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Gisele Agustini Lovatel,
Viviane Rostirola Elsner,
Karine Bertoldi,
Cláudia Vanzella,
Felipe Dos Santos Moysés,
Adriana Vizuete,
Christiano Spindler,
Laura Reck Cechinel,
Carlos Alexandre Netto,
Alysson Renato Muotri, Ionara Rodrigues Siqueira
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ABSTRACT: It has been described that exercise can modulate both inflammatory response and epigenetic modifications, although the effect of exercise on these parameters during the normal brain aging process yet remains poorly understood. Here, we investigated the effect of aging and treadmill exercise on inflammatory and epigenetic parameters specifically pro and anti-inflammatory cytokines levels, activation of NF-kB and histone H4 acetylation levels in hippocampus from Wistar rats. Additionally, we evaluated aversive memory through inhibitory avoidance task. Rats of 3 and 20 months of age were assigned to non-exercised (sedentary) and exercised (running daily for 20 min for 2 weeks) groups. The effect of daily forced exercise in the treadmill was assessed. The levels of inflammatory and epigenetic parameters were determined 1 h, 18 h, 3 days or 7 days after the last training session of exercise. It was observed an age-related decline on aversive memory, as well as aged rats showed increased hippocampal levels of inflammatory markers, such as TNFα, IL1-β and NF-kB and decreased IL-4 levels, an anti-inflammatory cytokine. Moreover, lower levels of global histone H4 acetylation were also observed in hippocampi from aged rats. Interestingly, there was a significant correlation between the biochemical markers and the inhibitory avoidance test performance. The forced exercise protocol ameliorated aging-related memory decline, decreased pro-inflammatory markers and increased histone H4 acetylation levels in hippocampi 20-months-old rats, while increased acutely IL-4 levels in hippocampi from young adult rats. Together, these results suggest that an imbalance of inflammatory markers might be involved to the aging-related aversive memory impairment. Additionally, our exercise protocol may reverse aging-related memory decline through improving cytokine profile.
Neurobiology of Learning and Memory 01/2013; · 3.42 Impact Factor
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ABSTRACT: Regular exercise improves learning and memory, including during aging process. Interestingly, the imbalance of epigenetic mechanisms has been linked to age-related cognitive deficits. However, studies about epigenetic alterations after exercise during the aging process are rare. In this preliminary study we investigated the effect of aging and exercise on DNA methyltransferases (DNMT1 and DNMT3b) and H3-K9 methylation levels in hippocampus from 3 and 20-months aged Wistar rats. The animals were submitted to two exercise protocols: single session or chronic treadmill protocol. DNMT1 and H3-K9 methylation levels were decreased in hippocampus from aged rats. The single exercise session decreased both DNMT3b and DNMT1 levels in young adult rats, without any effect in the aged group. Both exercise protocols reduced H3-K9 methylation levels in young adult rats, while the single session reversed the changes on H3-K9 methylation levels induced by aging. Together, these results suggest that an imbalance on DNMTs and H3-K9 methylation levels might be linked to the brain aging process and that the outcome to exercise seems to vary through lifespan.
Experimental gerontology 11/2012; · 3.34 Impact Factor
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ABSTRACT: The decomposition of solid waste in landfill is responsible for the formation of leachate, a dark liquid with an unpleasant odor; studies investigating its toxicity on mammals are rare. Oxidative stress has been considered as an important biochemical mechanism of the toxicity of several xenobiotics. The aim of this study was to evaluate the effects of landfill leachate on oxidative parameters in striatum, hippocampus and liver homogenates of mice and rats. In order to propose a clean technology for the treatment of leachate, we also investigated the effects of landfill leachate submitted to photoelectrooxidation process (PEO). The homogenates of cerebral structures and liver of Swiss albino mice and Wistar rats were incubated with different concentrations of non-PEO landfill leachate and PEO-treated landfill leachate. After the incubation, the levels of free radicals, determined by 2',7'-dichlorofluorescein diacetate probe, and the lipoperoxidation, quantified by the thiobarbituric acid reactive substances, were evaluated. There was an increase on the levels of free radicals in striatum of both mice and rats when exposed to non-PEO leachate. Moreover, PEO-treated leachate increased the lipoperoxidation in striatum homogenates from rodents. However, both leachates did not alter any of the parameters evaluated in the hippocampus. In the liver, the incubation with leachates induced an augment on levels of free radicals only in samples of mice. In addition, PEO-treated leachate increased the lipoperoxidation indexes in the liver of mice and rats. These results suggest that the landfill leachate can induce an oxidative stress state in the liver and the striatum of rodents. Additionally, the PEO process was unable to efficiently alter the toxic compounds of landfill leachate.
Ecotoxicology and Environmental Safety 08/2012; 84:319-24. · 2.29 Impact Factor
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Gisele Agustini Lovatel,
Karine Bertoldi,
Viviane Rostirola Elsner,
Cláudia Vanzella,
Felipe Dos Santos Moysés,
Christiano Spindler,
Vinicius Rafael Funck,
Leticia Meier Pereira,
Clarissa Vasconcelos de Oliveira,
Mauro Schneider Oliveira,
Carlos Alexandre Netto, Ionara Rodrigues Siqueira
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ABSTRACT: Exercise induces brain function adaptations and improves learning and memory; however the time window of exercise effects has been poorly investigated. Studies demonstrate an important role for cyclooxygenase-2 (COX-2) pathway function in the mechanisms underlying memory formation. The aim of present work was to investigate the effects of treadmill exercise on aversive memory and COX-2, PGE(2) and E-prostanoid receptors contents in the rat hippocampus at different time points after exercise has ended. Adult male Wistar rats were assigned to non-exercised (sedentary) and exercised (running daily for 20min, for 2weeks) groups. The inhibitory avoidance task was used to assess aversive memory and the COX-2, PGE(2) and E-prostanoid receptors (EP1, EP2, EP3 and EP4) levels were determined 1h, 18h, 3days or 7days after the last training session of treadmill exercise. The step down latency in the inhibitory avoidance, COX-2 and EP4 receptors levels were acutely increased by exercise, with a significant positive correlation between aversive memory performance and COX-2 levels. Increased EP2 content decreased PGE(2) levels were observed 7days after the last running session. The treadmill exercise protocol facilitates inhibitory avoidance memory and induces time-dependent changes on COX-2 pathways function (COX-2, PGE(2) and EP receptors).
Neurobiology of Learning and Memory 06/2012; 98(2):182-7. · 3.42 Impact Factor
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ABSTRACT: The aim of the present study was to evaluate the neuroprotective effects of environmental enrichment (EE), assessed by cognitive activity in the Morris water maze, and on brain oxidative status, through measurement of macromolecules damage, lipid peroxidation levels, total cellular thiols and antioxidant enzymes in hippocampus, striatum and cerebral cortex.
Adult male Wistar rats were submitted to the modified permanent bilateral occlusion of the common carotid arteries (2VO) method, with right common carotid artery being first occluded, and tested three months after the ischemic event. Cognitive and physical stimulation, named Environmental Enrichment, consisted of one-hour sessions run 3 times per week during 12weeks, following two different stimulation protocols: pre-ischemia and pre+post-ischemia. Rats were then tested for both reference and working spatial memory tasks in the water maze and later sacrificed for measurement of oxidative stress parameters.
A significant cognitive deficit was found in both spatial tasks after hypoperfusion; this effect was reversed in the 2VO enriched group. Moreover, hippocampal oxidative damage and antioxidant enzyme activity were decreased by environmental enrichment.
These results suggest that both stimulation protocols exert a neuroprotective effect against the cognitive impairment and the reduction of biomarkers for oxidative damage caused by chronic cerebral hypoperfusion.
Life sciences 06/2012; 91(1-2):29-36. · 2.56 Impact Factor
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ABSTRACT: Acetylcholinesterase (AChE), an enzyme that hydrolyses acetylcholine (ACh) at cholinergic synapses, is a target for pesticides and its inhibition by organophosphates leads to paralysis and death of arthropods. It has been demonstrated that the n-hexane extract of Calea serrata had acaricidal activity against larvae of Rhipicephalus (Boophilus) microplus and Rhipicephalus sanguineus. The aim of the present study was to understand the mechanism of the acaricidal action of C. serrata n-hexane extract are specifically to investigate the in vitro anticholinesterase activity on larvae of R. microplus and in brain structures of male Wistar rats. The n-hexane extract significantly inhibited in vitro acetylcholinesterase activity in R. microplus larvae and rat brain structures. The results confirm that inhibition of acetylcholinesterase is a possible mechanism of action of hexane extract at C. serrata.
Veterinary Parasitology 04/2012; 189(2-4):322-6. · 2.58 Impact Factor
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ABSTRACT: Neonatal hypoxic-ischemic encephalopathy (HI) is a major cause of nervous system damage and neurological morbidity. Perinatal malnutrition affects morphological, biochemical and behavioral aspects of neural development, including pathophysiological cascades of cell death triggered by ischemic events, so modifying resulting brain damage. Female Wistar rats were subjected to protein restriction during pregnancy and lactation (control group: 25% soybean protein; malnourished group: 7%). Seven days after delivery (PND7), their offspring were submitted to unilateral cerebral HI; rats were then tested for sensorimotor (PND7 and PND60) and memory (PND60) functions. Offspring of malnourished mothers showed marked reduction in body weight starting in lactation and persisting during the entire period of observation. There was a greater sensorimotor deficit after HI in malnourished (M) animals, in righting reflex and in home bedding task, indicating an interaction between diet and hypoxia-ischemia. At PND60, HI rats showed impaired performance when compared to controls in training and test sessions of rota-rod task, however there was no effect of malnutrition per se. In the open field, nourished HI (HI-N) presented an increase in crossings number; this effect was not present in HI-M group. Surprisingly, HI-M rats presented a better performance in inhibitory avoidance task and a smaller hemispheric brain damage as compared to HI-N animals. Our data points to a possible metabolic adaptation in hypoxic-ischemic animals receiving protein malnutrition during pregnancy and lactation; apparently we observed a neuroprotective effect of diet, possibly decreasing the brain energy demand, under a hypoxic-ischemic situation.
Brain research 02/2012; 1438:85-92. · 2.46 Impact Factor
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ABSTRACT: Physical activity impacts functional recovery following stroke in humans, however its effects in experimental animals submitted to chronic cerebral hypoperfusion have not been investigated. The aim of this study was to evaluate the therapeutic potential of exercise, as assessed by cognitive activity in the Morris water maze and the brain oxidative status, through measurement of macromolecules damage, TBARS levels and total cellular thiols, as well as antioxidant enzymes in hippocampus, striatum and cerebral cortex. Adult male Wistar rats were submitted to the modified permanent bilateral occlusion of the common carotid arteries (2VO) method, with right common carotid artery being first occluded, and tested 3 months after the ischemic event. The effects of three different exercise protocols were examined: pre-ischemia, post-ischemia and pre+post-ischemia. Physical exercise consisted of sessions of 20-min, 3 times per week during 12 weeks (moderate intensity). Rats were submitted to cognitive assessment, in both reference and working spatial memory and after the last testing session were sacrificed to have oxidative stress parameters determined. Hypoperfusion caused a significant cognitive deficit in both spatial water maze tasks and this effect was reversed in rats receiving exercise protocol post and pre+post the ischemic event. Moreover, forced regular treadmill exercise regulated oxidative damage and antioxidant enzyme activity in the hippocampus. These results suggest that physical exercise protects against cognitive and biochemical impairments caused by chronic cerebral hypoperfusion.
Neurobiology of Learning and Memory 01/2012; 97(1):90-6. · 3.42 Impact Factor
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ABSTRACT: The scope of this cross-sectional study was to assess a possible link between contact with pesticides and the prevalence of chronic disease in the rural population in the south of Brazil. Three municipalities were randomly chosen. The sample selected was recruited over three months (2005) and was composed of 298 subjects of both sexes, between 18 and 65 years of age, who frequented public or private pharmacies for the purchase of medication. Data obtained by means of structured interviews revealed that 68.4% of those interviewed worked in rural activities, and 74.8% of these were members of families working in agriculture with contact with pesticides. The average age was 51+16.5 years of age for the interviewees with contact with pesticides and 50+17.9 years for those without contact. The sample was composed of 36.2% of men, and 57.7% of the individuals had more than four years of education. Direct or indirect contact with pesticides was associated with the report of several diseases, with neurological and oral diseases being the most prevalent. There was a link with painful conditions and individuals with contact with pesticides reported twice as many diseases. The data corroborate the literature and draw attention to the need for promoting measures to protect the health of the rural population.
Ciencia & saude coletiva 08/2011; 16(8):3519-28.
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ABSTRACT: The leather industry is a major producer of wastewaters and releases large quantities of many different chemical agents used in hide processing into the environment. Since the central nervous system is sensitive to many different contaminants, our aim was to investigate the neurobehavioral effects of exposure of mice to tannery effluents using animal models of depression and anxiety, namely forced swim and elevated plus-maze. In order to propose a clean technology for the treatment of this effluent, we also investigated the exposure of mice to effluents treated by photoelectrooxidation process (PEO). Adult male Swiss albino mice (CF1 strain) were given free access to water bottles containing an effluent treated by a tannery (non-PEO) or PEO-treated tannery wastewater (0.1 and 1% in drinking water). Exposure to tannery wastewater induced behavioural changes in the mice in elevated plus-maze. Exposure to non-PEO 1% decreased the percentage of time spent in the open arms, indicating anxiety-like behaviour. Exposure to tannery wastewater did not alter immobility time in the forced swim test, suggesting that tannery effluents did not induce depression-like behaviour in the mice. These behavioural data suggest that non-PEO tannery effluent has an anxiogenic effect, whereas PEO-treated tannery effluents do not alter anxiety levels.
Neurotoxicology and Teratology 06/2011; 33(4):481-4. · 2.98 Impact Factor
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Ionara Rodrigues Siqueira,
Viviane Rostirolla Elsner,
Marina Concli Leite,
Cláudia Vanzella,
Felipe dos Santos Moysés,
Christiano Spindler,
Graça Godinho,
Cíntia Battú,
Suzana Wofchuk,
Diogo Onofre Souza,
Carlos Alberto Gonçalves,
Carlos Alexandre Netto
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ABSTRACT: Ascorbate, an intracellular antioxidant, has been considered critical for neuronal protection against oxidant stress, which is supported especially by in vitro studies. Besides, it has been demonstrated an age-related decrease in brain ascorbate levels. The aims of the present study were to investigate ascorbate uptake in hippocampal slices from old Wistar rats, as well as its neuroprotective effects in in vitro and in vivo assays. Hippocampal slices from male Wistar rats aged 4, 11 and 24 months were incubated with radiolabeled ascorbate and incorporated radioactivity was measured. Hippocampal slices from rats were incubated with different concentrations of ascorbate and submitted to H(2)O(2)-induced injury, cellular damage and S100B protein levels were evaluated. The effect of chronic administration of ascorbate on cellular oxidative state and astrocyte biochemical parameters in the hippocampus from 18-months-old Wistar rats was also studied. The ascorbate uptake was decreased in hippocampal slices from old-aged rats, while supplementation with ascorbate (2 weeks) did not modify any tested oxidative status in the hippocampus and the incubation was unable to protect hippocampal slices submitted to oxidative damage (H(2)O(2)) from old rats. Our data suggest that the decline of ascorbate uptake might be involved in the brain greater susceptibility to oxidative damage with advancing age and both in vitro and vivo assays suggest that ascorbate supplementation did not protect hippocampal cells.
Neurochemistry International 01/2011; 58(4):527-32. · 2.86 Impact Factor
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ABSTRACT: Regular and moderate exercise has been considered as an interesting neuroprotective strategy. However, the molecular mechanisms by which physical exercise alters brain function are unclear. Purinergic signaling seems to modulate the pathophysiology of ischemic neuronal damage, since it has been described a neuroprotective activity of adenosine and a dual role of ATP. In the present study, we investigated the effect of daily moderate intensity exercise on ectonucleotidase activities in synaptosomes from hippocampus and the soluble nucleotidases from blood serum of rats. Adult male Wistar rats were assigned to non-exercised (sedentary) group and exercised during 20-min sessions on different programs. The effects of physical activity on hydrolysis of ATP, ADP and AMP were assayed in the synaptosomal fraction obtained from the hippocampus and serum approximately 16 h after the last training session. Our data demonstrated that a neuroprotective exercise protocol, daily 20 min of training in treadmill during 2 weeks, diminished significantly the ADP hydrolysis and there is a trend to reduce the ATP hydrolysis in both hippocampal synaptosomes and blood serum of rats. We suggest that the neuroprotective exercise protocol may modulate nucleotidase activities.
Brain research 12/2009; 1316:173-80. · 2.46 Impact Factor
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ABSTRACT: Environmental enrichment recovers memory deficits without affecting atrophy of the hippocampus adult rats submitted to neonatal hypoxia-ischemia (HI). The present study was designed to investigate whether the modulation of brain oxidative status and/or BDNF content, as assessed in adulthood, are involved with the functional neuroprotection caused by environmental enrichment in animals receiving neonatal HI. Male Wistar rats, in the 7th postnatal day, were submitted to the Levine-Rice model of neonatal hypoxia-ischemia, comprising permanent occlusion of the right common carotid artery and a 90 min period of hypoxia (8% O(2)-92% N(2)). Starting 2 weeks after the HI event, animals were stimulated by the enriched environment (1 h/day for 9 weeks). Rats were sacrificed approximately 24 h after the end of enrichment period and some oxidative stress parameters, specifically the free radical levels, macromolecules damage and superoxide dismutase activity, in hippocampus and frontal cortex samples were determined. BDNF levels were also measured in the same encephalic structures. Indexes of macromolecules damage, TBARS levels and total cellular thiols, as well as free radical levels were unchanged in both studied structures. An increased SOD activity in the right hippocampus of HI group maintained in standard environment was found, this effect was reversed in HI enriched group. Moreover, BDNF levels were increased only in the hippocampus of non-stimulated HI group. These results suggest that the environmental enrichment protocol bearing cognitive protection is not associated to increases in BDNF expression nor SOD activity in hippocampus of the rats, as assessed in adulthood, submitted to neonatal hypoxia-ischemia.
Brain research 12/2008; 1247:188-95. · 2.46 Impact Factor
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ABSTRACT: Daily moderate intensity exercise (2 weeks of 20 min/day of treadmill training), which reduces damage to hippocampal slices from rats submitted to in vitro ischemia, did not modify oxidative stress parameters in the hippocampus nor the brain-derived neurotrophic factor (BDNF) levels in different brain regions. The aim was to investigate whether the modulation of hippocampal oxidative status and/or brain BDNF content is involved in exercise-induced neuroprotection. Wistar rats were submitted to daily exercise in the treadmill and were sacrificed approximately 16 h after the last treadmill running. Some several oxidative stress parameters were determined, specifically the free radical levels, the macromolecule damage, the total reactive antioxidant potential and reactivity levels, which represent the total antioxidant capacity, in the hippocampus. In addition, BDNF levels in different rat cerebral regions (hippocampus, cortex, striatum, and the cerebellum) were measured by ELISA. The used exercise protocol did not affect any oxidative stress parameters studied in the hippocampus, suggesting that it does not cause a significant oxidative stress nor induce adaptations of the cellular antioxidant system. Treadmill training also did not change the BDNF content in brain areas studied. Considering the fact that this exercise protocol have been shown to be neuroprotective, we might speculate that BDNF levels and oxidative status may not be directly involved with the mechanisms of exercise-induced neuroprotection after ischemia.
Brain Research 02/2008; 1188:182-8. · 2.73 Impact Factor
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ABSTRACT: We have recently demonstrated that high intensity training exercise exacerbates brain damage, while a moderate intensity (2 weeks of 20 min/day of treadmill training) reduces the injury caused by in vitro ischemia, oxygen and glucose deprivation (OGD), to hippocampal slices from Wistar rats. In the present paper, the effect of different running programs on severity of ischemic OGD lesion was examined, by the evaluation of three protocols designed to simulate exercise conditions common to humans: one or three 20-min sessions per week, during 12 weeks (moderate intensity), and two 20-min daily sessions for 3 weeks. OGD caused an increase of lactate dehydrogenase (LDH) release into the incubation media, a marker of tissue necrosis, and a decline of cell viability, as assessed by the decrease of mitochondrial dehydrogenase activity (MTT method). Moderate exercise, three times a week during 12-week treadmill training, decreased LDH release after OGD, while one weekly session and 3 weeks of two daily sessions did not affect OGD-induced LDH released. No exercise protocol evaluated altered MTT reduction. Our data support the hypothesis that moderate intensity exercise reduces hippocampal susceptibility to in vitro ischemia.
Brain Research 08/2007; 1157:121-5. · 2.73 Impact Factor
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ABSTRACT: We evaluated the effects of two levels of daily forced exercise intensity (moderate and high) in the treadmill over cell susceptibility to oxygen and glucose deprivation (OGD) in hippocampal slices from Wistar rats. Moderate exercise decreased lactate dehydrogenase (LDH) release after OGD, while a significant increase in LDH release was observed in the high intensity group submitted to OGD. Our data corroborate the hypothesis that higher training intensity exacerbates brain damage, while a moderate intensity reduces the injury caused by in vitro ischemia.
Brain Research Bulletin 01/2007; 71(1-3):155-9. · 2.82 Impact Factor
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ABSTRACT: Our data support a disproportion between free radicals levels and scavenging systems activity in different cerebral regions of the aging rat. We investigated the total reactive antioxidant potential and reactivity levels, which represent the total antioxidant capacity, in different cerebral regions of the aging rat (cortex, striatum, hippocampus and the cerebellum). In addition, we have determined several oxidative stress parameters, specifically the free radicals levels, the macromolecules damage (lipid peroxidation and carbonyl content), as well as the antioxidant enzymes activities in different cerebral areas from young (2 months-old), mature adult (6 months-old) and old (24 months-old) male Wistar rats. Free radicals levels, determined by 2',7'-dichlorofluorescein diacetate probe, were higher in striatum, cerebellum and hippocampus from aged rats. There was an age-related increase in lipoperoxidation in hippocampus and cerebral cortex. In the cerebellum, a high activity of superoxide dismutase and a decrease of catalase activity were observed. The striatum exhibited a significant catalase activity decrease; and glutathione peroxidase activity was diminished in the hippocampus of mature and aged rats. There was a marked decrease of total antioxidant capacity in hippocampus in both reactivity and potential levels, whereas striatum and cerebral cortex displayed a reduction on reactivity assay. We suggest that age-related variations of total antioxidant defenses in brain may predispose structures to oxidative stress-related neurodegenerative disorders.
International Journal of Developmental Neuroscience 01/2006; 23(8):663-71. · 2.42 Impact Factor
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ABSTRACT: The aging process is associated with cognitive impairment and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, as well as with oxidative stress. We determined some parameters of oxidative stress in homogenates of hippocampus, hypothalamus and adrenal glands from male 2-, 6- and 24-months-old Wistar rats. A significant age-dependent increase in the generation of free radicals was observed in hippocampus, hypothalamus and adrenal glands, as well as on lipid peroxidation in hippocampus and hypothalamus. The glutathione peroxidase (GPx) activity was significantly reduced in hypothalamus and hippocampus from 6-months-old rats; a decline on GPx and catalase activities in adrenal glands of 24-months-old animals was also present. Interestingly, a great decrease in total antioxidant capacity was found in all tissues tested. Reported findings support the idea that oxidative events participate on multiple neuroendocrine-metabolic impairments and suggest that the oxidative stress found in hippocampus, hypothalamus and adrenals might be associated with age-related physiological deficits.
Life Sciences 01/2006; 78(3):271-8. · 2.53 Impact Factor
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ABSTRACT: Aging is an important risk factor for stroke. We evaluated the effects of aging on cell susceptibility to oxygen and glucose deprivation (OGD) in slices of the hippocampus from Wistar rats aged 2, 11 and 24 months. Lactate dehydrogenase (LDH) released to the incubation media and free radical content were markedly increased in the 24-month group submitted to OGD. These results confirm that hippocampal tissue from old animals is more susceptible to ischemia-reoxygenation injury.
Brain Research 11/2004; 1025(1-2):226-30. · 2.73 Impact Factor
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ABSTRACT: The cholinergic hypothesis of Alzheimer disease (AD) has provided the rationale for the current pharmacotherapy of this disease, in an attempt to downgrade the cognitive decline caused by cholinergic deficits. Nevertheless, the search for potent and long-acting acetylcholinesterase (AChE) inhibitors that exert minimal side effects to AD patients is still an ongoing effort. Amazonian communities use traditional remedies prepared with Ptychopetalum olacoides (PO, Olacaceae) roots for treating various central nervous system conditions, including those associated with aging. The fact that PO ethanol extract (POEE) has been found to facilitate memory retrieval in the step down procedure in young and aged mice prompt us to evaluate its effects on AChE activity in memory relevant brain areas. POEE significantly inhibited AChE activity in vitro in a dose- and time-dependent manner in rat frontal cortex, hippocampus and striatum; a significant inhibition was also found in these same brain areas of aged (14 months) mice after acute administration of POEE (100 mg/kg ip). We propose that such AChE inhibitory activity is a neurochemical correlate of a number of therapeutic properties traditionally claimed for P. olacoides, particularly those associated with cognition.
Pharmacology Biochemistry and Behavior 07/2003; 75(3):645-50. · 2.53 Impact Factor
