Dolores Hidalgo Cuna de la Independencia Nacional, Mexico
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Ortiz-ButrOn R.,Laboratorio Of Neurobiologia | Blas-Valdivia V.,Laboratorio Of Neurobiologia | Pineda-Reynoso M.,Laboratorio Of Neurobiologia | Cano-Europa E.,Laboratorio Of Neurobiologia
Drug and Chemical Toxicology | Year: 2011

Methimazole is the most widely used antithyroid drug in Europe and North America, but it causes several undesirable side effects, such as hematological dysfunctions and immunosuppression. Our aim in this work was to compare, over a time course, markers of oxidative stress, the redox environment, the antioxidant enzymatic system, and the glutathione cycle in the spleen of rats with methimazole- or thyroidectomy-caused hypothyroidism. We used 70-male Wistar rats divided into four groups: 1) euthyroid; 2) sham thyroidectomy; 3) thyroidectomy-caused hypothyroidism, with parathyroid reimplant; and 4) methimazole-caused hypothyroidism. Five rats of the euthyroid- and methimazole-caused hypothyroidism groups were killed at the end of weeks 1, 2, 3, and 4 after treatment, and 5 rats of the sham thyroidectomy and thyroidectomy-caused hypothyroidism groups were killed at the end of weeks 2, 4, and 8 after the surgical procedure. Each spleen was excised and stored at -70°C until oxidative stress, REDOX environment, and the antioxidant enzymatic-system markers were tested. The histological study showed that only methimazole-induced hypothyroidism caused cell damage. This damage was associated with an increase of oxidative-stress markers that were not compensated for by the antioxidant system. The increase of the glutathione-cycle enzymes was insufficient to prevent oxidative-stress markers. Methimazole causes oxidative stress and cell damage in the spleen, whereas hypothyroidism per se does not cause cell damage in this organ. Therefore, it is necessary to develop new antithyroid drugs without causing oxidative stress and cellular damage. © 2011 Informa Healthcare USA, Inc.


Burgos H.,Laboratorio Of Biopsicologia | Burgos H.,Central University of Chile | Cofre C.,Laboratorio Of Biopsicologia | Hernandez A.,Laboratorio Of Neurobiologia | And 5 more authors.
Behavioural Brain Research | Year: 2015

Methylphenidate (MPH) is widely used as a "nootropic" agent and in the treatment of disorders of attention, and has been shown to modulate synaptic plasticity in vitro. Here we present in vivo evidence that this MPH-induced metaplasticity can last long after the end of treatment. MPH (0, 0.2, 1 and 5. mg/kg) was administered daily to male rats from postnatal day 42 for 15 days. The animals were tested daily in a radial maze. Long-term potentiation (LTP), a marker of neural plasticity, was induced in vivo in the prefrontal cortex after 2-3. h, 15-18 days or 5 months without treatment. The behavioral performance of the 1. mg/kg group improved, while that of animals that had received 5. mg/kg deteriorated. In the 1 and 5. mg/kg groups LTP induced 2-3. h after the last MPH treatment was twice as large as in the controls. Further, 15-18 days after the last MPH administration, in groups receiving 1 and 5. mg/kg, LTP was about fourfold higher than in controls. However, 5 months later, LTP in the 1. mg/kg group was similar to controls and in the 5. mg/kg group LTP could not be induced at all. No significant changes of LTP were seen in the low-dose group of animals (0.2. mg/kg). Thus, firstly, doses of MPH that improve learning coincide approximately with those that augment LTP. Secondly, MPH-induced increases in LTP can last for several weeks, but these may disappear over longer periods or deteriorate at high doses. © 2015 Elsevier B.V.


PubMed | University of Santiago de Chile, Laboratorio Of Biopsicologia, Autonomous University of Chile, Laboratorio Of Neurobiologia and 2 more.
Type: | Journal: Behavioural brain research | Year: 2015

Methylphenidate (MPH) is widely used as a nootropic agent and in the treatment of disorders of attention, and has been shown to modulate synaptic plasticity in vitro. Here we present in vivo evidence that this MPH-induced metaplasticity can last long after the end of treatment. MPH (0, 0.2, 1 and 5mg/kg) was administered daily to male rats from postnatal day 42 for 15 days. The animals were tested daily in a radial maze. Long-term potentiation (LTP), a marker of neural plasticity, was induced in vivo in the prefrontal cortex after 2-3h, 15-18 days or 5 months without treatment. The behavioral performance of the 1mg/kg group improved, while that of animals that had received 5mg/kg deteriorated. In the 1 and 5mg/kg groups LTP induced 2-3h after the last MPH treatment was twice as large as in the controls. Further, 15-18 days after the last MPH administration, in groups receiving 1 and 5mg/kg, LTP was about fourfold higher than in controls. However, 5 months later, LTP in the 1mg/kg group was similar to controls and in the 5mg/kg group LTP could not be induced at all. No significant changes of LTP were seen in the low-dose group of animals (0.2mg/kg). Thus, firstly, doses of MPH that improve learning coincide approximately with those that augment LTP. Secondly, MPH-induced increases in LTP can last for several weeks, but these may disappear over longer periods or deteriorate at high doses.


Durand D.,Institute Investigaciones Biomedicas INBIOMED | Carniglia L.,Institute Investigaciones Biomedicas INBIOMED | Beauquis J.,Laboratorio Of Neurobiologia | Beauquis J.,CONICET | And 4 more authors.
Neuropharmacology | Year: 2014

Abstract Amyloid precursor protein (APP) shedding yields the Alzheimer's disease (AD)-related peptide amyloid β (Aβ) through β- and γ-secretase cleavage. Alternatively, α-secretase cleavage generates a soluble and neuroprotective fragment (sAPPα) while precludes the production of Aβ. Although metabotropic glutamate (mGlu) receptors were associated with induction of sAPPα production in astrocytes, there was no further evidence regarding the specific subtype receptor or the mechanisms involved in this action. In the present study, we used the dual mGlu2/3 receptor agonist LY379268, which in pure astrocyte cultures selectively activates mGlu3 receptor subtype since mGlu2 receptor subtype is not expressed by these cells. We showed that LY379268 incremented sAPPα release from cultured astrocytes by inducing α-secretases expression, whereas it decreased β-secretase levels. LY379268-induced increase of PPAR-γ levels could be involved in the effect of the agonist on sAPPα release. Using the PDAPP-J20 murine model of AD we described a strong reduction in mGlu2/3 receptor expression in the hippocampus of 5- and 14-month-old transgenic mice compared to control littermates. Moreover, mGlu3 receptor expression is also decreased specifically in hippocampal astrocytes of these transgenic animals as a function of age. Therefore, diminished levels of hippocampal mGlu3 receptors might have implications in the development of the disease in these transgenic mice considering the anti-amyloidogenic action of mGlu3 receptors in astrocytes. © 2013 Elsevier Ltd. All rights reserved.


Introduction: Mechanical ventilation is a therapy for vital support used in a significant proportion of critically ill patients. The right time to successfully discontinue this therapy is a challenge for the intensive care specialist. For this reason it is still a subject for research. The echocardiographic evaluation of the diastolic dysfunction, the diaphragm, and the lung have become an invaluable tool for weaning from mechanical ventilation protocols, especially in patients with difficult or prolonged weaning from mechanical ventilation. There is still a need to validate, in controlled trials, the efficacy of an ultrasound protocol for weaning from mechanical ventilation that integrates the three modalities in a single protocol. Methods: Based on current literature, we developed a score justified by a mathematical model based on inequations. When ? ? 5 the risk of failure in the weaning process rises, the weaning process should be suspended; when ? ? 1 the risk of failure is low, the weaning process should be continued. Conclusions. The use of math models for decision-making is of great importance, as it sets an objective parameter within the existing evaluations. We proposed the use of inequations to set intervals of solution with the three points of care for ultrasound-guided weaning from mechanical ventilation. With this, the inequations proposed generate an area of certainty within the proposed values and the solution intervals. © 2016, Academia Nacional de Medicina. All rights reserved.


Cano-Europa E.,Laboratorio Of Neurobiologia | Blas-Valdivia V.,Laboratorio Of Neurobiologia | Lopez-Galindo G.E.,Laboratorio Of Neurobiologia | Franco-Colin M.,Laboratorio Of Metabolismo I Del | And 3 more authors.
Annals of Hepatology | Year: 2010

Our objective was to compare, over a time-course, markers of oxidative stress, the REDOX environment, and the antioxidant enzymatic system in the liver of rats with methimazole- or thyroidectomy-caused hypothyroidism. Methods. We used 60 male Wistar rats divided into four groups: 1) the euthyroid, which received only tap water, 2) false thyroidectomy, which received the surgery and postoperative treatment, 3) thyroidectomy-caused hypothyroidism, which had the thyroid gland removed and a parathyroid reim-plant, and 4) methimazole-caused hypothyroidism in rats that received 60 mg/kg/d of the anti thyroid drug in drinking water. Five rats of the euthyroid and methimazole-caused hypothyroidism groups were killed at the end of the first, second, third, and fourth week after treatment, and five rats of false thyroidectomy and thyroidectomy-caused hypothyroidism groups were killed at the end of the second and eighth week after the surgical procedure. Each liver was removed and stored at -70 °C until oxidative stress, REDOX environment, and antioxidant enzymatic system markers were tested. We also made a histological study at the end of the treatment. Results. The histological study revealed that only the methimazole-caused hypothyroidism caused cell damage. This damage is associated with an increase of oxidative stress markers that were not compensated for by the antioxidant system. The catalase activity is reduced and this allows H2O2-caused damage. In conclusion methimazole causes cell damage in the liver, whereas hypothyroidism per se does not cause hepatic-cell damage.


Rodriguez-Sanchez R.,Laboratorio Of Neurobiologia | Ortiz-Butron R.,Laboratorio Of Neurobiologia | Blas-Valdivia V.,Laboratorio Of Neurobiologia | Hernandez-Garcia A.,Laboratorio Of Neurobiologia | Cano-Europa E.,Laboratorio Of Neurobiologia
Food Chemistry | Year: 2012

Our objective was to determine if the phycobiliproteins of Arthrospira (Spirulina) maxima protect renal cells against mercury-caused oxidative stress and cellular damage in the kidney. We used 40 male mice that were assigned into eight groups: (1) a control group that received 100 mM phosphate buffer (PB) ig and 0.9% saline ip, (2) PB + HgCl2 (5 mg/kg ip), (3) PB plus phycobiliproteins (100 mg/kg ig), (4) PB plus C-phycocyanin (100 mg/kg ig), and four groups receiving HgCl2 + phycobiliproteins or C-phycocyanin (50, and 100 mg/kg ig). The left kidneys were used to determine lipid peroxidation, quantification of reactive oxygen species, and reduced glutathione and oxidised content. The right kidneys were processed for histology. The HgCl2 caused oxidative stress and cellular damage. All doses of phycobiliproteins or C-phycocyanin prevented enhancement of oxidative markers and they protected against HgCl2-caused cellular damage. © 2012 Elsevier Ltd. All rights reserved.


De Boni A.,Laboratorio Of Neurobiologia | De Riva V.,Laboratorio Of Neurobiologia | Galloni E.,Laboratorio Of Neurobiologia | Perini F.,Laboratorio Of Neurobiologia
Rivista Italiana della Medicina di Laboratorio | Year: 2011

Background: Antithrombotic therapy reduces the risk of recurrent ischaemic stroke by about 20%. Clinical failure has been ascribed to antiplatelet treatment resistance. The data reported in the literature are inconsistent. This is due to the heterogeneity of the clinical populations studied and to the different laboratory methods used. Light transmission aggregometry (LTA) is the gold standard for the study of platelet function. Several agonists at different concentrations were used in the studies reported in the literature. Methods. We studied a selected population of patients with ischaemic stroke by LTA using specific agonists for each antiplatelet drug in order to determine if there is an association between clinical failure and residual platelet activity. Results: In the population studied there were no clinical relapses or resistance to antiplatelet treatments. onclusion. Studies involving longer observational periods are needed to evaluate the possibility of emergence of resistance over a longer time as well as studies on a larger population to confirm our data. © Springer 2011.


Methimazole is the most widely used antithyroid drug in Europe and North America, but it causes several undesirable side effects, such as hematological dysfunctions and immunosuppression. Our aim in this work was to compare, over a time course, markers of oxidative stress, the redox environment, the antioxidant enzymatic system, and the glutathione cycle in the spleen of rats with methimazole- or thyroidectomy-caused hypothyroidism. We used 70-male Wistar rats divided into four groups: 1) euthyroid; 2) sham thyroidectomy; 3) thyroidectomy-caused hypothyroidism, with parathyroid reimplant; and 4) methimazole-caused hypothyroidism. Five rats of the euthyroid- and methimazole-caused hypothyroidism groups were killed at the end of weeks 1, 2, 3, and 4 after treatment, and 5 rats of the sham thyroidectomy and thyroidectomy-caused hypothyroidism groups were killed at the end of weeks 2, 4, and 8 after the surgical procedure. Each spleen was excised and stored at -70C until oxidative stress, REDOX environment, and the antioxidant enzymatic-system markers were tested. The histological study showed that only methimazole-induced hypothyroidism caused cell damage. This damage was associated with an increase of oxidative-stress markers that were not compensated for by the antioxidant system. The increase of the glutathione-cycle enzymes was insufficient to prevent oxidative-stress markers. Methimazole causes oxidative stress and cell damage in the spleen, whereas hypothyroidism per se does not cause cell damage in this organ. Therefore, it is necessary to develop new antithyroid drugs without causing oxidative stress and cellular damage.


PubMed | Laboratorio Of Neurobiologia
Type: Journal Article | Journal: Food chemistry | Year: 2012

Our objective was to determine if the phycobiliproteins of Arthrospira (Spirulina) maxima protect renal cells against mercury-caused oxidative stress and cellular damage in the kidney. We used 40 male mice that were assigned into eight groups: (1) a control group that received 100mM phosphate buffer (PB) ig and 0.9% saline ip, (2) PB+HgCl(2) (5mg/kg ip), (3) PB plus phycobiliproteins (100mg/kg ig), (4) PB plus C-phycocyanin (100mg/kg ig), and four groups receiving HgCl(2)+phycobiliproteins or C-phycocyanin (50, and 100mg/kg ig). The left kidneys were used to determine lipid peroxidation, quantification of reactive oxygen species, and reduced glutathione and oxidised content. The right kidneys were processed for histology. The HgCl(2) caused oxidative stress and cellular damage. All doses of phycobiliproteins or C-phycocyanin prevented enhancement of oxidative markers and they protected against HgCl(2)-caused cellular damage.

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