Homocysteine decreases extracellular nucleotide hydrolysis in rat platelets.

Hyperhomocysteinemia is an independent risk factor for atherothrombotic disease. Platelets play an important role in cardiovascular disease and release pro-aggregates mediators when activated, such as ADP, a physiological agonist involved in normal hemostasis and thrombosis. NTPDases and 5'-nucleotidase are ecto-enzymes that hydrolyze ATP, ADP and AMP to adenosine playing an important role on blood flow and thrombogenesis by regulating ADP catabolism.

Hyperhomocysteinemia selectively alters expression and stoichiometry of intermediate filament and induces glutamate- and calcium-mediated mechanisms in rat brain during development.

The aim of the present work was to investigate the actions of a chemically induced chronic hyperhomocysteinemia model on intermediate filaments (IFs) of cortical and hippocampal neural cells and explore signaling mechanisms underlying such effects. Results showed that in hyperhomocysteinemic rats the expression of neural IF subunits was affected. In cerebral cortex, glial fibrillary acidic protein (GFAP) expression was donwregulated while in hippocampus high and middle molecular weight neurofilament subunits (NF-H and NF-M, respectively) were up-regulated.

Methylphenidate treatment increases Na(+), K (+)-ATPase activity in the cerebrum of young and adult rats.

Methylphenidate is a central nervous system stimulant used for the treatment of attention-deficit hyperactivity disorder. Na(+), K(+)-ATPase is a membrane-bound enzyme necessary to maintain neuronal excitability. Considering that methylphenidate effects on central nervous system metabolism are poorly known and that Na(+), K(+)-ATPase is essential to normal brain function, the purpose of this study was to evaluate the effect of this drug on Na(+), K(+)-ATPase activity in the cerebrum of young and adult rats.

Exercise effects on activities of Na(+),K(+)-ATPase, acetylcholinesterase and adenine nucleotides hydrolysis in ovariectomized rats.

Hormone deficiency following ovariectomy causes activation of Na(+),K(+)-ATPase and acetylcholinesterase (AChE) that has been related to cognitive deficits in experimental animals. Considering that physical exercise presents neuroprotector effects, we decide to investigate whether exercise training would affect enzyme activation in hippocampus and cerebral cortex, as well as adenosine nucleotide hydrolysis in synaptosomes from cerebral cortex of ovariectomized rats. Female adult Wistar rats were assigned to one of the following groups: sham (submitted to surgery without removal of the ovaries), exercise, ovariectomized (Ovx) and Ovx plus exercise.

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.

Tyrosine administration decreases glutathione and stimulates lipid and protein oxidation in rat cerebral cortex.

Tyrosine levels are abnormally elevated in tissues and physiological fluids of patients with inborn errors of tyrosine catabolism especially in tyrosinemia type II which is caused by deficiency of tyrosine aminotransferase (TAT) and provokes eyes, skin and central nervous system disturbances. We have recently reported that tyrosine promoted oxidative stress in vitro but the exact mechanisms of brain damage in these disorder are poorly known. In the present study, we investigated the in vivo effect of L-tyrosine (500 mg/Kg) on oxidative stress indices in cerebral cortex homogenates of 14-day-old Wistar rats.

Acute homocysteine administration impairs memory consolidation on inhibitory avoidance task and decreases hippocampal brain-derived neurotrophic factor immunocontent: prevention by folic acid treatment.

In the present study, we first investigated the effect of single homocysteine administration on consolidation of short- and long-term memories of inhibitory avoidance task in Wistar rats. We also measured brain-derived neurotrophic factor levels in the hippocampus and parietal cortex of rats. The influence of pretreatment with folic acid on behavioral and biochemical effects elicited by homocysteine was also studied.

Altering and assessing persistence of genetically modified E. coli MG1655 in the large bowel.

One of the primary factors limiting the efficacy of probiotic therapies is short persistence time. Utilizing a novel method for assessment of persistence in the large bowel independent of survival of the organisms in the upper GI tract, we tested whether overexpression of the type 1 pilus, a colonization factor, or the presence of secretory immunoglobulin A (sIgA) might increase the persistence time of a laboratory strain of E. coli in the gut.

Homocysteine induces oxidative stress, inflammatory infiltration, fibrosis and reduces glycogen/glycoprotein content in liver of rats.

Hyperhomocysteinemia has been related to various diseases, including homocystinuria, neurodegenerative and hepatic diseases. In the present study we initially investigated the effect of chronic homocysteine administration on some parameters of oxidative stress, named total radical-trapping antioxidant potential, total antioxidant reactivity, catalase activity, chemiluminescence, thiobarbituric acid-reactive substances, and total thiol content in liver of rats. We also performed histological analysis, evaluating steatosis, inflammatory infiltration, fibrosis, and glycogen/glycoprotein content in liver tissue sections from hyperhomocysteinemic rats.

Hypermethioninemia provokes oxidative damage and histological changes in liver of rats.

In the present study we evaluated the effect of chronic methionine administration on oxidative stress and biochemical parameters in liver and serum of rats, respectively. We also performed histological analysis in liver. Results showed that hypermethioninemia increased chemiluminescence, carbonyl content and glutathione peroxidase activity, decreased total antioxidant potential, as well as altered catalase activity.

Effects of 1,4-butanediol administration on oxidative stress in rat brain: study of the neurotoxicity of gamma-hydroxybutyric acid in vivo.

gamma-Hydroxybutyric acid (GHB) is a naturally occurring compound in the central nervous system (CNS) whose tissue concentration are highly increased in the neurometabolic-inherited deficiency of succinic semialdehyde dehydrogenase (SSADH) activity or due to intoxication. SSADH deficiency is biochemically characterized by increased concentrations of GHB in tissues, cerebrospinal fluid, blood and urine of affected patients. Clinical manifestations are variable and include retardation of mental, motor, and language development along with other neurological symptoms, such as hypotonia, ataxia and seizures, whose underlying mechanisms are practically unknown.

Intracerebroventricular administration of N-acetylaspartic acid impairs antioxidant defenses and promotes protein oxidation in cerebral cortex of rats.

N-acetylaspartic acid (NAA) is the biochemical hallmark of Canavan Disease, an inherited metabolic disease caused by deficiency of aspartoacylase activity. NAA is an immediate precursor for the enzyme-mediated biosynthesis of N-acetylaspartylglutamic acid (NAAG), whose concentration is also increased in urine and cerebrospinal fluid of patients affected by CD. This neurodegenerative disorder is clinically characterized by severe mental retardation, hypotonia and macrocephaly, and generalized tonic and clonic type seizures.

Na+,K+-ATPase activity in an animal model of mania.

We evaluated Na(+),K(+)-ATPase activity in hippocampus of rats submitted to an animal model of mania which included the use of lithium and valproate. In the acute treatment, amphetamine or saline was administered to rats for 14 days, between day 8 and 14, rats were treated with lithium, valproate or saline. In the maintenance treatment, rats were treated with lithium, valproate or saline, between day 8 and 14, amphetamine or saline were administered.

Chronic hyperhomocysteinemia alters antioxidant defenses and increases DNA damage in brain and blood of rats: protective effect of folic acid.

We have previously demonstrated that acute hyperhomocysteinemia induces oxidative stress in rat brain. In the present study, we initially investigated the effect of chronic hyperhomocysteinemia on some parameters of oxidative damage, namely total radical-trapping antioxidant potential and activities of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase), as well as on DNA damage in parietal cortex and blood of rats. We also evaluated the effect of folic acid on biochemical alterations elicited by hyperhomocysteinemia.

NTPDase and 5'-nucleotidase activities in physiological and disease conditions: new perspectives for human health.

Extracellular nucleotides and nucleosides act as signaling molecules involved in a wide spectrum of biological effects. Their levels are controlled by a complex cell surface-located group of enzymes called ectonucleotidases. There are four major families of ectonucleotidases, nucleoside triphosphate diphosphohydrolases (NTPDases/CD39), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPs), alkaline phosphatases and ecto-5'-nucleotidase.

Stroke awareness among low literacy Latinos living in the South Carolina low country.

Background: Little is known about stroke awareness in Latinos with low literacy and living in regions with high stroke rates.

Methods: We surveyed a convenience sample of 60 adult Latinos living in Charleston South Carolina to examine recognition of 4 common warning signs of stroke and appropriate first action to call 9-1-1.

Results: Forty-six percent of the participants recognized sudden facial, arm, or leg weakness; 39% recognized sudden vision loss; 43% recognized sudden trouble walking; 45% recognized sudden headache; 17% recognized all four warning signs.

Influence of ketone bodies on oxidative stress parameters in brain of developing rats in vitro.

Pro-oxidant and antioxidant properties have been found for acetoacetate (AcAc) and beta-hydroxybutyrate (BHB) in peripheral tissues. In the present study we investigated the role of AcAc and BHB at concentrations found in diabetic patients during ketoacidotic crises and in individuals affected by succinyl CoA: 3-oxoacid CoA transferase and acetoacetyl-CoA thiolase deficiencies, disorders clinically characterized by neurological symptoms, on a large number of oxidative stress parameters in fresh cerebral cortex of developing rats. Lipid peroxidation (chemiluminescence and thiobarbituric acid-reactive substances levels), protein oxidative damage (carbonyl formation and sulfhydryl oxidation), 2',7'-dichlorofluorescin diacetate oxidation and the non-enzymatic (total antioxidant reactivity and glutathione levels) and enzymatic (glutathione peroxidase, superoxide dismutase and catalase activities) antioxidant defenses were not changed by doses of BHB and AcAc as high as 25 mM in cortical supernatants under basal conditions.

Intrastriatal injection of hypoxanthine alters striatal ectonucleotidase activities: a time-dependent effect.

The aim of this study was to investigate the effects of intrastriatal injection of hypoxanthine on ectonucleotidase (E-NTPDases and ecto-5'-nucleotidase) activities and expressions in the striatum of rats. The effect of pre-treatment with vitamins E and C on the effects elicited by this oxypurine on enzymatic activities and on thiobarbituric reactive substances (TBARS) was also investigated. The effect of pre-incubation with hypoxanthine on nucleotide hydrolysis in striatum homogenate was also determined.

Optimal control strategy of malaria vector using genetically modified mosquitoes.

The development of transgenic mosquitoes that are resistant to diseases may provide a new and effective weapon of diseases control. Such an approach relies on transgenic mosquitoes being able to survive and compete with wild-type populations. These transgenic mosquitoes carry a specific code that inhibits the plasmodium evolution in its organism.

Ovariectomy impairs spatial memory: prevention and reversal by a soy isoflavone diet.

Since a previous study has shown that ovariectomy impairs spatial memory, we, herein, investigate the influence of pre- and post-treatment with a soy diet on the effects elicited by ovariectomy on spatial memory. In the pre-treatment, 20-day-old female Wistar rats were first fed for 60 days on a standard diet with casein (control) or a soy diet. At 80 days of age, the animals were assigned to one of the following groups: sham (submitted to surgery without removal of ovaries) and ovariectomized.

Tyrosine promotes oxidative stress in cerebral cortex of young rats.

Tyrosine accumulates in inborn errors of tyrosine catabolism, especially in tyrosinemia type II, where tyrosine levels are highly elevated in tissues and physiological fluids of affected patients. In tyrosinemia type II, high levels of tyrosine are correlated with eyes, skin and central nervous system disturbances. Considering that the mechanisms of brain damage in these disorders are poorly known, in the present study, we investigated whether oxidative stress is elicited by l-tyrosine in cerebral cortex homogenates of 14-day-old Wistar rats.

Effects of chronic proline administration on lipid contents of rat brain.

In the present work we investigated the effects of chronic proline administration on ganglioside, cholesterol and phospholipid total contents, as well as on ganglioside profile in cerebral cortex, hippocampus, hypothalamus and cerebellum of rats. We also evaluated the ganglioside content and profile in detergent-soluble and resistant microdomains isolated from synaptic membranes obtained from cerebral cortex. Proline solution (hyperprolinemic) or saline (control) were subcutaneously administered to rats from 6th to 28th post-natal day, according to body weight.

Intrastriatal injection of hypoxanthine impairs memory formation of step-down inhibitory avoidance task in rats.

The aim of this study was to investigate the effects of intrastriatal injection of hypoxanthine, the major compound accumulated in Lesch-Nyhan disease, on performance step-down inhibitory avoidance task in the rat. Male adult Wistar rats were divided in two groups: (1) saline-injected and (2) hypoxanthine-injected group. Treated-group received intrastriatal hypoxanthine solution 30 min before training session (memory acquisition) or immediately after training session (memory consolidation) or 30 before test session (memory retrieval) on step-down inhibitory avoidance task.

Guanidinoacetate administration increases acetylcholinesterase activity in striatum of rats and impairs retention of an inhibitory avoidance task.

Guanidinoacetate methyltransferase deficiency (GAMT-deficiency) is an inborn error of metabolism biochemically characterized by accumulation of guanidinoacetate (GAA) and depletion of creatine; the pathogenesis of brain dysfunction in this disorder is not yet established. In the present study we investigated the effect of intrastriatal administration of GAA on acetylcholinesterase (AChE) activity and on memory acquisition, consolidation and retrieval of step-down inhibitory avoidance task in rat. Results showed that GAA significantly increased AChE activity in rat striatum 30 min (50%) and 3 h (25%), but not 6 h after drug administration.