidant enzyme activities in brain and reduced lipid peroxidation. Therefore, positive effects of deprenyl and estradiol on spatial memory may occur due not only to their antioxidant activities but also to the different actions.


Subject(s)
Brain/drug effects , Estradiol/pharmacology , Memory/drug effects , Neuroprotective Agents/pharmacology , Oxidative Stress/drug effects , Selegiline/pharmacology , Age Factors , Animals , Brain/anatomy & histology , Brain/physiology , Female , Glutathione Peroxidase/metabolism , Maze Learning/drug effects , Rats , Spatial Behavior/drug effects , Thiobarbituric Acid Reactive Substances/metabolism , Time Factors
17.
Eur J Appl Physiol ; 87(2): 141-4, 2002 Jun.
Article in English | MEDLINE | ID: mdl-12070624

ABSTRACT

Although numerous studies have tested the effects of continuous exercise regimens on antioxidant defences, information on the effect of sprint exercise on the antioxidant defence system and lipid peroxidation levels of tissues is scant. The present study was designed to determine the effects of sprint exercise on the lipid peroxidation and antioxidant enzyme system in liver and skeletal muscle during the post-exercise recovery period in untrained mice. Mice performed 15 bouts of exercise, each comprising running on a treadmill for 30 s at 35 m.min(-1) and a 5 degrees slope, with a 10-s rest interval between bouts. They were then killed by cervical dislocation either immediately (0 h), 0.5 h, 3 h or 24 h after completion of the exercise. Their gastrocnemius muscle and liver tissues were quickly removed. It was found that blood lactate levels increased immediately after the exercise, but had returned to control levels by 0.5 h post-exercise. This exercise regimen had no effect on the activity of superoxide dismutase and glutathione peroxidase in these tissues. Levels of muscle thiobarbituric acid reactive substances (TBARS) had increased at 0.5 and 3 h post-exercise, and then returned to control levels by 24 h post-exercise. In conclusion, acute sprint exercise in mice resulted in an increase in TBARS levels in skeletal muscle; no change was observed in the liver. Antioxidant enzyme activities remained unaffected by acute sprint exercise in these tissues.


Subject(s)
Glutathione Peroxidase/metabolism , Liver/metabolism , Muscle, Skeletal/metabolism , Oxidative Stress , Physical Conditioning, Animal/physiology , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/metabolism , Animals , Exercise Test , Lactic Acid/blood , Male , Mice , Mice, Inbred BALB C , Physical Endurance/physiology , Reference Values , Running/physiology
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