Goizane Marcaida

Hospital Clínico San Carlos

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Vicente Felipo

Centro de Investigacion Principe Felipe

Marı́a-Dolores Miñana

Hospital General Universitario De Valencia

Santiago Grisolı́a

Generalitat Valenciana

Maite López‐Garrigós

Hospital Universitari Sant Joan D'Alacant

Joaquín Uris

University of Alicante

Enrique Rodríguez–Borja

Hospital Clínico Universitario de Valencia

Begoña Laíz

Hospital Universitari i Politècnic La Fe

María Salinas

Hospital Universitari Sant Joan D'Alacant

MÁ

Miguel Ángel Lorente

Roche (Spain)

Arturo Carratalá

Hospital Clínico Universitario de Valencia

Cooperative Institutions

Hospital Universitario La Paz

Instituto de Salud Carlos III

Hospital de Poniente

Universidad Internacional De La Rioja

Hospital General Universitario de Alicante Doctor Balmis

Hospital Universitario Puerta de Hierro Majadahonda

Hospital Clínico San Carlos

Hospital General Universitario Gregorio Marañón

Centro de Investigación Biomédica en Red

Universidad San Pablo CEU

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Prenatal Exposure of Rats to Ammonia Impairs NMDA Receptor Function and Affords Delayed Protection Against Ammonia Toxicity and Glutamate Neurotoxicity

Journal of Neuropathology & Experimental Neurology (1995)

María‐Dolores Miñana Goizane Marcaida Santiago Grisolı́a Vicente Pelipo

The aim of this work was to assess whether perinatal hyperammonemia impairs the function of NMDA receptors and whether this impairment affords protection against acute ammonia toxicity and glutamate and NMDA neurotoxicity. Rats were exposed to ammonia during the prenatal and lactation periods by feeding the female rats an ammonium-containing diet since day 1 of pregnancy. After weaning (at postnatal day 21), the pups were fed a normal diet with no ammonia added. This treatment resulted in a marked decrease of the growth rate of the animals, which was maintained even 1 month after normalization of ammonia levels. Rats exposed to ammonia were more resistant than controls to acute ammonia toxicity 13 days after feeding a normal diet but not at 3 months. Primary cultures of cerebellar neurons from hyperammonemic rats showed decreased binding of [3H]MK-801 and were remarkably more resistant than controls to glutamate and NMDA toxicities. Also, the increase in aspartate aminotransferase activity induced by low concentrations of NMDA was not produced in such cultures. These results indicate that exposure to ammonia during the prenatal and lactation periods results in long-lasting impairment of NMDA receptor function. This would be the reason for the delayed protection afforded by exposure to low ammonia levels against acute ammonia toxicity in animals and against glutamate and NMDA toxicity in neuronal cultures.

Neurotoxicity

Hyperammonemia

10.1097/00005072-199509000-00005

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Citations (21)

Prevalence of HTLV-1/2 Infections in Spain: A Cross-Sectional Hospital-Based Survey

AIDS Research and Human Retroviruses (2010)

Ana Treviño Juan González‐García Carmen de Mendoza Rafael Benito Antonio Aguilera

The presence of antibodies to human T-lymphotropic virus (HTLV) types 1 and 2 was examined in 5742 sera belonging to consecutive adult outpatients attended during June 2008 at 13 different hospitals across Spain. Overall, 58.8% were female. Foreigners represented 8% of the study population. Seven individuals were seropositive for HTLV-2 (overall prevalence 0.12%). No cases of HTLV-1 infection were found. All HTLV-2(+) subjects were Spanish natives, of whom six were coinfected with HIV-1 and five with hepatitis C virus (HCV). Moreover, all but one of the HTLV-2(+) subjects had been intravenous drug users. In summary, this cross-sectional survey suggests that the rate of HTLV infection in Spain is low, and is mostly represented by HTLV-2. Infected individuals are generally Spanish natives with a prior history of intravenous drug use and are coinfected with HIV-1 and/or HCV.

Cross-sectional study

Intravenous drug

Prevalence

Hepatitis C

10.1089/aid.2009.0234

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Citations (16)

Brain ATP Depletion Induced by Acute Ammonia Intoxication in Rats Is Mediated by Activation of the NMDA Receptor and Na⁺, K⁺‐ATPase

Journal of Neurochemistry (1994)

Еlena Kosenko Yuri Kaminsky Eugenio Grau María‐Dolores Miñana Goizane Marcaida

Abstract: Injection of large doses of ammonia into rats leads to depletion of brain ATP. However, the molecular mechanism leading to ATP depletion is not clear. The aim of the present work was to assess whether ammonium‐induced depletion of ATP is mediated by activation of the NMDA receptor. It is shown that injection of MK‐801, an antagonist of the NMDA receptor, prevented ammonia‐induced ATP depletion but did not prevent changes in glutamine, glutamate, glycogen, glucose, and ketone bodies. Ammonia injection increased Na + ,K + ‐ATPase activity by 76%. This increase was also prevented by previous injection of MK‐801. The molecular mechanism leading to activation of the ATPase was further studied. Na + ,K + ‐ATPase activity in samples from ammonia‐injected rats was normalized by “in vitro” incubation with phorbol 12‐myristate 13‐acetate, an activator of protein kinase C. The results obtained suggest that ammonia‐induced ATP depletion is mediated by activation of the NMDA receptor, which results in decreased protein kinase C‐mediated phosphorylation of Na + ,K + ‐ATPase and, therefore, increased activity of the ATPase and increased consumption of ATP.

10.1046/j.1471-4159.1994.63062172.x

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Citations (192)

Effects of hyperammonemia on brain protein kinase C substrates

Metabolic Brain Disease (1996)

Eugenio Grau Goizane Marcaida Carmina Montoliú María‐Dolores Miñana Santiago Grisolı́a

Hyperammonemia

10.1007/bf02237958

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Citations (17)

Susceptibilidad genética del síndrome de Gilbert en población valenciana; eficiencia del test de ayuno

Revista Clínica Española (2016)

Alfredo Torres Nicolás Elórtegui Escartín Carolina Monzó C. Guzmán Isidró Ferrer

10.1016/j.rce.2016.10.001

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Citations (4)

Lack of correlation between glutamate-induced depletion of ATP and neuronal death in primary cultures of cerebellum

Brain Research (1995)

Goizane Marcaida María-Dolores Min ̃ana Santiago Grisolı́a Vicente Felipo

10.1016/0006-8993(95)00703-s

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Citations (56)

Evaluación del patrón de solicitud de hemoglobina glucosilada por Atención Primaria: estudio piloto regional en la Comunidad Valenciana

Endocrinología y Nutrición (2011)

María Salinas Maite López‐Garrigós Arturo Carratalá Cristina Aguado Julián Ruiz Díaz

10.1016/j.endonu.2011.02.009

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Citations (3)

Ammonia Prevents Activation of NMDA Receptors by Glutamate in Rat Cerebellar Neuronal Cultures

European Journal of Neuroscience (1995)

Goizane Marcaida María‐Dolores Miñana María Burgal Santiago Grisolı́a Vicente Felipo

Acute ammonia toxicity is mediated by activation of NMDA receptors and is prevented by chronic moderate hyperammonaemia. The aim of this work was to assess whether the protective effect of chronic hyperammonaemia is due to impaired activation of the NMDA receptor. It is shown that chronic hyperammonaemia in rats decreases the binding of [3H]MK-801 to synaptosomal membranes from the hippocampus but not the amount of NMDAR1 receptor protein as determined by immunoblotting. In primary cultures of cerebellar neurons, long-term treatment with 1 mM ammonia also decreased significantly the binding of [3H]MK-801. These results suggest that ammonia impairs NMDA receptor activation. To confirm this possibility we tested the effect of long-term treatment of the cultured neurons with 1 mM ammonia on three well known events evoked by activation of the NMDA receptor: neuronal death induced by glutamate, increase in aspartate aminotransferase activity and increase in free intracellular [Ca2+]. Long-term treatment with ammonia prevented noticeably the effects of glutamate or NMDA on all these parameters. These results indicate that long-term treatment of neurons with 1 mM ammonia leads to impaired function of the NMDA receptor, which cannot be activated by glutamate or NMDA. Activation of protein kinase C by a phorbol ester restored the ability of the NMDA receptor to be activated in neurons treated with ammonia. This suggests that ammonia impairs NMDA receptor function by decreasing protein kinase C-dependent phosphorylation.

Long-term depression

10.1111/j.1460-9568.1995.tb01036.x

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Citations (75)

Clinical Presentation of Individuals With Human T-Cell Leukemia Virus Type-1 Infection in Spain

Open Forum Infectious Diseases (2019)

Carmen de Mendoza María Pirón Rocío González Ana Belén Jiménez Estrella Caballero

Although only 8%-10% of persons infected with human T-cell leukemia virus type 1 (HTLV-1) may develop virus-associated diseases lifelong, misdiagnosis of asymptomatic infected carriers frequently leads to late diagnoses.A nationwide HTLV-1 register was created in Spain in 1989. A total of 351 infected persons had been reported by the end of 2017. We examined all new HTLV-1 diagnoses during the last decade and compared their clinical presentation.A total of 247 individuals with HTLV-1 infection had been reported in Spain since year 2008. The incidence has remained stable with 20-25 new diagnoses yearly. Women represented 62%. Only 12% were native Spaniards, most of whom were foreigners from Latin America (72.5%). Up to 57 (23%) individuals presented clinically with HTLV-1-associated conditions, including subacute myelopathy (n = 24; 42.1%), T-cell lymphoma (n = 19; 33.3%), or Strongyloides stercoralis infestation (n = 8; 14%). Human T-cell leukemia virus type 1 diagnosis had been made either at blood banks (n = 109; 44%) or at clinics (n = 138; 56%). It is interesting to note that Spaniards and especially Africans were overrepresented among patients presenting with HTLV-1-associated illnesses, suggesting that misdiagnosis and late presentation are more frequent in these populations compared to Latin Americans.Given that 23% of new HTLV-1 diagnoses in Spain are symptomatic, underdiagnosis must be common. Although screening in blood banks mostly identifies asymptomatic Latin American carriers, a disproportionately high number of Spaniards and Africans are unveiled too late, that is, they already suffer from classic HTLV-1 illnesses.

Asymptomatic carrier

10.1093/ofid/ofz036

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Citations (9)

Determination of intracellular ATP in primary cultures of neurons

Brain Research Protocols (1997)

Goizane Marcaida María‐Dolores Miñana Santiago Grisolı́a Vicente Felipo

Primary (astronomy)

10.1016/s1385-299x(96)00009-8

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Citations (18)