Marisela Méndez-Armenta

Instituto Nacional de Neurología y Neurocirugía, Tlalpam, Mexico City, Mexico

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Publications (38)90.86 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Epilepsy is a neurological disorder that has been associated with oxidative stress therefore epilepsy models have been develop such as kainic acid and pentylenetetrazol are usually used to understanding of the molecular mechanisms of this disease. We examined the metallothionein expression in rat brains of treated with kainic acid and pentylenetetrazol. Increase in metallothionein and nitrotirosyne immunoreactivity of both seizures epilepsy models was observed. Moreover, we show a significant increase on levels of MT expression. These results suggest that the increase of metallothionein expression is related with kainic acid and pentylenetetrazol treatments as response to damage mediated by oxidative stress. Published by Elsevier B.V.
    08/2015; 40(2):530-534. DOI:10.1016/j.etap.2015.08.006
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    ABSTRACT: In developing animals, Cadmium (Cd) induces toxicity to many organs including brain. Reactive oxygen species (ROS) are often implicated in Cd-inducedtoxicity and it has been clearly demonstrated that oxidative stress interferes with the expression of genes as well as transcriptional factors such as Nrf2-dependent Antioxidant Response Element (Nrf2-ARE). Cd-generated oxidative stress and elevated Nrf2 activity have been reported in vitro and in situ cells. In this study we evaluated the morphological changes and the expression pattern of Nrf2 and correlated them with the Cd concentrations in different ages of developing rats in heart, lung, kidney, liver, and brain. The Cd content in different organs of rats treated with the metal was increased in all ages assayed. Comparatively, lower Cd brain levels were found in rats intoxicated at the age of 12 days, then pups treated at 5, 10, or 15 days old, at the same metal dose. No evident changes, as a consequence of cadmium exposure, were evident in the morphological analysis in any of the ages assayed. However, Nrf2-ARE immunoreactivity was observed in 15-day-old rats exposed to Cd. Our results support that fully developed blood-brain barrier is an important protector against Cd entrance to brain and that Nrf2 increased expression is a part of protective mechanism against cadmium-induced toxicity.
    Oxidative medicine and cellular longevity 06/2015; 2015:1-9. DOI:10.1155/2015/570650 · 3.36 Impact Factor
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    ABSTRACT: Spinal cord injury (SCI) is a condition producing irreversible damage to the neurological function. Among the leading mechanisms associated to cell death after SCI, excitotoxicity, oxidative stress, inflammatory response and apoptosis are considered potential targets to prevent tissue damage. We recently reported that dapsone an anti-inflammatory drug, decreases the activity of myeloperoxidase, lipid peroxidation, improve neurological function and increase the amount of spared tissue after SCI in rats. In this study, we characterized the anti-apoptotic effect of dapsone administered at 12.5 mg/kg/24 h dose, starting at 3 and 5 h after SCI. We monitored the activity of caspases-8, 9, and 3 and quantitated Annexin V and TUNEL positive cells in the core of the lesion. Results showed increased activities of caspase-8, 9 and 3 at 72 h by SCI to reach increments of 69, 143 and 293 %, respectively, as compared to sham group. Meanwhile, dapsone, administered at 3 and 5 after SCI, reduced caspase-8 activity by 36 and 44 % respectively, whereas the activity of caspase-9 was diminished by 37 %. Likewise, the activity of caspase-3 showed a decrease of 38 %. Finally, both Annexin V and TUNEL-positive cells were significantly reduced by DDS as compared to untreated SCI animals. Results showed that dapsone exerted anti-apoptotic effect after SCI.
    Neurochemical Research 05/2015; 40(6). DOI:10.1007/s11064-015-1588-z · 2.59 Impact Factor
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    ABSTRACT: Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy.
    Oxidative medicine and cellular longevity 12/2014; 2014:293689. DOI:10.1155/2014/293689 · 3.36 Impact Factor
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    ABSTRACT: After transient cerebral ischemia and reperfusion (I/R), damaging mechanisms, such as excitotoxicity and oxidative stress, lead to irreversible neurological deficits. The induction of metallothionein-II (MT-II) protein is an endogenous mechanism after I/R. Our aim was to evaluate the neuroprotective effect of MT-II after I/R in rats. Male Wistar rats were transiently occluded at the middle cerebral artery for 2 h, followed by reperfusion. Rats received either MT (10 μ g per rat i.p.) or vehicle after ischemia. Lipid peroxidation (LP) was measured 22 h after reperfusion in frontal cortex and hippocampus; also, neurological deficit was evaluated after ischemia, using the Longa scoring scale. Infarction area was analyzed 72 hours after ischemia. Results showed increased LP in frontal cortex (30.7%) and hippocampus (26.4%), as compared to control group; this effect was fully reversed by MT treatment. Likewise, we also observed a diminished neurological deficit assessed by the Longa scale in those animals treated with MT compared to control group values. The MT-treated group showed a significant (P < 0.05) reduction of 39.9% in the infarction area, only at the level of hippocampus, as compared to control group. Results suggest that MT-II may be a novel neuroprotective treatment to prevent ischemia injury.
    Oxidative Medicine and Cellular Longevity 02/2014; 2014:436429. DOI:10.1155/2014/436429 · 3.36 Impact Factor
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    ABSTRACT: Characterization of auto-destructive mechanisms, leading to cell death after spinal cord injury (SCI) is important to prevent further damage to tissue. Heme oxygenase (HO) catalyzes the oxidation of heme to biliverdin and carbon monoxide (CO), as a response to cell damage. Products of HO action have biological effects, as antioxidant biliverdin. We evaluated the changes of HO activity after injury, and the effect of pharmacological treatments with hemin (an inducer) and (Sn)-protoporphyrin (an inhibitor) of HO, upon motor recovery after SCI. Female Wistar rats were submitted to SCI by trauma and sacrificed at several times (2, 4, 8, 12 and 24h) after injury to evaluate HO activity. Additional groups of rats were treated with either hemin or Sn-PPIX, to evaluate motor recovery, spared spinal cord tissue and HO activity. Results showed that HO control activity was increased by effect of SCI, at all times evaluated, as compared to sham group values. Twenty-four h after injury, HO activity was increased 7.2-fold by Hemin treatment, as compared to SCI plus vehicle group values. In addition, animals treated with hemin 2 and 8h after SCI, showed a better motor recovery and higher spared cord tissue, as compared to control group values. Our findings indicate that activation of HO is a beneficial mechanism when attained during the acute phase after SCI.
    Neuroscience Letters 10/2013; 556. DOI:10.1016/j.neulet.2013.08.067 · 2.03 Impact Factor
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    ABSTRACT: Excitotoxicity due to glutamate receptors (GluRs) overactivation is a leading mechanism of oxidative damage and neuronal death in various diseases. We have shown that dapsone (DDS) was able to reduce both neurotoxicity and seizures associated to the administration of kainic acid (KA), an agonist acting on AMPA/KA receptors (GluK1-GluK5). Recently, it has been shown that phenobarbital (PB) is also able to reduce epileptic activity evoked by that receptor. In the present study, we tested the antioxidative, anticonvulsive and neuroprotective effects of DDS and PB administered alone or in combination upon KA toxicity to rats. Results showed that KA increased lipid peroxidation and diminished reduced glutathione (GSH), 24 h after KA administration and both drugs in combination or individually inhibited these events. Likewise, KA promotes mortality and this event was antagonized by effect of both treatments. Additionally, the behavioral evaluation showed that DDS and PB administered alone or in combination decreased the number of limbic seizures and reduced the percentage of animals showing tonic-clonic seizures versus the control group, which was administered only with KA. Finally, our study demonstrated that all of the treatments prevented the neuronal death of the pyramidal cell layer of hippocampal CA-3. In conclusion, the treatment with DDS and PB administrated alone or in combination exerted antioxidant, anticonvulsive and neuroprotective effects against the neurotoxicity induced by KA in rats, but their effects were not additive. Thus, it may be good options of treatment in diseases such as epilepsy and status epilepicus, administered separately.
    Neurochemical Research 06/2013; 38(9). DOI:10.1007/s11064-013-1087-z · 2.59 Impact Factor
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    ABSTRACT: We studied the use of three biocompatible materials obtained by plasma polymerization of pyrrole (PPy), pyrrole doped with iodine (PPy/I) and a copolymer formed with pyrrole and polyethylene glycol (PPy/PEG), implanted, separately, after a complete spinal cord transection in rats. Motor function assessed with the BBB scale and somatosensory evoked potentials (SEPs) in the implanted rats were studied. Results showed that the highest motor recovery was obtained in rats with PPy/I implants. They also showed a significant reduction in the latency of SEPs. Histological analyses showed no signs of implant rejection; on the contrary, implants based on PPy improved the SEPs conduction and motor function after lesion.
    Journal of Materials Science Materials in Medicine 07/2012; 23(10):2583-92. DOI:10.1007/s10856-012-4715-2 · 2.59 Impact Factor
  • Concepción Nava-Ruiz · Marisela Méndez-Armenta · Camilo Ríos ·
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    ABSTRACT: Lead (Pb), a ubiquitous and potent neurotoxicant, induces several neurophysiological and behavioural changes, while Pb alters the function of multiple organs and systems, it primarily affects the central nervous system. In human adults, encephalopathy resulting from Pb intoxication is often characterized by sleeplessness, poor attention span, vomiting, convulsions and coma; in children, Pb-induced encephalopathy is associated with mental dullness, vomiting, irritability and anorexia; diminished cognitive function resulting in a mental deficit has been also observed during Prolonged exposure to Pb. Pb can produce oxidative stress, disrupt the blood-brain barrier and alter several Ca(2+)-dependent processes, including physiological processes that involve nitric oxide synthesis on central nervous system in development and adult animals. This review summarizes recent evidence showing that Pb can interfere with the production of nitric oxide and can disrupt the function of nitric oxide synthase. Lead interferes with nitric oxide-related physiological mechanisms, and Pb neurotoxicity may affect processes involved in learning and memory.
    Journal of molecular histology 04/2012; 43(5):553-63. DOI:10.1007/s10735-012-9414-2 · 1.82 Impact Factor
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    ABSTRACT: After spinal cord injury (SCI), a complex cascade of pathophysiological processes rapidly damages the nervous tissue. The initial damage spreads to the surrounding tissue by different mechanisms, including oxidative stress. We have recently reported that the induction of metallothionein (MT) protein is an endogenous rapid-response mechanism after SCI. Since the participation of MT in neuroprotective processes after SCI is still unknown, the aim of the present study was to evaluate the possible neuroprotective effect of exogenously administered MT-II during the acute phase after SCI in rats. Female Wistar rats weighing 200-250g were submitted to spinal cord contusion by means of a computer-controlled device (NYU impactor). Rats received several doses of MT-II (3.2, 10 and 100μg) at 2 and 8h after SCI. Results of the BBB scale were statistically analysed using an ANOVA of repeated-measures, followed by Tukey's test. Among the three doses tested, only 10 and 100μg were able to significantly increase (p<0.05) BBB scale scores eight weeks after SCI from a mean of 7.88 in the control group, to means of 12.63 and 10.88 for the 10 and 100μg doses of MT-II, respectively. The amount of spared tissue was also higher in the groups treated with 10 and 100μg, as compared to the control group values. Results from the present study demonstrate a significant neuroprotective effect of exogenously administered MT-II. Further studies are needed in order to characterize the mechanisms involved in this neuroprotective action.
    Neuroscience Letters 03/2012; 514(1):102-5. DOI:10.1016/j.neulet.2012.02.068 · 2.03 Impact Factor
  • M Méndez-Armenta · C Nava-Ruiz · F Fernández-Valverde · A Sánchez-García · C Rios ·
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    ABSTRACT: Heavy metals are ubiquitous in the environment and exposure through food and water as well as occupational sources can constitute a potential threat to human health. The mechanisms of heavy metal damage include the production of free radicals that alter mitochondrial activity, affecting cellular types like neurons and muscular fibres. We examined whether rats exposed subchronically via drinking water to low doses of heavy metals can produce alterations in muscle. Results showed that the proportion of ragged red fibres increased in muscle of rats exposed to lead and thallium, likewise slight changes in enzymatic activity of muscular fibres were also observed.
    07/2011; 32(1):107-12. DOI:10.1016/j.etap.2011.03.001
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    ABSTRACT: After spinal cord injury (SCI), a complex cascade of pathophysiological processes increases the primary damage. The inflammatory response plays a key role in this pathology. Recent evidence suggests that myeloperoxidase (MPO), an enzyme produced and released by neutrophils, is of special importance in spreading tissue damage. Dapsone (4,4'-diaminodiphenylsulfone) is an irreversible inhibitor of MPO. Recently, we demonstrated, in a model of brain ischemia/reperfusion, that dapsone has antioxidant, antiinflammatory, and antiapoptotic effects. The effects of dapsone on MPO activity, lipid peroxidation (LP) processes, motor function recovery, and the amount of spared tissue were evaluated in a rat model of SCI. MPO activity had increased 24.5-fold 24 hr after SCI vs. the sham group, and it had diminished by 38% and 19% in the groups treated with dapsone at 3 and 5 hr after SCI, respectively. SCI increased LP by 45%, and this increase was blocked by dapsone. In rats treated with dapsone, a significant motor function recovery (Basso-Beattie-Bresnahan score, BBB) was observed beginning during the first week of evaluation and continuing until the end of the study. Spontaneous recovery 8 weeks after SCI was 9.2 ± 1.12, whereas, in the dapsone-treated groups, it reached 13.6 ± 1.04 and 12.9 ± 1.17. Spared tissue increased by 42% and 33% in the dapsone-treated groups (3 and 5 hr after SCI, respectively) vs. SCI without treatment. Dapsone significantly prevented mortality. The results show that inhibition of MPO by dapsone significantly protected the spinal cord from tissue damage and enhanced motor recovery after SCI.
    Journal of Neuroscience Research 03/2011; 89(3):373-80. DOI:10.1002/jnr.22555 · 2.59 Impact Factor
  • M A Benitez · M Mendez-Armenta · S Montes · D Rembao · L H Sanin · C Rios ·
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    ABSTRACT: This study was designed to assess the effect of Cadmium (Cd) and lead (Pb) exposure during pregnancy in rats and their correlation with metallothionein (MT). Rats were exposed to either 10 ppm Cd or 300 ppm Pb through drinking water during pregnancy. Both metals were measured in placenta, fetus brain and fetal and maternal blood. MT was quantified in placenta and fetus brain and it was also observed in placenta by immunohistochemical technique. Offspring weight was found to be significantly lower for the Cd exposure group than for the control group. A Cd increase in the placenta of the exposed group was accompanied by MT induction; these effects were related to a limited accumulation of Cd in fetus brain. In contrast, dam Pb exposure caused an accumulation of Pb in the fetus brain and induced damage to placenta. The results account for differences in the transference of these metals during pregnancy that could be related to their toxicity.
    Histology and histopathology 12/2009; 24(12):1523-30. · 2.10 Impact Factor
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    ABSTRACT: This study examined the neuroprotective ability of tetrapeptide L-Asp-Ala-His-Lys (DAHK) in permanent middle cerebral artery occlusion in rats. One DAHK dose (16 mg/kg) or saline solution were i.v. administered 30 min after occlusion and neurological deficit was evaluated at 2, 24, 48, 72 and 96 h using Longa scoring scale. The striatum infarction area was evaluated until 96 h after occlusion in both groups after staining with hematoxylin-eosin. DAHK-treated group showed a significant (P < 0.05) protection of 70% of neurological deficit at 96 h after occlusion, in comparison with the control-group that showed permanent neurological deficit. The DAHK-treated group showed a significant (P < 0.05) reduction of 52% infarction area in the striatum, as compared to control values. Results presented here support the possible therapeutic application of DAHK as a neuroprotective agent in human patients with stroke, as the peptide is part of human serum albumin, already being tested in clinical trials.
    Neurochemical Research 09/2009; 35(2):343-7. DOI:10.1007/s11064-009-0060-3 · 2.59 Impact Factor
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    ABSTRACT: Interference with nitric oxide production is a possible mechanism for lead neurotoxicity. In this work, we studied the effects of sub-acute lead administration on the distribution of NOS isoforms in the hippocampus with respect to blood and hippocampal lead levels. Lead acetate (125, 250 and 500ppm) was given via drinking water to adult male Wistar rats for 14 days. We determined blood and hippocampal lead levels by atomic absorption spectrophotometry. Antibodies against three isoforms of NOS were used to analyze expression and immunolocalization using western blotting and immunohistochemistry, respectively. Blood and hippocampal lead levels were increased in a dose-dependent manner in groups treated with lead acetate. We found diminished expression and immunoreactivity of nNOS and eNOS at 500ppm as compared to the control group. No expression and immunoreactivity was observed in hippocampus for iNOS. The observed high levels of lead in the blood reflect free physiological access to this metal to the organism and were related to diminished expression and immunoreactivity for nNOS and eNOS.
    Experimental and toxicologic pathology: official journal of the Gesellschaft fur Toxikologische Pathologie 07/2009; 62(3):311-6. DOI:10.1016/j.etp.2009.04.006 · 1.86 Impact Factor
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    ABSTRACT: Spinal cord injury (SCI) is a world-wide health problem. After traumatic injury, spinal cord tissue starts a series of self-destructive mechanisms, known as the secondary lesion. The leading mechanisms of damage after SCI are excitotoxicity, free radicals' overproduction, inflammation and apoptosis. Metallothionein (MT) and reduced glutathione (GSH) are low-molecular-weight, cysteine-rich peptides able to scavenge free radicals. MT and GSH participation as neuroprotective molecules after SCI is unknown. The aim of the present study is to describe the changes of MT and GSH contents and GSH peroxidase (GPx) activity in the acute phase after SCI in rats. Female Wistar rats weighing 200-250g were submitted to spinal cord contusion model, by means of a computer-controlled device (NYU impactor). Rats receiving laminectomy were used as a control group. Animals were killed 2, 4, 12 and 24h after surgery. MT was quantified by the silver-saturation method, using atomic absorption spectrophotometry. GSH and GPx were assayed by spectrophotometry. Results indicate an increased MT content by effect of SCI, only at 4 and 24h, as compared to sham group values. Meanwhile, GSH was found decreased at 4, 12 and 24h after SCI. Interestingly, GPx activity was raised at all time points, indicating that this enzymatic defense is activated soon after SCI. Results suggest that thiol-based defenses, MT and GSH, are differentially expressed by spinal cord tissue to cope with the various processes of damage after lesion.
    Neuroscience Letters 02/2009; 452(1):56-9. DOI:10.1016/j.neulet.2009.01.020 · 2.03 Impact Factor
  • M.I. Castro-González · M Méndez-Armenta ·
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    ABSTRACT: Metals are being utilized of ways in industries and agriculture; particularly heavy metals such as mercury, cadmium, lead and arsenic constitute a significant potential threat to human health because they are associated to many adverse effects on health. The consumption of fish is recommended because it is a good source of omega-3 fatty acids, which have been associated with health benefits due to its cardio-protective effects. However, the content of heavy metals discovered in some fish makes it difficult to establish clearly the role of fish consumption on a healthy diet. Therefore the present mini-review accounts for the recent evidence of the effect of these toxic metals on the human health and their possible implications in fish consumption.
    Environmental Toxicology and Pharmacology 11/2008; 26(3):263-71. DOI:10.1016/j.etap.2008.06.001 · 2.08 Impact Factor
  • Marisela Méndez-Armenta · Camilo Ríos ·
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    ABSTRACT: The Cd has been recognized as one of the most toxic environmental and industrial pollutants due to its ability to induce disturbances in several organs and tissues following either acute or chronic exposure. This review accounts for the recent evidence on its mechanisms to induce neurotoxicity, the role of the blood-brain barrier, oxidative stress, interference with calcium, and zinc-dependent processes and apoptosis induction as well as the modulatory effect of metallothionein. Discussion about cadmium neurotoxicity is centered on mechanisms of induction of cellular disfunctions. Future investigations must address those neuronal mechanisms in detail in order to understand cadmium-induced neurotoxicity.
    Environmental Toxicology and Pharmacology 05/2007; 23(3):350-8. DOI:10.1016/j.etap.2006.11.009 · 2.08 Impact Factor
  • M A Benitez · M Mendez-Armenta · L H Sanin · S Montes · C Rios ·

    Epidemiology 11/2006; 17(Suppl). DOI:10.1097/00001648-200611001-01306 · 6.20 Impact Factor
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    ABSTRACT: Cadmium (Cd) is neurotoxic metal which induces histopathological damage and oxidative stress through free radicals over production. Metallothionein (MT) is a protein able to scavenge free radicals and to chelate metals. In this study we describe the lipid peroxidation (LPO) and MT content in the brain of developing rats exposed at Cd 1 mg/kg/day intra peritoneally (i.p.) and dexamethasone (Dx) 2 mg/kg/day (i.p.) alone and combined during 5 days. At those doses, cadmium significantly increases the levels of LPO in parietal cortex, striatum and cerebellum as compared to a control group while, in the hippocampus no modifications in the LPO levels were observed. In the group treated with Cd+Dx, Dx significantly diminished the levels of LPO in parietal cortex, striatum and cerebellum. On the other hand, the MT levels showed a significant increase in all regions of the groups treated with Dx and Cd+Dx as compared with the control group. These results show that Dx treatment prevented the increase in LPO levels associated to Cd exposure, probably through the increase in MT content.
    Toxicology Letters 10/2003; 144(2):151-7. DOI:10.1016/S0378-4274(03)00199-1 · 3.26 Impact Factor

Publication Stats

535 Citations
90.86 Total Impact Points


  • 1996-2014
    • Instituto Nacional de Neurología y Neurocirugía
      • Clinical Laboratory of Neurodegenerative Diseases
      Tlalpam, Mexico City, Mexico
  • 2006
    • Research Center for Food and Development A.C.
      Hermosillo, Sonora, Mexico
  • 1999-2002
    • The National Institute of Neurology and Neurosurgery
      Tlalpam, The Federal District, Mexico