The protective effect of extra-virgin olive oil in the experimental model of multiple sclerosis in the rat.

This study has evaluated the effect of EVOO (Extra-Virgin olive oil), OA (oleic acid) and HT (hydroxytyrosol) in an induced model of MS through experimental autoimmune encephalomyelitis (EAE).Dark Agouti 2-month old rats (25 males) were divided into five groups: (i) control group, (ii) EAE group, (iii) EAE+EVOO, (iv) EAE+HT, and (v) EAE+OA. At 65 days, the animals were sacrificed and the glutathione redox system and bacterial lipopolysaccharide (LPS) and LPS-binding protein (LBP) products of the microbiota in brain, spinal cord, and blood were evaluated.Gastric administration of EVOO, OA, and HT reduced the degree of lipid and protein oxidation, and increased glutathione peroxidase, making it a diet-based mechanism for enhancing protection against oxidative damage. In addition, it reduced the levels of LPS and LBP, which appeared as being increased in the EAE correlated with the oxidative stress produced by the disease.

Dose-dependent S-allyl cysteine ameliorates multiple sclerosis disease-related pathology by reducing oxidative stress and biomarkers of dysbiosis in experimental autoimmune encephalomyelitis.

Garlic is a component of the Mediterranean diet. S-allyl cysteine (SAC), the most common organosulphur present in garlic, possesses neuroprotective properties. This investigation was performed to evaluate the dose-dependent protective action of SAC on oxidative damage, inflammation and gut microbiota alterations biomarkers. Experimental autoimmune encephalomyelitis (EAE) as a model of multiple sclerosis (MS) was induced by the myelin oligodendrocyte glycoprotein (MOG), whose effects were quantified by examining the changes in: clinical score, lipid peroxidation products, carbonylated proteins, glutathione system, tumor necrosis factor alpha (TNFα), and lipopolysaccharide membrane bacteria (LPS). Our results reveal that MOG induces paralysis, oxidative damage and increases in LPS binding protein (LBP) and LPS levels. In this work, two doses of SAC were compared with two dose of N-acetyl cysteine (NAC). SAC was more effective than NAC and it prevented the harmful effects induced by MOG more effectively at the dose of 50mg/kg than that of 18mg/kg. Surprisingly, NAC increases LBP levels while SAC had not such negative effect. In conclusion the data show the ability of SAC to modify EAE evolution.

Transcranial magnetic stimulation and aging: Effects on spatial learning and memory after sleep deprivation in Octodon degus.

The benefits of neuromodulatory procedures as a possible therapeutic application for cognitive rehabilitation have increased with the progress made in non-invasive modes of brain stimulation in aged-related disorders. Transcranial magnetic stimulation (TMS) is a non-invasive method used to examine multiple facets of the human brain and to ameliorate the impairment in cognition caused by Alzheimer's disease (AD). The present study was designed to evaluate how a chronic TMS treatment could improve learning and memory functions after sleep deprivation (SD) in old Octodon degus. SD was executed by gently handling to keep the animals awake throughout the night. Thirty young and twenty-four old O. degus females were divided in six groups (control, acute and chronic TMS treatment). Behavioral tests included; Radial Arm Maze (RAM), Barnes Maze (BM) and Novel Object Recognition (NOR). Although learning and memory functions improved in young animals with only one session of TMS treatment, a significant improvement in cognitive performance was seen in old animals after 4 and 7days of TMS, depending on the task that was performed. No side effects were observed following, which showed therapeutic potential for improving age-related cognitive performance.

Cognitive Impairment After Sleep Deprivation Rescued by Transcranial Magnetic Stimulation Application in Octodon degus.

Sleep is indispensable for maintaining regular daily life activities and is of fundamental physiological importance for cognitive performance. Sleep deprivation (SD) may affect learning capacity and the ability to form new memories, particularly with regard to hippocampus-dependent tasks. Transcranial magnetic stimulation (TMS) is a non-invasive procedure of electromagnetic induction that generates electric currents, activating nearby nerve cells in the stimulated cortical area. Several studies have looked into the potential therapeutic use of TMS. The present study was designed to evaluate how TMS could improve learning and memory functions following SD in Octodon degus. Thirty juvenile (18 months old) females were divided into three groups (control, acute, and chronic TMS treatment-with and without SD). TMS-treated groups were placed in plastic cylindrical cages designed to keep them immobile, while receiving head magnetic stimulation. SD was achieved by gently handling the animals to keep them awake during the night. Behavioral tests included radial arm maze (RAM), Barnes maze (BM), and novel object recognition. When TMS treatment was applied over several days, there was significant improvement of cognitive performance after SD, with no side effects. A single TMS session reduced the number of errors for the RAM test and improved latency and reduced errors for the BM test, which both evaluate spatial memory. Moreover, chronic TMS treatment brings about a significant improvement in both spatial and working memories.

Prepubertal children with suitable fitness and physical activity present reduced risk of oxidative stress.

To assess the impact of fitness status and physical activity on oxidative stress in prepubertal children, we measured selected biomarkers such as protein carbonyls (PC), lipid peroxidation products, and total nitrites, as well as the antioxidant system: total glutathione (TG), oxidized glutathione (GSSG), reduced glutathione (GSH), superoxide dismutase activity, and glutathione peroxidase. A total of 132 healthy children ages 7-12, at prepubertal stage, were classified into two groups according to their fitness level: low fitness (LF) and high fitness (HF). They were observed while engaged in an after-school exercise program, and a questionnaire was created to obtain information on their physical activity or sedentary habits. Plasma and red blood cells were obtained to analyze biomarkers. Regarding oxidative stress markers, the LF group and the sedentary group showed higher levels of TG and GSSG and a lower GSH/GSSG ratio than the HF group and the children engaged in physical activity. A negative association was found between PC and GSSG and TG and between TG and the GSH/GSSG ratio. Moreover, a negative correlation was found between GSSG and fitness, with a positive correlation with the GSH/GSSG ratio. TG, GSSG, and the GSH/GSSG ratio seem to be reliable markers of oxidative stress in healthy prepubertal children with low fitness or sedentary habits. This research contributes to the recognition that an adequate level of fitness and recreational physical activity in childhood leads to better health and oxidative status.

[Natalizumab and reduction of carbonylated proteins in patients with multiple sclerosis]. / Natalizumab y reduccion de los niveles de proteinas carboniladas en pacientes con esclerosis multiple.

INTRODUCTION: The sensitivity of the central nervous system to oxidative damage and its relationship with inflammatory response are well known. Recent studies have shown that oxidative stress is present in the establishment and development of multiple sclerosis (MS). One of the most recent treatments in this process is natalizumab, a monoclonal antibody. AIM: To evaluate whether the therapeutic effect of natalizumab is associated with the severity of the disease and the oxidative damage. PATIENTS AND METHODS: Researchers recruited twenty patients with relapsing-remitting MS (RRMS) undergoing therapy with natalizumab and distributed, according to the Expanded Disability Status Scale (EDSS), in two groups: RRMS-1 (EDSS < 5) and RRMS-2 (EDSS ≥ 5). Blood samples were taken for an oxidative profile study. RESULTS: Data showed a decrease in carbonylated proteins following treatment with natalizumab. The reduction in oxidative damage rated as protein oxidation is significant between the previous (baseline) situation of the patient and after 14 months' treatment. The most significant decrease coincided with the patients with the highest levels of severity in the process. Although it has not been possible to establish a correlation, the statistical significance is higher for patients in the RRMS-2 group treated with natalizumab. The antioxidant systems, on the other hand, did not display any statistically significant changes. CONCLUSIONS: Natalizumab brings about a reduction in carbonylated protein levels.

Neuroprotective effects of extremely low-frequency electromagnetic fields on a Huntington's disease rat model: effects on neurotrophic factors and neuronal density.

There is evidence to suggest that the neuroprotective effect of exposure of extremely low-frequency electromagnetic fields (ELF-EMF) may be due, at least in part, to the effect of these fields on neurotrophic factors levels and cell survival, leading to an improvement in behavior. This study was undertaken to investigate the neuroprotective effects of ELFEF in a rat model of 3-nitropropionic acid (3NP)-induced Huntington's disease. Behavior patterns were evaluated, and changes in neurotrophic factor, cell damage, and oxidative stress biomarker levels were monitored in Wistar rats. Rats were given 3NP over four consecutive days (20 mg/kg body weight), whereas ELFEF (60 Hz and 0.7 mT) was applied over 21 days, starting after the last injection of 3NP. Rats treated with 3NP exhibited significantly different behavior in the open field test (OFT) and the forced swim test (FST), and displayed significant differences in neurotrophic factor levels and oxidative stress biomarkers levels, together with a neuronal damage and diminished neuronal density, with respect neuronal controls. ELFEF improved neurological scores, enhanced neurotrophic factor levels, and reduced both oxidative damage and neuronal loss in 3NP-treated rats. ELFEF alleviates 3NP-induced brain injury and prevents loss of neurons in rat striatum, thus showing considerable potential as a therapeutic tool.

Olive oil reduces oxidative damage in a 3-nitropropionic acid-induced Huntington's disease-like rat model.

Free radicals contribute to altered neuronal functions in neurodegenerative diseases and brain aging, by producing lipid- and other molecule-dependent modifications. The Mediterranean diet has been associated with a reduced risk of neurodegenerative disease. This study sought to verify whether extra-virgin olive oil (EVOO) exerted a brain antioxidant effect, protecting the brain against the oxidative stress caused by 3-nitropropionic acid (3NP). 3NP was administered intraperitoneally (i.p.) at a dose of 20 mg/kg body weight over four consecutive days. EVOO (representing 10% of calorie intake in the total standard daily diet of rats) and hydroxytyrosol (HT; 2.5 mg/kg body weight) were administered for 14 days. In all studied samples, 3NP caused a rise in lipid peroxides (LPO) and a reduction in glutathione (GSH) content. While the results showed that EVOO and HT reduces lipid peroxidation product levels and blocks the GSH depletion prompted by 3NP in both striatum and rest of the brain in Wistar rats. In addition, EVOO blocks and reverses the effect of 3NP on succinate dehydrogenase activity. In brief, the data obtained indicate that EVOO and HT act as a powerful brain antioxidant.

Cardiorespiratory fitness and oxidative stress: effect of acute maximal aerobic exercise in children and adolescents.

AIM: Evaluate the effects of oxidative stress in saliva in young males, according to their cardiorespiratory fitness and taking acute maximal aerobic exercise into consideration. An incremental exercise test (20 meter shuttle run) was used. METHODS: Seventy healthy male subjects, aged 10 to 14 years, were included in the study and were classified into two groups according to fitness parameters. Subjects were expected to take the 20 meter shuttle run test. RESULTS: Group I had high cardiorespiratory fitness while group II had low cardiorespiratory fitness below the mean for their age. Saliva samples were taken before and immediately after exercise in order to measure levels of reduced glutathione, lipoperoxides, glutathione/lipoperoxides ratio and catalase. The values of reduced glutathione were significantly diminished regardless the subjects' cardiorespiratory fitness. The glutathione/lipoperoxides ratio was significantly diminished in group I. In addition, positive correlations were observed between lipoperoxides values after the 20 meter shuttle run test. CONCLUSION: High cardiorespiratory fitness does not seem to be an essential factor effecting in the oxidative stress values before exercise. However, oxidative stress could be greater with more intensity and duration after and acute maximal physical exercise.

Mice lacking the peroxisome proliferator-activated receptor α gene present reduced number of dopamine neurons in the substantia nigra without altering motor behavior or dopamine neuron decline over life.

Peroxisome proliferator-activated receptor alpha (PPAR-α), which is expressed by neurons of the nigrostriatal circuit, plays a prominent role in oxidative stress and neuroinflammation. The objectives were: (i) to discern if levels of antioxidant molecules and pro-inflammatory cytokines, along with PPAR-γ expression are modified in the nigrostriatal region of null PPAR-α mice, (ii) to discern whether dopaminergic neuronal features of the substantia nigra pars compacta (SNpc) and dorsal striatum are affected in null mice, and (iii) to establish if aging-induced decline of nigral neurons is different in null PPAR-α mice relative to wild-type littermates. A substantial decrease in antioxidant molecules was found in SNpc of null mice, by using ELISA. The pro-inflammatory factors TNF-α and IL-3 were found to be reduced in the substantia nigra, suggesting dual and opposite effects of PPAR-α deficiency on oxidative and pro-inflammatory molecules. Immunohistological and stereological studies revealed that young null mice present a smaller SNpc (-19.8%; TH downregulation was discarded). Normal locomotion in an open-field was not affected in null mice. Dopamine cell death could be caused by reduced protection against oxidative stress. Old null mice showed a percentage reduction of nigral dopamine neurons similar to that of young null animals, with a rate of decline over life of around 44%, the same value than that of wild-type littermates. These findings suggest that nuclear PPAR-α is necessary for the normal development of the substantia nigra along with normal levels of antioxidant molecules. Lack of PPAR-α does not modify the normal motor behavior of mice or decline of nigral dopamine neurons throughout life.

Huntingtons Disease: The Value of Transcranial Meganetic Stimulation

Huntington's disease (HD) is a genetic neurodegenerative process whose etiology is based on a localized disturbance in the short arm of chromosome 4 that encodes the huntingtin protein (Htt). The elongation of triple CAG for glutamine characterizes this change. Mutated Htt (mHtt) causes the appearance of intracellular aggregates inducing alterations in mitochondrial metabolism in the form of reactive oxygen species (ROS) and ATP depletion. The oxidative imbalance caused by mHtt leads the neurons to a state of oxidative stress resulting in damage to macromolecules and cellular death. Since the discovery of certain mechanisms underlying the pathogenesis of HD, several therapeutic procedures have been shown to delay or slow the evolution of the condition and have demonstrated the biochemical and molecular mechanism involved. The studies have reported that transcranial magnetic stimulation (TMS) may improve motor and other symptoms associated with neurodegenerative and neuropsychiatric processes such as major depression, schizophrenia, epilepsy, neuropathic pain, amyotrophic lateral sclerosis, progressive muscle atrophy, multiple sclerosis, stroke, Alzheimer's disease, Parkinson's disease or HD. This study focuses on the effect of TMS on oxidative stress and neurogenesis in studies and its possible usefulness in HD.

Olfactory bulbectomy induced oxidative and cell damage in rat: protective effect of melatonin.

In this study we analyzed the effects of melatonin (Mel, 1 mg/kg ip) on behavioral changes as well as cell and oxidative damage prompted by bilaterally olfactory bulbectomy. Olfactory bulbectomy caused an increase in lipid peroxidation products and caspase-3, whereas it prompted a decrease of reduced glutathione (GSH) content and antioxidative enzymes activities. Additionally, olfactory bulbectomy induced behavioral changes characterized by the enhancement of immobility time in the forced swim test and hyperactivity in the open field test. All these changes were normalized by treatment of Mel (14 days). Our data show that Mel has a beneficial neuropsychiatric action against oxidative stress, cell damage and behavior alterations.

[The molecular bases of Huntington's disease: the role played by oxidative stress]. / Bases moleculares de la enfermedad de Huntington: papel del estrés oxidativo.

INTRODUCTION: Huntington's disease is a neurodegenerative, autosomal dominant disease that mainly affects the basal ganglia. The disorder is caused by mutation in the gene encoding the huntingtin protein (Htt), producing intracellular aggregates. The adult form (chorea with dementia) is the most frequent. It is characterized by unpredictable, spasmodic, involuntary and constant movements, mostly associated with psychiatric and cognitive alterations. DEVELOPMENT: The main characteristics of Huntington's disease are: neuronal loss, glyosis, and accumulations of mutated Htt, all associated with different underlying channels in the pathogenesis of the disease, such as: excitotoxicity, energy deficit (ATP depletion), reduction in the synthesis and release of neurotrophic factors (BDNF and GDNF), and oxidative stress. Oxidative stress is involved in the pathogenesis of various neurodegenerative diseases, including Huntington's disease, and numerous studies have shown the existence of oxidative damage in the plasma and tissue of patients suffering from this disease. CONCLUSIONS: Oxidative stress in patients with Huntington's disease may be used as an evolutionary-prognostic marker of both the disease and therapeutic effectiveness, as well as an interesting field of research for the development of new therapeutic strategies.

Bases moleculares de la enfermedad de Huntington: papel del estrés oxidativo / The molecular bases of Huntington’s disease: the role played by oxidative stress

Introducción. La enfermedad de Huntington es un proceso de naturaleza neurodegenerativa, autosómica dominante,que afecta principalmente a los ganglios de la base. Está causada por mutación en el gen que codifica para la proteínahuntingtina (Htt), originando agregados intracelulares. La forma adulta, coreica y con demencia es la más frecuente. Cursacon movimientos impredecibles, espasmódicos, involuntarios y constantes, en la mayoría de los casos asociados a alteracionespsiquiátricas y cognitivas. Desarrollo. La enfermedad de Huntington se caracteriza principalmente por pérdida neuronal,gliosis y acúmulos de Htt mutada, todo ello asociado a diferentes vías subyacentes en la patogénesis, como son, entre otras,excitotoxicidad, déficit energético (depleción de adenosín trifosfato), reducción en la síntesis y liberación de factores neurotróficos(factor neurotrófico derivado del cerebro y factor neurotrófico derivado de una línea celular glial), y estrés oxidativo.El estrés oxidativo está involucrado en la patogénesis de varias enfermedades neurodegenerativas, entre ellas la enfermedad de Huntington, y son varios los estudios que muestran la existencia de daño oxidativo en el plasma y el tejido de estos pacientes.Conclusiones. El estrés oxidativo acontecido en la enfermedad de Huntington puede utilizarse como marcador de evolución- pronóstico de la enfermedad y de efectividad terapéutica, y es un foco de interés para el desarrollo de nuevas estrategias terapéuticas (AU)

Introduction. Huntington’s disease is a neurodegenerative, autosomal dominant disease that mainly affects thebasal ganglia. The disorder is caused by mutation in the gene encoding the huntingtin protein (Htt), producing intracellularaggregates. The adult form (chorea with dementia) is the most frequent. It is characterized by unpredictable, spasmodic,involuntary and constant movements, mostly associated with psychiatric and cognitive alterations. Development. The maincharacteristics of Huntington’s disease are: neuronal loss, glyosis, and accumulations of mutated Htt, all associated withdifferent underlying channels in the pathogenesis of the disease, such as: excitotoxicity, energy deficit (ATP depletion),reduction in the synthesis and release of neurotrophic factors (BDNF and GDNF), and oxidative stress. Oxidative stress isinvolved in the pathogenesis of various neurodegenerative diseases, including Huntington’s disease, and numerous studieshave shown the existence of oxidative damage in the plasma and tissue of patients suffering from this disease. Conclusions.Oxidative stress in patients with Huntington’s disease may be used as an evolutionary-prognostic marker of both the diseaseand therapeutic effectiveness, as well as an interesting field of research for the development of new therapeutic strategies (AU)

Effect of melatonin on myocardial oxidative stress induced by experimental obstructive jaundice.

OBJECTIVE: melatonin has been demonstrated to have active antioxidant properties in different tissues during experimental cholestasis. The aim of this research was to study myocardial oxidative stress on obstructive jaundice, and to analyze the effect of melatonin on myocardial oxidative lesions. MATERIAL AND METHODS: we achieved cholestasis by ligature and sectioning of the main bile duct. Melatonin was administered intraperitoneally (500 microg/kg/day). We measured malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxydase (GPx) antioxidant enzyme levels in the heart tissue. RESULTS: obstructive cholestasis increased MDA and decreased GSH as well as all antioxidant enzymes. Melatonin administration significantly decreased MDA values, and increased GSH and antioxidant enzymes on the icteric animal myocardium. CONCLUSIONS: melatonin treatment prevents oxidative stress in the cardiac tissue as induced by experimental cholestasis.

Effect of melatonin on myocardial oxidative stress induced by experimental obstructive jaundice

Objective: melatonin has been demonstrated to have activeantioxidant properties in different tissues during experimentalcholestasis. The aim of this research was to study myocardial oxidativestress on obstructive jaundice, and to analyze the effect ofmelatonin on myocardial oxidative lesions.Material and methods: we achieved cholestasis by ligatureand sectioning of the main bile duct. Melatonin was administeredintraperitoneally (500 ìg/kg/day). We measured malondialdehyde(MDA), reduced glutathione (GSH), catalase (CAT), superoxidedismutase (SOD) and glutathione peroxydase (GPx) antioxidantenzyme levels in the heart tissue.Results: obstructive cholestasis increased MDA and decreasedGSH as well as all antioxidant enzymes. Melatonin administrationsignificantly decreased MDA values, and increased GSH and antioxidantenzymes on the icteric animal myocardium.Conclusions: melatonin treatment prevents oxidative stressin the cardiac tissue as induced by experimental cholestasis(AU)

Cambios en biomarcadores del estrés oxidativo inducidos por la pubertad / Changes in oxidative stress biomarkers induced by puberty

Objetivos: Estudiar la influencia del estrés oxidativo (EO) en la adolescencia, dado que éste se produce por un desequilibrio entre sustancias oxidantes y mecanismos de defensa antioxidante y se ha descrito como uno de los factores que más influye en la disminución progresiva de las funciones biológicas con el avance de la edad. Material y métodos: Se han seleccionado 38 varones prepúberes con estadio de Tanner G1-P1 y 32 varones púberes sanos con estadio de Tanner G3−4-P3−4 de 10 a 14 años, que presentaban peso, talla, índice de masa corporal, frecuencia cardíaca y presión arterial en el percentil 50 de su edad (desviación estándar ±1). Se midieron en saliva las concentraciones basales de los productos de lipoperoxidación, glutatión reducido y catalasa, ya que se ha demostrado una buena correlación entre las concentraciones plasmáticas y salivares de los biomarcadores del EO. Resultados: Los varones puberales presentaron concentraciones superiores significativas de los productos de lipoperoxidación (p<0,001), no se obtuvieron diferencias significativas en los demás biomarcadores estudiados. Se encontró una correlación significativa positiva entre los productos de lipoperoxidación y el glutatión reducido (p<0,001). Conclusión: Se describe por primera vez que en la pubertad hay un aumento de los productos de lipoperoxidación y que podrían estar influyendo en la aparición de EO en esta etapa de la vida (AU)

Aim: Evaluate the influence of puberty in oxidative stress. Subjects and methods: The study included 38 prepubescent males with Tanner G1-P1 and 32 healthy pubescent boys with Tanner G3−4-P3−4. Weight, height and body mass index, heart rate, blood pressure values were within the 50 percentile 50±1SD for their age. The biomarkers were measured in saliva, as a good correlation between saliva and plasma levels has been reported in lipoperoxidation products, reduced glutathione and catalase. Results: Pubescent boys had significantly higher levels of lipoperoxidation products (P<0.001) compared with the prepubertal group, with no significant differences in the other parameters measured. There was a significant positive correlation between lipoperoxides and reduced glutathione in these children. Conclusion: It is the first time that an increase of lipoperoxidation products has been reported in pubertal boys and this biomarker could play a role in the development of oxidative stress in this stage of life (AU)

[Model of Huntington's disease induced with 3-nitropropionic acid]. / Modelo de enfermedad de Huntington inducido con ácido 3-nitropropiónico.

INTRODUCTION: Huntington's disease is an autosomal dominant hereditary disorder. This neurodegenerative illness is characterized by mutation of the huntingtin protein gene, causing the formation of intracellular protein aggregates. DEVELOPMENT: Intensive research efforts have been made to investigate the molecular mechanism involved. For this reason, the development of animal and cellular models of Huntington's disease has offered alternative approaches to study of this disease. The alteration of succinate dehydrogenase activity has been linked to Huntington's disease. 3-nitropropionic acid is an inhibitor of this enzyme, prompting oxidative stress and death neuronal, mimic some aspects of Huntington's disease as anatomical, physiological and chemical changes. CONCLUSION: This model is a useful tool to study the mechanisms involved in this disease and to evaluate new therapeutic strategies.

[Changes in oxidative stress biomarkers induced by puberty]. / Cambios en biomarcadores del estrés oxidativo inducidos por la pubertad.

AIM: Evaluate the influence of puberty in oxidative stress. SUBJECTS AND METHODS: The study included 38 prepubescent males with Tanner G(1)-P(1) and 32 healthy pubescent boys with Tanner G(3-4)-P(3-4). Weight, height and body mass index, heart rate, blood pressure values were within the 50 percentile 50+/-1SD for their age. The biomarkers were measured in saliva, as a good correlation between saliva and plasma levels has been reported in lipoperoxidation products, reduced glutathione and catalase. RESULTS: Pubescent boys had significantly higher levels of lipoperoxidation products (P<0.001) compared with the prepubertal group, with no significant differences in the other parameters measured. There was a significant positive correlation between lipoperoxides and reduced glutathione in these children. CONCLUSION: It is the first time that an increase of lipoperoxidation products has been reported in pubertal boys and this biomarker could play a role in the development of oxidative stress in this stage of life.

Modelo de enfermedad de Huntington inducido con ácido 3-nitropropiónico / Model of huntington disease induced with-3 nitropropionic acid

Introducción. La enfermedad de Huntington es un trastorno hereditario autosómico dominante. Esta patología neurodegenerativa se genera aparentemente por la mutación del gen que codifica para la proteína huntingtina, y resulta en la formación de agregados intracelulares. Desarrollo. Se han llevado a cabo hasta ahora diversos esfuerzos para investigar los mecanismos moleculares patogénicos. Por ello, el desarrollo de modelos animales y celulares de la enfermedad de Huntington ofrece valiosas aproximaciones para el estudio de esta enfermedad. La alteración de la actividad de la enzima succinato deshidrogenasa se ha ligado al desarrollo de la enfermedad de Huntington. El ácido 3-nitropropiónico es un inhibidor de esta enzima que induce estrés oxidativo y muerte neuronal, así como mimetiza algunos aspectos de la enfermedad de Huntington como los cambios neuroanatómicos, fisiológicos y químicos. Conclusión. Este modelo constituye una herramienta útil para el estudio fenomenológico de los mecanismos involucrados en esta enfermedad y para el análisis de nuevas estrategias terapéuticas (AU)

Introduction. Huntington’s disease is an autosomal dominant hereditary disorder. This neurodegenerative illness is characterized by mutation of the huntingtin protein gene, causing the formation of intracellular protein aggregates. Development. Intensive research efforts have been made to investigate the molecular mechanism involved. For this reason, the development of animal and cellular models of Huntington’s disease has offered alternative approaches to study of this disease. The alteration of succinate dehydrogenase activity has been linked to Huntington’s disease. 3-nitropropionic acid is an inhibitor of this enzyme, prompting oxidative stress and death neuronal, mimic some aspects of Huntington’s disease as anatomical, physiological and chemical changes. Conclusion. This model is a useful tool to study the mechanisms involved in this disease and to evaluate new therapeutic strategies (AU)