Antioxidant effect of phenolic compounds (PC) at different concentrations in IEC-6 cells: A spectroscopic analysis.

Phenolic compounds (PC) have been proposed as natural antioxidant agents that protect cells against oxidative stress-related diseases. Nonetheless, their low bioavailability forecasts controversy about mechanisms on their in vivo scavenging activity against reactive oxygen species (ROS). It has been proposed that PC reduce directly ROS concentration. An alternative or complementary action of PC could be the activation of the cell's antioxidant pathway, involving the regulation of gene expression, like that initiated by the Nrf2 transcription factor. To date there is not enough experimental data to support or discard this possibility. In the present study, we evaluated the use of several PC to prevent peroxidation of macromolecules and to elicit the activation of the Nrf2 transcription factor in H2O2-stresed IEC-6 enterocytic cell line. Synchrotron microspectroscopy demonstrated that PC compounds protected proteins, lipids and nucleic acids against oxidation induced by H2O2. Immunofluorescence results showed that treatment with quercetin (Qc), catechin (Cat) and capsaicin (Cap) induced the translocation of Nrf2 into the nucleus, at the same level as did H2O2 treatment, thus mimicking the action of the endogenous cell response to peroxidation. Even though the detailed mechanism still needs to be elucidated, we demonstrated the activation of Nrf2 by PCs in response to oxidative stress.

Inhibition of α-amylase by flavonoids: Structure activity relationship (SAR).

Flavonoids are recognized to regulate animals' food digestion processes trough interaction with digestive enzymes. The binding capacity of hesperetin (HES), luteolin (LUT), quercetin (QUE), catechin (CAT) and rutin (RUT) with pancreatic α-amylase were evaluated, using UV-Vis spectroscopy, fluorescence and molecular docking. Using p-nitrophenyl-α-d-maltopentoside (pNPG5) as substrate analog, LUT showed the best inhibitory capacity, even better than that of the positive control, acarbose (ACA). A mixed-type inhibition was observed for HES, LUT and QUE, a competitive-type for ACA, while no inhibition was observed with CAT and RUT. In agreement with kinetic results, α-amylase presented a higher affinity for LUT, when analyzed by fluorescence quenching. The binding of flavonoids to amylase followed a static mechanism, where the binding of one flavonoid per enzyme molecule was observed. Docking analysis showed that flavonoids bound near to enzyme active site, while ACA bound in another site behind the catalytic triad. Extrinsic fluorescence analysis, together with docking analysis pointed out that hydrophobic interactions regulated the flavonoid-α-amylase interactions. The present study provides evidence to understand the relationship of flavonoids structure with their inhibition mechanism.

Trombosis de senos venosos durales. Diagnóstico inesperado cerebral / Dural venous sinuses thrombosis; an unexpected diagnosis

No disponible

Relación entre la grasa corporal y la expresión de ira en personas que realizan ejercicio regularmente / Relacionamento entre gordura corporal e expressão de raiva em pessoas que se exercitam regularmente / Relationship between body fat mass and the expression of anger in people who practice exercise customarily

La actividad física proporciona beneficios, tanto a la población sana como enferma, pero también puede derivar en problemas psicológicos y emocionales como respuesta al estrés. Además, aquellos atletas con menor peso corporal presentan indicadores más elevados de depresión e ira. Se plantea determinar la relación de la grasa corporal sobre la expresión de ira y entender la relación entre distintos comportamientos psicológicos, en personas físicamente activas. 264 sujetos cumplimentaron el Inventario de Expresión de Ira Estado-Rasgo, versión 2, para el estudio sobre las características de la ira y sus efectos en la salud mental y física. Se tomaron medidas antropométricas (peso, talla, IMC, porcentaje de grasa corporal, masa libre de grasa). Se calcularon distintos percentiles en función del género y edad, clasificando a los participantes en tres grupos: percentil 55 de grasa corporal. Se analizaron distintos comportamientos en relación al STAXI-2 y a los distintos percentiles, pero sin encontrar diferencias significativas entre la ira y los tres grupos (AU)

Physical activity provides benefits, both to healthy as to ill population, but can also lead to psychological and emotional problems in response to stress. Furthermore, those athletes with lower body weight have higher indicators of depression and anger. We propose to relate body fat on the expression of anger and to understand the relationship between different psychological behaviors in physically active people. 264 subjects completed the Anger Expression Inventory State Trait version 2 (STAXI-2), which studies the characteristics of anger and its effects on mental and physical health. Anthropometric measurements (weight, height, BMI, percent body fat, fat-free mass) were taken. Various body fat percentiles, 55 were calculated according to gender and age, classifying participants into three percentile groups. Different behaviors were recorded in relation to STAXI-2 and percentiles, but with no significant differences between anger and those groups (AU)

A atividade física proporciona benefícios tanto para pessoas saudáveis como doentes, mas também pode levar a problemas psicológicos e emocionais, como resposta ao estresse. Além disso, os atletas com menor peso corporal têm indicadores mais altos de depressão e raiva. Prevê-se a determinar a influência da gordura corporal sobre a modulação do comportamento e entender a relação entre os vários comportamentos psicológicos entre as pessoas fisicamente ativas. 264 pessoas preencheram um questionário ad hoc, que incluiu Anger Expression Inventory State Trait version 2 (STAXI-2). Medidas antropométricas (peso, altura, IMC, percentual de gordura corporal, massa livre de gordura) foram tomadas. Vários percentis foram calculados por sexo e idade, classificando os participantes em três grupos: percentil 55 de gordura corporal. Diferentes comportamentos foram registrados em relação ao STAXI-2 e os vários percentis, mas sem diferenças significativas entre a raiva e os três grupos (AU)

Hernia diafragmática congénita de aparición tardía: la importancia de la clínica / Tardive appearing congenital diaphragmatic hernia: the importance of the symptoms

El diagnóstico de hernia diafragmática es raro después del período neonatal. Presentamos a un lactante de 8 meses con decaimiento y diagnóstico final de hernia diafragmática, ya que se trata de una presentación atípica, en una edad poco común y que presentó una evolución tórpida, a fin de difundir el conocimiento de esta entidad y sus posibles presentaciones a la comunidad científica (AU)

Diaphragmatic hernia diagnosis after neonatal period is a rare issue. We show a 8 month-baby with decay and final diagnosis of late-onset diaphragmatic hernia, because it is an atypical presentation, an uncommon age, and a torpid evolution, thus, it would be interesting to spread this subject to scientific community (AU)

IGF-1 deficiency causes atrophic changes associated with upregulation of VGluT1 and downregulation of MEF2 transcription factors in the mouse cochlear nuclei.

Insulin-like growth factor 1 (IGF-1) is a neurotrophic protein that plays a crucial role in modulating neuronal function and synaptic plasticity in the adult brain. Mice lacking the Igf1 gene exhibit profound deafness and multiple anomalies in the inner ear and spiral ganglion. An issue that remains unknown is whether, in addition to these peripheral abnormalities, IGF-1 deficiency also results in structural changes along the central auditory pathway that may contribute to an imbalance between excitation and inhibition, which might be reflected in abnormal auditory brainstem responses (ABR). To assess such a possibility, we evaluated the morphological and physiological alterations in the cochlear nucleus complex of the adult mouse. The expression and distribution of the vesicular glutamate transporter 1 (VGluT1) and the vesicular inhibitory transporter (VGAT), which were used as specific markers for labeling excitatory and inhibitory terminals, and the involvement of the activity-dependent myocyte enhancer factor 2 (MEF2) transcription factors in regulating excitatory synapses were assessed in a 4-month-old mouse model of IGF-1 deficiency and neurosensorial deafness (Igf1 (-/-) homozygous null mice). The results demonstrate decreases in the cochlear nucleus area and cell size along with cell loss in the cochlear nuclei of the deficient mouse. Additionally, our results demonstrate that there is upregulation of VGluT1, but not VGAT, immunostaining and downregulation of MEF2 transcription factors together with increased wave II amplitude in the ABR recording. Our observations provide evidence of an abnormal neuronal cytoarchitecture in the cochlear nuclei of Igf1 (-/-) null mice and suggest that the increased efficacy of glutamatergic synapses might be mediated by MEF2 transcription factors.

Dietary fiber and phenolic compounds as functional ingredients: interaction and possible effect after ingestion.

Dietary fiber and phenolic compounds are two recognized dietary factors responsible for potential effects on human health; therefore, they have been widely used to increase functionality of some foods. This paper focuses on showing the use of both substances as functional ingredients for enriching foods, and at the same time, describes the use of a single material that combines the properties of the two types of substances. The last part of the work describes some facts related to the interaction between dietary fiber and phenolic compounds, which could affect the bioaccessibility and absorption of phenolics in the gut. In this sense, the purpose of the present review is to compile and analyze evidence relating to the use of dietary fiber and phenolic compounds to enhance technological and nutritional properties of foods and hypothesize some of the possible effects in the gut after their ingestion.

Age-related functional and structural retinal modifications in the Igf1-/- null mouse.

BACKGROUND: Mutations in the gene encoding human insulin-like growth factor-I (IGF-I) cause syndromic neurosensorial deafness. To understand the precise role of IGF-I in retinal physiology, we have studied the morphology and electrophysiology of the retina of the Igf1(-/-) mice in comparison with that of the Igf1(+/-) and Igf1(+/+) animals during aging. METHODS: Serological concentrations of IGF-I, glycemia and body weight were determined in Igf1(+/+), Igf1(+/-) and Igf1(-/-) mice at different times up to 360days of age. We have analyzed hearing by recording the auditory brainstem responses (ABR), the retinal function by electroretinographic (ERG) responses and the retinal morphology by immunohistochemical labeling on retinal preparations at different ages. RESULTS: IGF-I levels are gradually reduced with aging in the mouse. Deaf Igf1(-/-) mice had an almost flat scotopic ERG response and a photopic ERG response of very small amplitude at postnatal age 360days (P360). At the same age, Igf1(+/-) mice still showed both scotopic and photopic ERG responses, but a significant decrease in the ERG wave amplitudes was observed when compared with those of Igf1(+/+) mice. Immunohistochemical analysis showed that P360 Igf1(-/-) mice suffered important structural modifications in the first synapse of the retinal pathway, that affected mainly the postsynaptic processes from horizontal and bipolar cells. A decrease in bassoon and synaptophysin staining in both rod and cone synaptic terminals suggested a reduced photoreceptor output to the inner retina. Retinal morphology of the P360 Igf1(+/-) mice showed only small alterations in the horizontal and bipolar cell processes, when compared with Igf1(+/+) mice of matched age. CONCLUSIONS: In the mouse, IGF-I deficit causes an age-related visual loss, besides a congenital deafness. The present results support the use of the Igf1(-/-) mouse as a new model for the study of human syndromic deaf-blindness.

Carbon paste electrodes modified with biosolids, soils and biocomposites utilized to study the interaction between organic matter and copper.

Carbon paste electrodes (CPEs) modified with a biosolid, two types of soils with different amounts of organic matter (OM), and two biocomposites (soils mixed with a biosolid) were used to assess and compare the Cu(II) ion retention properties of the organic matter contained in the samples. The accumulation of Cu(II) on the surface of the modified carbon paste electrodes (MCPEs) was performed under open-circuit conditions. When comparing the response of the MCPEs while assessing parameters such as pH, preconcentration time, and adsorption/desorption capacity, it was found that the reaction mechanism of the two soils is different between the soils and dissimilar from the biosolid; while the biocomposites show reaction mechanisms that are intermediate between those of the soils and the biosolid. This was proven with the use of infrared spectroscopy, since the FTIR spectra show similarities between the two soils and significant differences between the soils and the biosolid.

Registro de traumatismos craneoencefálicos leves: estudio multicéntrico de la Sociedad Española de Urgencias Pediátricas / Registry of mild craniocerebral trauma: Multicentre study from the Spanish Association of Pediatric emergencies

Objetivo: Revisar la actuación habitual ante un traumatismo craneal (TCE) leve en los Servicios de Urgencias y determinar los factores predictivos más importantes de lesión intracraneal (LIC). Material y métodos: Estudio multicéntrico prospectivo de 18 meses de duración realizado en 9 hospitales españoles. Se recogieron los datos de los pacientes menores de 18 años atendidos en Urgencias por TCE leve (puntuación en la escala de Glasgow de 13 a 15) en las 72h previas. Resultados: Se incluyeron 1.070 pacientes (61,2% de sexo masculino). La mediana de edad fue de 2,4 años (P 25-75%; de 0,9 a 6,4 años). La mediana de tiempo trascurrido desde el TCE hasta la consulta fue de 1h (P 25-75%; de 0,6 a 2,5h). Se practicó radiografía simple de cráneo al 64,5% de los niños y tomografía computarizada al 9%, resultó normal el 91,4% y el 84,4%, respectivamente. La prevalencia de LIC fue del 1,4% en la muestra total (intervalo de confianza [IC] del 95%: de 0,8 a 2,3). Precisó ingreso el 25,3% de los pacientes, 4 (3,7%) requirieron neurocirugía y ningún niño falleció. En el análisis multivariante, las variables que se asociaron a un riesgo incrementado de LIC fueron la pérdida de conciencia (odds ratio [OR] de 4,2; IC del 95%: de 1,1 a 17; p = 0,045), el deterioro neurológico (OR de 8,8; IC del 95%: de 2,1 a 37,6; p = 0,003) y la detección de un cefalohematoma (OR de 14,6; IC del 95%: de 4,9 a 44; p<0,001). Conclusiones: La combinación de parámetros clínicos permite seleccionar de forma adecuada a los pacientes con TCE leve que precisan exploraciones complementarias. En consecuencia, el uso rutinario de la radiografía de cráneo no parece justificado (AU)

Objective: To determine management practices of minor head trauma in children evaluated at Spanish Hospital Emergency Departments and to determine patient variables associated with intracranial injury. Methods: Multicenter and prospective study during 18 months in 9 hospitals in Spain. Patients up to the age of 18 years with minor head trauma (Glasgow Coma Scale score higher than or equal to 13 on admission), treated in Emergency Departments and with a maximum onset of 72h since the traumatism, were included in the study. Results: A total of 1070 patients were studied with a median age of 2.4 years (p25-75 0.9 6.4 years); 61.2% were male. The median time between head trauma and medical consultation was 1 hour (p25-75 0.6 2.5h). Skull X-rays were performed on 64.5% of the children and a head CT scan on 9%; 91.4% of X-ray and 84.4% of CT were normal. The prevalence of intracranial injury was 1.4% (95% CI: 0.8 2.3). Twenty-five point three percent of the patients were admitted; 4 (3.7%) required neurosurgical intervention during admission. None of the patients died. Multiple logistic regression analysis identified loss of consciousness (OR 4.2, 95% CI: 1.1 17; P=0.045), neurological deterioration (OR 8.8, 95% CI: 2.1 37.6; P=0.003) and cephalhaematoma (OR 14.6, 95% CI: 4.9 44; P <0.001) as independent predictors of intracranial injury. Conclusions: The combination of clinical parameters allows selection of patients with minor head trauma who need complementary explorations. In consequence, the routine use of skull X-ray in their initial evaluation is unnecessary (AU)

[Registry of mild craniocerebral trauma: multicentre study from the Spanish Association of Pediatric emergencies]. / Registro de traumatismos craneoencefálicos leves: estudio multicéntrico de la Sociedad Española de Urgencias Pediátricas.

OBJECTIVE: To determine management practices of minor head trauma in children evaluated at Spanish Hospital Emergency Departments and to determine patient variables associated with intracranial injury. METHODS: Multicenter and prospective study during 18 months in 9 hospitals in Spain. Patients up to the age of 18 years with minor head trauma (Glasgow Coma Scale score higher than or equal to 13 on admission), treated in Emergency Departments and with a maximum onset of 72h since the traumatism, were included in the study. RESULTS: A total of 1070 patients were studied with a median age of 2.4 years (p25-75 0.9-6.4 years); 61.2% were male. The median time between head trauma and medical consultation was 1 hour (p25-75 0.6-2.5h). Skull X-rays were performed on 64.5% of the children and a head CT scan on 9%; 91.4% of X-ray and 84.4% of CT were normal. The prevalence of intracranial injury was 1.4% (95% CI: 0.8-2.3). Twenty-five point three percent of the patients were admitted; 4 (3.7%) required neurosurgical intervention during admission. None of the patients died. Multiple logistic regression analysis identified loss of consciousness (OR 4.2, 95% CI: 1.1-17; P=0.045), neurological deterioration (OR 8.8, 95% CI: 2.1-37.6; P=0.003) and cephalhaematoma (OR 14.6, 95% CI: 4.9-44; P <0.001) as independent predictors of intracranial injury. CONCLUSIONS: The combination of clinical parameters allows selection of patients with minor head trauma who need complementary explorations. In consequence, the routine use of skull X-ray in their initial evaluation is unnecessary.

Oxidative and nitrosative stress and fibrogenic response.

Uncontrolled production of collagen I is the main feature of liver fibrosis. Following a fibrogenic stimulus such as alcohol, hepatic stellate cells (HSC) transform into an activated collagen-producing cell. In alcoholic liver disease, numerous changes in gene expression are associated with HSC activation, including the induction of several intracellular signaling cascades, which help maintain the activated phenotype and control the fibrogenic and proliferative state of the cell. Detailed analyses for understanding the molecular basis of the collagen I gene regulation have revealed a complex process involving reactive oxygen species (ROS) as key mediators. Less is known, however, about the contribution of reactive nitrogen species (RNS). In addition, a series of cytokines, growth factors, and chemokines, which activate extracellular matrix (ECM)-producing cells through paracrine and autocrine loops, contribute to the fibrogenic response.

[Hepatocyte oxidant stress and alcoholic liver disease]. / Estrés oxidativo hepatocitario y hepatopatía alcohólica.

Acute and chronic alcohol consumption increases the production of reactive oxygen species (ROS), and enhances lipid peroxidation of lipids, proteins, and DNA. The mechanism by which alcohol causes cell injury is still not clear but a major role for ROS and lipid peroxidation-end products is considered. Many pathways have been suggested to play a role on how ethanol induces a state of "oxidative stress", including redox-state changes, acetaldehyde production, damage to the mitochondria, membrane injury, apoptosis, ethanol-induced hypoxia, effects on the immune system and altered cytokine production, increased endotoxin levels and activation of Kupffer cells, mobilization of iron, changes in the antioxidant defense, particularly mitochondrial glutathione (GSH), one electron oxidation of ethanol to 1-hydroxy-ethyl radical, and induction of CYP2E1. These pathways are not exclusive of one another and it is likely that several, indeed many systems contribute to the ability of ethanol to induce a state of oxidative stress.

Estrés oxidativo hepatocitario y hepatopatía alcohólica / No disponible

El consumo agudo y crónico de alcohol aumenta la producciónde especies de oxígeno reactivas (EOR) y potencia la peroxidaciónde los lípidos, las proteínas y el ADN. El mecanismo por el que elalcohol produce lesión celular sigue sin estar claro, pero se piensaque las EOR y los productos de la peroxidación lipídica intervienende forma decisiva. Se ha señalado la intervención de muchasvías en la manera que tiene el etanol de inducir un estado de “estrésoxidativo”, incluidos los cambios de estado redox, la producciónde acetaldehído, el daño mitocondrial, las lesiones membranosas,la apoptosis, la hipoxia inducida por etanol, los efectossobre el sistema inmunitario y la producción alterada de citocinas,el aumento de los niveles de endotoxinas y de activación de las célulasde Kupffer, la movilización del hierro, la modulación de ladefensa antioxidante, especialmente del glutatión mitocondrial(GSH), la oxidación monoelectrónica del etanol a un radical 1-hidroxi-etilo y la inducción de la CYP2E1. Estas vías no son excluyentesentre sí y es probable que sean varios, ciertamente muchos,los sistemas que contribuyan a la capacidad que posee eletanol de inducir un estado de estrés oxidativo

Acute and chronic alcohol consumption increases the productionof reactive oxygen species (ROS), and enhances lipid peroxidationof lipids, proteins, and DNA. The mechanism by which alcoholcauses cell injury is still not clear but a major role for ROSand lipid peroxidation-end products is considered. Many pathwayshave been suggested to play a role on how ethanol induces a stateof “oxidative stress”, including redox-state changes, acetaldehydeproduction, damage to mitochondria, membrane injury, apoptosis,ethanol-induced hypoxia, effects on the immune system andaltered cytokine production, increased endotoxin levels and activationof Kupffer cells, mobilization of iron, modulation of the antioxidantdefense, particularly mitochondrial glutathione (GSH),one electron oxidation of ethanol to 1-hydroxy-ethyl radical, andinduction of CYP2E1. These pathways are not exclusive of oneanother and it is likely that several, indeed many, systems contributeto the ability of ethanol to induce a state of oxidative stress

[Neurotrophic action of insulin-like growth factor-I in the inner ear]. / Acciones neurotróficas del factor de crecimiento similar a la insulina de tipo I en el oído interno.

INTRODUCTION: Loss of hearing constitutes one of the most frequent disabling sensory impairments in the developed world. Different therapeutic approaches are currently being studied, including treatment with stem cells, genetic manipulation and pharmacological protection. AIM: To evaluate the role played by insulin-like growth factor-I (IGF-I) in the development, maintenance and repair of auditory functioning. DEVELOPMENT: Proper development of the inner ear is dependent on a suitable coordination of the cell processes of proliferation, differentiation, neurogenesis and programmed cell death, which are regulated by different factors, one of which is IGF-I. During the embryogenesis of the inner ear, this factor is expressed in abundance and is essential for cell survival and maintaining neuronal precursors. Studies conducted in Igf-1-/- null mice have highlighted its importance in the development and continued functioning of the inner ear. Mice with a deficit in this gene display morphological disorders that correspond to severe functional deficiencies, which are confirmed by analysing brainstem auditory evoked potentials. A deficit of IGF-I in humans is also accompanied by profound sensory hypoacusis. CONCLUSIONS: In a scenario like this, IGF-I appears as a key factor in the development of auditory functioning and a candidate for regenerative therapy of the inner ear.

Acciones neurotróficas del factor de crecimiento similar a la insulina de tipo I en el oído interno / Neurotrophic action of insulin-like growth factor-i in the inner ear

Introducción. La pérdida de audición constituye una de las deficiencias sensoriales invalidantes más frecuentes en el mundo desarrollado. En la actualidad se estudian diferentes abordajes terapéuticos, entre los que se incluyen el tratamiento con células madre, la manipulación genética y la protección farmacológica. Objetivo. Evaluar el papel del factor de crecimientosimilar a la insulina de tipo I (IGF-I) en el desarrollo, el mantenimiento y la reparación de la función auditiva. Desarrollo. El desarrollo del oído interno depende de la adecuada coordinación de los procesos celulares de proliferación, diferenciación, neurogénesis y muerte celular programada, que se encuentran regulados por distintos factores entre los que se encuentra el IGF-I. Durante la embriogénesis del oído interno, este factor se expresa abundantemente y es fundamental para la supervivencia celular y el mantenimiento de los precursores neuronales. El estudio del ratón nulo Igf-1–/– ha puesto de manifiesto su importancia en el desarrollo y mantenimiento funcional del oído interno. Los ratones deficientes en este gen presentan alteraciones morfológicas que se corresponden con graves deficiencias funcionales, confirmadas mediante el análisis de los potenciales evocados auditivos de tronco cerebral. El déficit de IGF-I en humanos también se acompaña de hipoacusia sensorial profunda. Conclusión. En este escenario, se perfila el IGF-I como un factor clave para el desarrollo de la función auditiva y un candidato para la terapia regenerativa del oído interno

Introduction. Loss of hearing constitutes one of the most frequent disabling sensory impairments in the developed world. Different therapeutic approaches are currently being studied, including treatment with stem cells, genetic manipulation and pharmacological protection. Aim. To evaluate the role played by insulin-like growth factor-I (IGF-I) in the development, maintenance and repair of auditory functioning. Development. Proper development of the inner ear is dependent on a suitable coordination of the cell processes of proliferation, differentiation, neurogenesis and programmed cell death, which are regulated by different factors, one of which is IGF-I. During the embryogenesis of the inner ear, this factor is expressed in abundance and is essential for cell survival and maintaining neuronal precursors. Studies conducted in Igf-1–/– null mice have highlighted its importance in the development and continued functioning of the inner ear. Mice with a deficit in this gene display morphological disorders that correspond to severe functional deficiencies, which are confirmed by analysing brainstem auditory evoked potentials. A deficit of IGF-I in humans is also accompanied by profound sensory hypoacusis. Conclusions. In a scenario like this, IGF-I appears as a key factor in the development of auditory functioning and a candidate for regenerative therapy of the inner ear

Dimethylsphingosine increases cytosolic calcium and intracellular pH in human T lymphocytes.

N,N-Dimethyl-D-erythro-sphingosine (DMS) is the N-methyl derivative of sphingosine; both are activators of sphingosine-dependent protein kinases. The aim of this work was to study the effect of DMS on cytosolic calcium and intracellular pH (pHi) in human T lymphocytes. The variations of calcium and pH were determined by fluorescence digital imaging using Fura-2-AM and BCECF-AM, respectively. DMS increased both pHi and Ca(2+)-cytoslic in human T lymphocytes. These effects were dose-dependent. This drug induced a fast increase in pHi and a release of calcium from different intracellular calcium pools than thapsigargin. DMS also induced a Ca(2+)-influx different from the store-operated calcium channels, since drug effect was not modified by 30 microM SKF 96365. The influx of calcium induced by DMS was completely blocked by preincubation in the presence of nickel, or lanthanum, while the increase in pHi was no affected. However, the presence of cadmium reduced but does not block Ca(2+)-influx. The inhibition of G-protein by 100 ng/mL pertussis toxin, and the inhibition of tyrosine kinases by genistein significantly reduced the cytosolic calcium increase induced by DMS by an inhibition of both, release of calcium from intracellular pools and influx from extracellular medium. The inhibition of pools emptiness by these drugs was related with the inhibition that they induce in the DMS cytosolic alcalinization. In summary, DMS increases pHi and as consequence releases calcium from intracellular pools, and it increases calcium-influx through a channel different from store-operated channel (SOC). Both cytosolic calcium and pHi increase are modulated by G-proteins and tyrosine kinases.