Protective effect of an adenosine A1 receptor agonist against metamidophos-induced toxicity and brain oxidative stress.

The aim of this study was to evaluate the effects of different doses of an adenosine A(1) selective agonist, phenylisopropyl adenosine (PIA), on metamidophos-induced cholinergic symptoms, mortality, diaphragm muscle necrosis, and brain oxidative stress. A LD(50) dose of metamidophos (20 mg/kg body weight, p.o.) was followed by 1 mL/kg body weight of 0.9% NaCl or 1 mg/kg, 2 mg/kg, 3 mg/kg, or 5 mg/kg body weight PIA ip. Incidence of clinical signs including chewing, salivation, convulsion, and respiratory distress did not show any significant difference among all treatment groups (p > 0.05). PIA was found to be effective to reverse the necrotic changes in diaphragm muscle induced by metamidophos significantly in all groups. Brain Thiobarbituric Acid Reactive Substance (TBARS) levels were significantly increased after the metamidophos poisoning. Administration of 2 to 5 mg/kg body weight PIA decreased brain TBARS levels compared to 0.9% NaCl treated rats. The results indicate that, although different doses of PIA reduced the OP-induced oxidative stress and diaphragm necrosis, a single dose of PIA was not able to recover cholinergic signs and symptoms of metamidophos poisoning.

Antioxidant and antiapoptotic activities of deprenyl and estradiol co-administration in aged rat kidney.

Aging is a progressive degeneration process in living organisms. Deprenyl is an irreversible monoamine-oxidase B inhibitor which has antioxidant, antiapoptotic and neuroprotective effects. Estradiol is also a neuroprotective and antioxidant hormone. The objective of this study was to determine whether the antioxidative effects of deprenyl can suppress apoptotic activity, with or without estradiol, in aged female rat kidney. Wistar Albino female rats were divided into six groups as follows; young (3 months old) control, aged (24 months old) control, aged deprenyl treated, aged estradiol treated, aged deprenyl plus estradiol treated and sham. All rats except for the sham group were injected for 21 days. Determination of oxidative stress parameter was performed spectrophotometrically. To detect apoptotic cells, TUNEL staining and caspase-3 immunohistochemistry were performed. Deprenyl and estradiol administration, alone or in combination, decreased significantly the levels of lipid peroxidation relative to aged control and sham-injected rats. The number of TUNEL positive cells decreased significantly in deprenyl and estradiol-treated rats compared with aged control and sham rats. Deprenyl and estradiol replacement attenuated age-related changes in renal morphology. The results indicate that deprenyl treatment alone, or in combination with estradiol, may modulate age-related apoptotic changes in rat kidney by decreasing oxidative stress.

Acute exhaustive exercise does not alter lipid peroxidation levels and antioxidant enzyme activities in rat hippocampus, prefrontal cortex and striatum.

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.

The effects of regular aerobic exercise in adolescent period on hippocampal neuron density, apoptosis and spatial memory.

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.

The effect of the acute submaximal exercise on thrombin activatable fibrinolysis inhibitor levels in young sedentary males.

Depending on type, duration, and intensity of the exercise, changes occur in hemostasis. In this study, we evaluated the changes in the parameters of coagulation and fibrinolytic systems that happened after the submaximal aerobic exercises by bicycle ergomater. Twelve healthy male participants whose ages were between 21 and 28 have been included. The venous samples have been drawn before the exercise as well as at the 0 th, 15th, and 60th minutes after the submaximal exercise. The values of prothrombin time (PT), active partial thromboplastin time (aPTT), D-dimer, fibrinogen, plasminogen activator inhibitor 1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI) have been measured. Plasminogen activator inhibitor 1 values have shown an insignificant increase after exercise (P = .328), whereas, it has decreased significantly during the resting period (P = .033) Postexercise 15th and 60th minutes TAFI values have decreased significantly comparing to basal and postexercise (0 th minute) values (P = .001). Fibrinolytic system activation is observed after acute submaximal aerobic exercise of sedentary healthy participants.

Effect of acute and chronic exercise on oxidant-antioxidant equilibrium in rat hippocampus, prefrontal cortex and striatum.

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.