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Felipe Dal-Pizzol

Publications and source records attributed to Felipe Dal-Pizzol.

At least 37 records · Page 2Linked to original sources
PubMed2006

Oxidative stress effects on the central nervous system of rats after acute exposure to ultra high frequency electromagnetic fields.

Mobile telephones and their base stations are an important source of ultra high frequency electromagnetic fields (UHF-EMFs; 800-1800 MHz) and their utilization is increasing all over the world. Epidemiological studies have suggested that low energy UHF-EMFs may have biological effects, such as changes in oxidative metabolism after exposure. Therefore, we have investigated the effect of acute UHF-EMF exposure on non-enzymatic antioxidant defense and lipid and protein oxidative damage in the rat frontal cortex and hippocampus. We have used malondialdehyde (MDA) and carbonyl assays to assess lipid and protein oxidative damages, respectively. No changes in lipid and protein damage, and also in non-enzymatic defense were found in frontal cortex or hippocampus. These results suggest that acute UHF-EMF exposure is not able to produce detectable oxidative stress in rats from any age tested. However, more tests using a longer period of exposure and evaluating other tissues are necessary to ensure that there is no health risk associated with the use of mobile phones.

Animals↗
PubMed2006

Lipid peroxidative damage on malathion exposure in rats.

Lipid peroxidation is one of the major outcomes of free radical-mediated injury to tissue in vivo, including the central nervous system (CNS). The aim of this study was to examine whether malathion, a commonly used organophosphorus (OP), might induce oxidative stress in cerebrospinal fluid, blood serum and brain structures in male Wistar rats. Malathion was administered intraperitoneally in the doses of 25, 50, 100 and 150 mg/kg for 28 days. Oxidative damage was determined by measuring the thiobarbituric acid reactive species (TBARS) content, as an index of lipid peroxidation. TBARS concentration in the cerebrospinal fluid (CSF) and brain structures were increased, but a decrease in TBARS concentration in serum was observed. The results of the present study suggest the usefulness of TBARS measurement as a good biomarker in the estimation of malathion-induced oxidative stress affecting CSF and brain structures.

Analysis of Variance↗
PubMed2006

Influence of malathion on acetylcholinesterase activity in rats submitted to a forced swimming test.

The organophosphorus insecticides, including malathion, are used indiscriminately in large amounts, causing environmental pollution and risk to human health. Classically, this toxicity is attributed mainly to the accumulation of acetylcholine (ACh), due to inhibition of acetylcholinesterase (AChE), and consequently overstimulation of the nicotinic and muscarinic receptors. The present study investigated the effects of acute and chronic malathion administration in immobility time in the forced swimming test (FST), open-field test and AChE activity in neural tissue of rats. Malathion was administered intraperitoneally once a day for one day (acute) or for 28 days (chronic) (in both protocols malathion was administered at 25, 50, 100 and 150 mg/kg). No significant effect was seen in immobility time in the FST after acute malathion treatment. The chronic malathion treatment induced an increase in the time of immobility in the FST. Both treatments do not interfere in locomotor activity evaluated in a novel environment. The inhibition of AChE activity was significant in the hippocampus (25, 50, 100 and 150 mg/kg), cortex (100 and 150 mg/kg) and striatum (150 mg/kg) after chronic treatment, but not significantly after acute treatment. These data suggest a possible interaction between increased immobility time in the FST and activation of cholinergic receptors by accumulated ACh subsequent to AChE inhibition.

Acetylcholinesterase↗
PubMed2006

Effects of N-acetylcysteine plus deferoxamine in lipopolysaccharide-induced acute lung injury in the rat.

OBJECTIVES: Interventions that reduce the generation or the effects of reactive oxygen species exert controversial effects in animal models of lung injury, and these could be secondary to the pro-oxidant effects of antioxidants generally by their interaction with iron. We here describe the effects of N-acetylcysteine, deferoxamine, or both in the treatment of acute lung injury induced by intratracheal lipopolysaccharide injection. DESIGN: Prospective, randomized, controlled experiment. SETTING: Animal basic science laboratory. SUBJECTS: Male Wistar rats, weighing 200-250 g. INTERVENTIONS: Rats exposed intratracheally to lipopolysaccharide were treated with N-acetylcysteine (20 mg/kg subcutaneously 3, 6, and 12 hrs after lipopolysaccharide instillation), deferoxamine (20 mg/kg subcutaneously 3 hrs after lipopolysaccharide instillation), N-acetylcysteine (20 mg/kg, 3, 6, and 12 hrs after lipopolysaccharide instillation) plus deferoxamine (20 mg/kg 3 hrs after lipopolysaccharide instillation), or vehicle. MEASUREMENTS AND MAIN RESULTS: Acute lung injury was induced by intratracheal instillation of lipopolysaccharide in Wistar rats. The animals were randomly divided into five groups: group 1, control with instillation of isotonic saline; group 2, lipopolysaccharide treated with saline; group 3, lipopolysaccharide treated with N-acetylcysteine; group 4, lipopolysaccharide treated with deferoxamine; and group 5, lipopolysaccharide treated with N-acetylcysteine plus deferoxamine. Several times after lipopolysaccharide instillation, the rats were killed and a bronchoalveolar lavage was performed to determine thiobarbituric acid reactive species, protein carbonyls, superoxide dismutase and catalase activities, mitochondrial superoxide production (oxidative stress variables), the degree of the alveolar-capillary membrane compromise, and inflammatory infiltration. Samples from the lung were isolated and assayed for oxidative stress variables or histopathologic analyses. N-acetylcysteine plus deferoxamine decreased bronchoalveolar lavage fluid protein, inflammatory cells, oxidative damage variables, and proinflammatory cytokines. N-acetylcysteine plus deferoxamine treatment significantly attenuated lung oxidative damage, mitochondrial superoxide production, and histopathologic alterations after lipopolysaccharide instillation. CONCLUSIONS: Our data provide the first experimental demonstration that N-acetylcysteine plus deferoxamine decreases oxidative stress and mitochondrial dysfunction and limits inflammatory response and alveolar pathology induced by lipopolysaccharide in the rat.

Acetylcysteine↗
PubMed2006

Oxidative variables in the rat brain after sepsis induced by cecal ligation and perforation.

OBJECTIVE: The underlying mechanisms of the changes in mental status, septic encephalopathy, and long-term cognitive symptoms in sepsis survivors have only been defined in part. The present study was undertaken to assess different variables of oxidative stress in several brain structures after cecal ligation and perforation in the rat. DESIGN: Prospective animal study. SETTING: Animal basic science laboratory. SUBJECTS: Male Wistar rats, weighing 250-350 g. INTERVENTIONS: Rats were subjected to cecal ligation and perforation (sepsis group) with saline resuscitation (at 50 mL/kg immediately and 12 hrs after cecal ligation and perforation) or sham operation (control group). MEASUREMENTS AND MAIN RESULTS: Oxidative damage, assessed by the thiobarbituric acid reactive species and the protein carbonyl assays, occurred early (after 6 hrs) in the course of sepsis development in the hippocampus, cerebellum, and cortex. At longer times after sepsis induction (12-96 hrs), there was no evidence of oxidative damage in all analyzed structures. Except for the striatum, earlier in sepsis development (6 hrs) we demonstrated an increase in superoxide dismutase activity without a proportional increase in catalase activity with a consequent increase in the relation of superoxide dismutase/catalase. The balance between these enzymes was restored in the studied structures 12-96 hrs after sepsis induction. CONCLUSIONS: The short-term oxidative damage demonstrated here could participate in the development of central nervous system symptoms during sepsis development, or even septic encephalopathy. The alterations in the superoxide dismutase/catalase relation were temporally related to the occurrence or not of oxidative damage in the central nervous system.

Animals↗
PubMed2006

Increased oxidative stress after repeated amphetamine exposure: possible relevance as a model of mania.

BACKGROUND: Acute mania can be modeled in animals using D-amphetamine (AMPH). Acute AMPH injections are associated with monoamine depletion, loss of neurofilaments and neurite degeneration. However, the precise mechanisms underlying AMPH-induced neurotoxicity are still unclear. Several studies have demonstrated that oxidative stress may play a role in the behavioral and neurochemical changes observed after AMPH administration. METHODS: The effects of a single and repeated injections (seven daily injections) of AMPH administered intraperitonially on locomotion and the production of lipid and protein oxidative markers in rat cortex, striatum and hippocampus were assessed. Locomotion was assessed in an open-field task and markers of oxidative stress were assessed in brain tissue. RESULTS: Both single and repeated injections of AMPH increased protein carbonyl formation in rat brain. Repeated exposure to AMPH induced an additional increase in thiobarbituric acid reactive species in brain tissue. CONCLUSIONS: Longer periods of exposure to AMPH were associated with increased oxidative stress in rat brain. This adds to the notion that repeated manic episodes may be associated with greater brain damage and, therefore, poorer outcomes.

Animals↗
PubMed2006

Effects of lithium and valproate on amphetamine-induced oxidative stress generation in an animal model of mania.

OBJECTIVE: Previous studies have suggested that oxidative stress may play a role in the pathophysiology of bipolar disorder (BD). Moreover, recent studies indicate that lithium and valproate exert neuroprotective effects against oxidative stress. We studied the effects of the mood stabilizers lithium and valproate on amphetamine-induced oxidative stress in an animal model of mania. METHODS: In the first model (reversal treatment), adult male Wistar rats received d-amphetamine or saline for 14 days, and between the 8th and 14th days, they were treated with lithium, valproate or saline. In the second model (prevention treatment), rats were pretreated with lithium, valproate or saline, and between the 8th and 14th days, they received d-amphetamine or saline. We assessed locomotor activity with the open-field task. We measured thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation, as parameters of oxidative stress, and superoxide dismutase (SOD) and catalase (CAT), the major antioxidant enzymes, in the prefrontal cortex and hippocampus. RESULTS: Lithium and valproate reversed (reversal treatment model) and prevented (prevention treatment model) amphetamine-induced hyperactivity and reversed and prevented amphetamine-induced TBARS formation in both experiments. However, the co-administration of lithium or valproate with amphetamine increased lipid peroxidation, depending on the brain region and treatment regimen. No changes in protein carbonyl formation were observed. SOD activity varied with different treatment regimens, and CAT activity increased when the index of lipid peroxidation was more robust. CONCLUSION: Our findings suggest that lithium and valproate exert protective effects against amphetamine-induced oxidative stress in vivo, further supporting the hypothesis that oxidative stress may be associated with the pathophysiology of BD.

Animals↗
PubMed2005

Hypertonic saline and hemorrhagic shock: hepatocellular function and integrity after six hours of treatment.

PURPOSE: The comparison after 6 h of hemorrhagic shock (HS) treatment with NaCl 7.5% (Hypertonic Saline Solution-SSH) or Ringer Lactate (RL) on liver function and integrity. METHODS: Male Wistar rats were submitted to HS (Mean Arterial Pressure-MAP= 45 mmHg) during 60 min and then treated with NaCl 7.5% (SSH, 10% of blood loss, n=8) or Ringer Lactate (RL, 400% of blood loss, n=8). After 6 h rats were anesthetized, hepatic function was assessed by bile flow measurement and liver integrity evaluated by determination of alanine aminotransferase (ALT) and bilirubin activities. RESULTS: There was no difference in MAP between the groups during the whole experiments. Biliary flow showed a significant recovery after SSH treatment (p<0.05), and significant decrease of ALT (p<0.001) and bilirubin levels (p<0.001) in comparison to RL. CONCLUSION: Resuscitation of HS with NaCl 7.5% promoted better recovery of liver function and lesser hepatocellular damage after 6 h of treatment compared to RL. The improvement is very likely related to increased microvascular perfusion provided by small volume resuscitation.

Alanine Transaminase↗
PubMed2005

Gastrin-releasing peptide receptor antagonist effects on an animal model of sepsis.

RATIONALE: Several new therapeutic strategies have been described for the treatment of sepsis, but to date none are related to alterations in the bombesin/gastrin-releasing peptide (GRP) receptor pathways. OBJECTIVES: To determine the effects of a selective GRP receptor antagonist, RC-3095, on cytokine release from macrophages and its in vivo effects in the cecal ligation and puncture (CLP) model of sepsis and in acute lung injury induced by intratracheal instillation of LPS. METHODS: We determined the effects of RC-3095 in the CLP model of sepsis and in acute lung injury induced by intratracheal instillation of LPS. In addition, we determined the effects of RC-3095 on tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-10, and nitric oxide release from activated macrophages. MEASUREMENTS AND MAIN RESULTS: The GRP antagonist attenuated LPS- or CLP-induced TNF-alpha, IL-1beta, and nitric oxide release in cultured macrophages and decreased the mRNA levels of inducible nitric oxide synthase. The administration of RC-3095 (0.3 mg/kg) 6 h after sepsis induction improved survival in the CLP model, and diminished lung damage after intratracheal instillation of LPS. These effects were associated with attenuation on the circulating TNF-alpha and IL-1beta levels and decreased myeloperoxidase activity in several organs. CONCLUSIONS: We report that a selective GRP receptor antagonist attenuates the release of proinflammatory cytokines in vitro and in vivo and improves survival in "established" sepsis. These are consistent with the involvement of a new inflammatory pathway relevant to the development of sepsis.

Animals↗
PubMed2005

Pro-oxidant action of diphenyl diselenide in the yeast Saccharomyces cerevisiae exposed to ROS-generating conditions.

Organoselenium compounds have a potential thiol peroxidase-like activity. Diphenyl diselenide (DPDS) is an electrophilic reagent used in the synthesis of a variety of pharmacologically active organic selenium compounds. Using TRAP assay of chemiluminescense we have shown that diphenyl diselenide clearly possesses a pro-oxidant property. For an investigation on the mechanisms of this property, we used mutant strains of Saccharomyces cerevisiae defective in antioxidant defenses, i.e. in superoxide dismutase, in biosynthesis of glutathione, and the transcription factor yAP-1-lacking yap 1 mutant that cannot activate genes of the oxidative stress response. Exposure of growing cultures to the drug increased cell sensitivity to oxidizing agents. The pro-oxidant effect was independent of the metabolic condition or of the oxidative mutagen tested. N-acetylcysteine, a precursor of glutathione biosynthesis, could neutralize the pro-oxidant effects of diphenyl diselenide by stimulating an increase of endogenous glutathione biosynthesis or by directly binding to the drug. Vitamin E (Trolox), a known antioxidant, was also able to protect S. cerevisiae against the pro-oxidant effect of diphenyl diselenide. In vitro assays showed that diphenyl diselenide interacts non-enzymatically with the thiol group of glutathione.

Antimetabolites, Antineoplastic↗
PubMed2005

Selegiline protects against recognition memory impairment induced by neonatal iron treatment.

Excess of iron in the brain has been implicated in the pathogenesis of several human neurodegenerative diseases, for example Alzheimer's disease and Parkinson's disease. It has been shown that the neonatal period is critical for the establishment of normal iron content in the adult brain. Moreover, it is known that aging alters the cerebral distribution of this metal. We have recently described that neonatal administration of iron severely impaired novel object recognition memory in rats. The aim of the present study was to determine whether selegiline, a monoamine oxidase (MAO) inhibitor known for its neuroprotective properties, could protect rats against cognitive impairment induced by neonatal administration of iron. In the first experiment, male Wistar rats received vehicle (5% sorbitol in water) or iron (10.0 mg/kg) orally from postnatal days 12 to 14 and saline (0.9% NaCl) or selegiline (1.0 or 10.0 mg/kg) intraperitoneally for 21 days, starting 24 h before the first iron dosing. In the second experiment, rats were given either vehicle or iron (10.0 mg/kg) orally from postnatal days 12 to 14 followed by saline or selegiline (1.0 or 10.0 mg/kg) intraperitoneally for 21 days, starting when rats reached adulthood (50th day after birth). Iron-treated rats given selegiline in both doses showed no deficits in recognition memory. Rats receiving iron but no selegiline presented memory deficits. This is the first study reporting the reversion of iron-induced memory impairment, supporting the view that our model can be considered as a useful tool in the search for new drugs with neuroprotective and/or memory enhancing properties.

Animals↗
PubMed2005

Effect of protein malnutrition on redox state of the hippocampus of rat.

The protein malnutrition is a worldwide problem, affecting mainly newborns and children of developing countries. This deficiency reaches the brain in the most critical period of the development. Various consequences are related to this insult, such as memory disturbance, learning, and behavioral impairment. Protein content of the diet plays an important role on antioxidant mechanisms. This study observed the effects of protein malnutrition on rat hippocampus redox state. Wistar rats were separate in four groups, receiving different diets: first group with 25% casein, protein deficient group with 8% casein, and the same two groups supplemented with methionine (0.15%). Diets were isocaloric and were administered since the prenatal period up to the sacrifice. Rats were decapitated at 21 or 75 days old and hippocampus were isolated for measuring the lipoperoxidation by TBARS method, protein oxidative damage by carbonyl (DNPH) levels, and the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). There was significant alterations in the activities of the enzyme SOD, lipoperoxidation, and protein oxidation in hippocampus of 21 and 75 day-old rats fed with 25% of protein with methionine and the groups fed with low levels of protein (8%) both supplemented or not with methionine. Our data suggest that both the content of protein in the diet and the essential amino acid methionine may alter the antioxidant system and the redox state of the brain.

Animal Nutritional Physiological Phenomena↗
PubMed2005

Oxidative parameters differences during non-lethal and lethal sepsis development.

BACKGROUND: The participation of oxidative stress in the development of sepsis is still unclear. The aim of this study was to determine which aspect of antioxidant/pro-oxidant has the major importance in differentiation between non-lethal and lethal sepsis. MATERIALS AND METHODS: Non-lethal and lethal sepsis were induced by cecal ligation and puncture (CLP) in adult Wistar rats, using 18 and 14 gauge needle, respectively. Rats were sacrificed within 12, 24, 48, and 96 h and organs (heart, lung, diaphragm, liver, and kidney) were isolated. The main antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) were measured, as well as protein carbonyls and TBARS, as an index of oxidative damage. RESULTS: Twelve hours after lethal sepsis induction we observed an increase in the oxidative damage in all of the organs studied. In contrast, during non-lethal sepsis, the oxidative damage occurs late in the course of the disease (after 48 h) and the increase in protein carbonyls is of less magnitude when compared to the lethal sepsis. During non-lethal sepsis, in contrast to the lethal sepsis, there is no sustained increase in the SOD/CAT relation. CONCLUSIONS: The present study is the first report showing a different profile of oxidative damage when comparing non-lethal and lethal sepsis. The oxidative damage in proteins seems to be a differential parameter between non-lethal and lethal sepsis. In addition, the SOD/CAT imbalance seems to be an important factor in the oxidative stress during the lethal sepsis, but seems not to happen, in a sustained way, during the non-lethal sepsis.

Animals↗
PubMed2005

Morphological and oxidative alterations on Sertoli cells cytoskeleton due to retinol-induced reactive oxygen species.

Retinol (vitamin A) is involved in several cellular processes, like cell division, differentiation, transformation and apoptosis. Although it has been shown that retinol is a limitant factor for all these processes, the precise mechanisms by which retinol acts are still unknown. In the present study we hypothesised that alterations in the cytoskeleton of Sertoli cells induced by retinol supplementation could indicate an adaptive maintenance of its functions, since it plays an important role in the transformation process that we observed. Previous results demonstrated that Sertoli cells treated with retinol showed an oxidative imbalance, that leads the cell to two phenotypes: apoptosis or transformation. Our group has identified characteristics of Sertoli cells transformed by retinol which results in normal cell functions modification. In the present study the actin filament fluorescence assay and the deformation coefficient showed a modification in the morphology induced by retinol. We also observed an oxidative alteration in isolated cytoskeleton proteins and did not show alterations when these proteins are analyzed by electrophoreses. Our results showed an increase in mitochondria superoxide production and a decrease in nitric oxide levels. All results were partially or completely reverted by co-treatment of the antioxidant Trolox. These findings suggest that the cytoskeleton components suffer individual alterations in different levels and that these alterations generate a global phenotype modification and that these processes are probably ROS dependent. We believe that the results from this study indicate an adaptation of the cytoskeleton to oxidative imbalance since there was not a loss of its function.

Actin Cytoskeleton↗
PubMed2005

Effects of follicle-stimulating hormone and vitamin A upon purinergic secretion by rat Sertoli cells.

Follicle-stimulating hormone (FSH) and vitamin A (retinol) are two of the main regulators of the male reproductive system. Recently, it has been described that extracellular purines can affect some important reproductive-related functions in Sertoli cells and germinative cells, by activating specific purinergic receptors. In this work, we report that both FSH and retinol are able to induce changes in the levels of extracellular purines of cultured rat Sertoli cells. FSH induced an increase in adenosine, mainly caused by enhanced ecto-ATPase activity, while retinol increased xanthine and hypoxanthine levels, and decreased uric acid concentration by an unknown mechanism. These data indicate that purinergic signaling may be involved in the control and/or regulation of some of the reproductive-related actions of these hormones.

Animals↗
PubMed2005

N-acetylcysteine and deferoxamine reduce pulmonary oxidative stress and inflammation in rats after coal dust exposure.

Coal dust inhalation induces oxidative damage and inflammatory infiltration on lung parenchyma. Thus, the aim of this study was to determine whether N-acetylcysteine (NAC) administered alone or in combination with deferoxamine (DFX), significantly reduced the inflammatory infiltration and oxidative damage in the lungs of rats exposed to coal dust. Forty-two male Wistar rats (200-250 g) were exposed to the coal dust (3mg/0.5 mL saline, 3 days/week, for 3 weeks) by intratracheal instillation. The animals were randomly divided into three groups: saline 0.9% (n=8), supplemented with NAC (20mg/kg of body weight/day, intraperitoneal injection (i.p.)) (n=8), and supplemented with NAC (20 mg/kg of body weight/day, i.p.) plus DFX (20 mg/kg of body weight/week) (n=8). Control animals received only saline solution (0.5 mL). Lactate dehydrogenase activity and total cell number were determined in the bronchoalveolar lavage fluid. We determined lipid peroxidation and oxidative protein damage parameters and catalase and superoxide dismutase activities in the lungs of animals. Intratracheal instillation of coal dust in the lungs of rats led to an inflammatory response and induced significant oxidative damage. The administration of NAC alone or in association with DFX reduced the inflammatory response and the oxidative stress parameters in rats exposed to coal dust.

Acetylcysteine↗
PubMed2005

Cognitive impairment in sepsis survivors from cecal ligation and perforation.

OBJECTIVE: Critical illness survivors present long-term cognitive impairment, including problems with memory and learning. We evaluated cognitive performance in rats that survived from sepsis induced by cecal ligation and puncture (CLP). DESIGN: Prospective, controlled experiment. SETTING: Animal basic science laboratory. SUBJECTS: Male Wistar rats, weighing 300-350 g. INTERVENTIONS: The rats underwent CLP (sepsis group) with "basic support" (saline at 50 mL/kg immediately and 12 hrs after CLP plus ceftriaxone at 30 mg/kg and clindamycin at 25 mg/kg 6, 12, and 18 hrs after CLP) or sham-operated (control group). MEASUREMENTS AND MAIN RESULTS: Ten days after surgery, the animals underwent three behavioral tasks: a) inhibitory avoidance task; b) habituation to an open field; and c) continuous multiple-trials step-down inhibitory avoidance task (CMSIA). In the habituation to an open-field task, there were no differences in the number of crossings and rearings. The sepsis group showed significantly decreased performance in latency retention compared with the sham group in inhibitory avoidance. Furthermore, when tested by the habituation to an open-field task, the sepsis group did not show any difference between training and test, indicating memory impairment. In the CMSIA, the sepsis group showed a significant increase in the number of training trials required to reach the acquisition criterion. CONCLUSION: Our data provide the first experimental demonstration that survivors from CLP show learning and memory impairment after complete physical recovery from sepsis.

Animals↗