Physical exercise reverses glutamate uptake and oxidative stress effects of chronic homocysteine administration in the rat.

The influence of physical exercise on the effects elicited by homocysteine on glutamate uptake and some parameters of oxidative stress, namely thiobarbituric acid-reactive substances, 2',7'-dichlorofluorescein (H(2)DCF) oxidation, as well as enzymatic antioxidant activities, superoxide dismutase, catalase and glutathione peroxidase in rat cerebral cortex were investigated. Wistar rats received subcutaneous administration of homocysteine or saline (control) from the 6th to 29th day of life. The physical exercise was performed from the 30th to 60th day of life; 12 h after the last exercise session animals were sacrificed and the cerebral cortex was dissected out.

Chronic methylphenidate administration alters antioxidant defenses and butyrylcholinesterase activity in blood of juvenile rats.

Methylphenidate (MPH), a psychostimulant that affects both dopaminergic and noradrenergic systems, is one of the most frequently prescribed treatments for attention-deficit hyperactivity disorder. The present study investigated the effects of chronic administration of MPH on some parameters of oxidative stress, as well as on butyrylcholinesterase (BuChE) activity in blood of young rats. Rats received intraperitoneal injections of MPH (2.

Acute hyperhomocysteinemia alters the coagulation system and oxidative status in the blood of rats.

In the present study, we investigated the effect of the acute administration of homocysteine (Hcy) on parameters of the coagulation system, as well as fibrinogen and nitrite levels in the blood of rats. In addition, we evaluated the effect of acute hyperhomocysteinemia on thiobarbituric acid-reactive substances in plasma and on antioxidant enzymes activities (superoxide dismutase, catalase, and gluthatione peroxidase) in the erythrocytes of rats. Wistar rats, aged 29 days, received a single subcutaneous dorsal injection of saline (control) or Hcy (0.

Development of an animal model for chronic mild hyperhomocysteinemia and its response to oxidative damage.

The purpose of this study was to develop a chronic chemically induced model of mild hyperhomocysteinemia in adult rats. We produced levels of Hcy in the blood (30μM), comparable to those considered a risk factor for the development of neurological and cardiovascular diseases, by injecting homocysteine subcutaneously (0.03μmol/g of body weight) twice a day, from the 30th to the 60th postpartum day.

Chronic variable stress induces oxidative stress and decreases butyrylcholinesterase activity in blood of rats.

Depressive disorders, including major depression, are serious and disabling, whose mechanisms are not clearly understood. Since life stressors contribute in some fashion to depression, chronic variable stress (CVS) has been used as an animal model of depression. In the present study we evaluated some parameters of oxidative stress [thiobarbituric acid reactive substances (TBARS), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)], and inflammatory markers (interleukin 6, C reactive protein, tumor necrosis factor-alpha and nitrites), as well as the activity of butyrylcholinesterase in blood of rats subjected to chronic stress.

Proline impairs energy metabolism in cerebral cortex of young rats.

In the present study we investigated the effect of acute hyperprolinemia on some parameters of energy metabolism, including the activities of succinate dehydrogenase and cytocrome c oxidase and (14)CO(2) production from glucose and acetate in cerebral cortex of young rats. Lipid peroxidation determined by the levels of thiobarbituric acid-reactive substances, as well as the influence of the antioxidants alpha-tocopherol plus ascorbic acid on the effects elicited by Pro on enzyme activities and on the lipid peroxidation were also evaluated. Wistar rats of 12 and 29 days of life received one subcutaneous injection of saline or proline (12.

Protective effect of antioxidants on cerebrum oxidative damage caused by arginine on pyruvate kinase activity.

We have demonstrated that acute arginine administration decreases antioxidant defenses and compromises enzymes of respiratory chain in rat brain. In this study we evaluated in vivo and in vitro effect of arginine on pyruvate kinase activity, as well as its effect on an important parameter of oxidative stress namely thiobarbituric acid-reactive substances (TBA-RS) in cerebrum of rats. We also tested the influence of antioxidants, namely alpha -tocopherol plus ascorbic acid on the effects elicited by arginine in order to investigate the possible participation of free radicals on the effects of arginine on these parameters.

Protective effect of nitric oxide synthase inhibition or antioxidants on brain oxidative damage caused by intracerebroventricular arginine administration.

We have previously demonstrated that acute arginine administration induces oxidative stress and compromises energy metabolism in rat hippocampus. In the present study, we initially investigated the effect of intracerebroventricular infusion of arginine (0.1, 0.

Proline promotes decrease in glutamate uptake in slices of cerebral cortex and hippocampus of rats.

In the present study we first investigated the in vitro and in vivo effects of proline on glutamate uptake in the cerebral cortex and hippocampus slices of rats. The action of alpha-tocopherol and/or ascorbic acid on the effects elicited by administration of proline was also evaluated. For in vitro studies, proline (30.

Inhibition of CO(2) production from glucose by arginine in brain slices of rats.

In the present study we evaluated the in vivo effect of arginine on CO(2) production from glucose in a medium with physiological and high extracellular K(+) concentrations. We also tested the influence of the nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), on the effects elicited by arginine in order to investigate the possible participation of NO and/or its derivatives on the effects of arginine on CO(2) production from glucose. Sixty-day-old rats were treated with a single intraperitoneal injection of saline (control; group I), arginine (0.

Proline induces alterations on nucleotide hydrolysis in synaptosomes from cerebral cortex of rats.

In the present study we investigated the in vivo (acute and chronic) and in vitro effects of proline on NTPDase and 5'-nucleotidase activities in synaptosomes obtained from cerebral cortex of rats. For acute administration, 29-day-old rats received one subcutaneous injection of proline (18.2 micromol/g body weight) or an equivalent volume of 0.

NTPDase and 5'-nucleotidase activities of synaptosomes from hippocampus of rats subjected to hyperargininemia.

ATP is an important excitatory neurotransmitter and adenosine acts as a neuromodulatory structure inhibiting neurotransmitters release in the central nervous system. Since the ecto-nucleotidase cascade that hydrolyzes ATP to adenosine is involved in the control of brain functions and previous studies realized in our laboratory have recently reported that acute administration of Arg decreases the NTPDase and 5'-nucleotidase activities of rat blood serum, in the present study we investigated the effect of arginine administration on NTPDase and 5'-nucleotidase activities by synaptosomes from hippocampus of rats. First, sixty-days-old rats were treated with a single or a triple intraperitoneal injection of arginine (0.

Arginine administration reduces creatine kinase activity in rat cerebellum.

In the present study were evaluated the in vivo effects of arginine administration on creatine kinase (CK) activity in cerebellum of rats. We also tested the influence of antioxidants, namely alpha-tocopherol and ascorbic acid and the nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), on the effects elicited by Arg in order to investigate the possible participation of nitric oxide (NO) and/or its derivatives peroxynitrite (ONOO(-)) and other/or free radicals on the effects of arginine on CK activity. Sixty-day-old rats were treated with a single i.

Proline reduces brain cytochrome c oxidase: prevention by antioxidants.

In the present study, we initially investigated the in vivo (acute and chronic) and in vitro effects of proline on cytochrome c oxidase (complex IV) activity in rat cerebral cortex to test the hypothesis that proline might alter energy metabolism and that this alteration could be provoked by oxidative stress. The action of alpha-tocopherol and ascorbic acid on the effects produced by proline was also evaluated. For acute administration, 29- and 60-day-old rats received one subcutaneous injection of proline (18.

Proline induces alterations in nucleotide hydrolysis in rat blood serum.

The main objective of the present study was to evaluate the in vivo (acute and chronic) and in vitro effects of proline on serum nucleotide hydrolysis. For acute administration, 29-day-old rats received one subcutaneous injection of proline (18.2 (micromol/g body weight) or an equivalent volume of 0.

Alpha-tocopherol and ascorbic acid administration prevents the impairment of brain energy metabolism of hyperargininemic rats.

1. We have previously demonstrated that arginine administration induces oxidative stress and compromises energy metabolism in rat hippocampus. In the present study we initially investigated the influence of pretreatment with alpha-tocopherol and ascorbic acid on the effects produced by arginine on hippocampus energy metabolism.

Arginine administration decreases cerebral cortex acetylcholinesterase and serum butyrylcholinesterase probably by oxidative stress induction.

In the present study we investigated the action of vitamins E and C on the inhibition of acetylcholinesterase and butyrylcholinesterase activities provoked by arginine in cerebral cortex and serum of 60-day-old rats. Animals were pretreated for 1 week with daily intraperitoneal administration of saline (control) or vitamins E (40 mg/kg) and C (100 mg/kg). Twelve hours after the last injection, animals received one injection of arginine (0.

Reduction of energy metabolism in rat hippocampus by arginine administration.

Hyperargininemia is an inherited metabolic disease biochemically characterized by tissue accumulation of arginine. Mental retardation and other neurological features are common symptoms in hyperargininemic patients. Considering that the underlying mechanisms of brain damage in this disease are poorly established, in this work we investigated the effect of arginine administration to adult Wistar rats on some parameters of energy metabolism (CO(2) production, glucose uptake, lactate release and the activities of succinate dehydrogenase, complexes II and IV of the respiratory chain) in rat hippocampus.

Brain energy metabolism is compromised by the metabolites accumulating in homocystinuria.

Homocystinuria is an inborn error of metabolism caused by severe deficiency of cystathionine beta-synthase activity. It is biochemically characterized by tissue accumulation of homocysteine (Hcy) and methionine (Met). Homocystinuric patients present a variable degree of neurological dysfunction whose pathophysiology is poorly understood.

Proline reduces acetylcholinesterase activity in cerebral cortex of rats.

In the present study we investigated the in vivo and in vitro effect of proline (Pro) on acetylcholinesterase (AChE) activity in rat cerebral cortex. The action of vitamins E and C on the effects produced by Pro was also tested. Twelve-day-old rats received one s.

Arginine administration reduces catalase activity in midbrain of rats.

Hyperargininemia is an inherited neurometabolic disorder biochemically characterized by tissue accumulation of arginine and clinically by severe neurological symptoms whose pathophysiology is poorly understood. In the present study we investigated the effect of arginine administration on the antioxidant enzyme activities catalase, glutathione peroxidase and superoxide dismutase in rat midbrain. We also tested the effect of L-NAME on the effects produced by Arg.