Early detection of toxic events induced by xenobiotics is necessary for a proper assessment of human risk after the exposure to those agents. The aim of this work was to evaluate the cell line HEp-2 as an experimental model to determine the genotoxic effects of sodium arsenate. To this end, we determined the metabolic activity cells by the MTT test on seven concentrations of arsenate that range from 27 to 135,000 μM, obtaining the median lethal concentration (LC50), the lowest observed effect concentration (LOEC), and the not observed effect concentration (NOEC) of sodium arsenate at 24 h of exposition. According to the cytotoxic response obtained, we evaluated the genotoxic effect of the 27 and 270 μM concentrations by using the micronucleus assay and chromosomal aberrations test. We found a statistically significant increase (p<0.05) in the frequency of micronuclei between control cultures and those exposed to the highest concentration of sodium arsenate. Furthermore, the frequencies of nucleoplasmic bridges and tripolar mitosis were significantly higher in cell cultures exposed to the above concentrations compared to the control cultures (p<0.05). The participation of the glutathione system as response to the arsenate exposition was also analyzed, and a statistically significant increase in the glutathione content was found in those cells exposed to 27 μM of arsenate. The Glutathione S-transferase activity did not increase in the exposed cells compared to control cells, suggesting that the arsenate reduction involved other metabolic pathways in the HEp-2 cells. These results confirm that, under the conditions carried out in this study, sodium arsenate is genotoxic for HEp-2 cells. Therefore, we suggest that this cell line would be a good model for the assessment of the cytotoxic and genotoxic effects of xenobiotics on human cells.

La detección temprana de eventos tóxicos inducidos por xenobióticos es necesaria para una adecuada evaluación del riesgo humano ante la exposición a dichos agentes. El objetivo de este trabajo fue evaluar a la línea celular HEp-2 como modelo experimental para determinar los efectos genotóxicos del arseniato de sodio. Para ello, se determinó la actividad metabólica de las células mediante el ensayo de MTT, en siete concentraciones de arseniato de sodio en el rango 27-135.000 μM, determinando la concentración letal media (LC50), la menor concentración de efecto observado (LOEC) y la mayor concentración de efecto no observado (NOEC) de arseniato de sodio para una exposición de 24 h. Teniendo en cuenta los datos de citotoxicidad, se evaluó el efecto genotóxico a las concentraciones 27 y 270 μM por medio del ensayo de micronúcleos y aberraciones cromosómicas, encontrando un aumento estadísticamente significativo en la frecuencia de micronúcleos entre el control y la mayor concentración arseniato de sodio ensayada. Además, la presencia de puentes nucleoplasmáticos y mitosis tripolar fue significativamente mayor en ambas concentraciones estudiadas con respecto al control. Se analizó la participación del sistema de glutatión como respuesta a la exposición al arseniato, encontrándose un aumento estadísticamente significativo en el contenido de glutatión en la concentración de arseniato de 27 μM. La actividad de la glutatión S-transferasa no aumentó, lo que sugiere que la reducción del arseniato implicó otra vía metabólica en las células HEp-2. Estos resultados confirman que el arseniato de sodio induce genotoxicidad en células HEp-2 en las condiciones realizadas en este estudio y por lo tanto este tipo de línea celular es un buen modelo para ensayos de citotoxicidad y genotoxicidad en los cuales se quiere evaluar el riesgo humano.

Puberty refers to the final stage of children's growth and development in which adult height, reproductive and psychosocial maturity are reached. It is initiated in the central nervous system by neuroendocrine factors (under genetic control and environmental influence) that activate the hypothalamic- pituitary-gonadal axis and its regulatory mechanisms. Precocious puberty is defined as the progressive onset of pubertal signs at an age more than 2.5 SD below the mean of a population. It may be gonadotropin-dependent (central) or gonadotropin-independent (peripheral). Most of the cases are idiopathic, but occasionally the cause may be an underlying organic disease with variable severity. Treatment is recommended because of the negative effects it may have on the child's development.

La pubertad es el período final del crecimiento y maduración del niño en el que se alcanza la talla final y la madurez psicosocial y reproductiva. Se inicia en el sistema nervioso central por factores neuroendocrinos que activan el eje hipotálamo-hipofisario-gonadal y sus mecanismos reguladores. Estos factores actúan bajo control genético e influencia ambiental. La pubertad precoz se define como la aparición progresiva de signos puberales a una edad por debajo de 2,5 DS de la media para una población determinada. Puede ser dependiente de gonadotropinas (central) o independiente de gonadotropinas (periférica). La mayoría de los casos son de origen idiopático, aunque también puede estar causada por enfermedades orgánicas de severidad variable. Por la repercusión desfavorable que tiene en la maduración del niño se recomienda tratar adecuadamente.

There is evidence showing a close relationship between diet and the occurrence of non-communicable chronic diseases. The present study assessed food consumption in a 2002/2004 cohort of young adults born in 1978/79 in Ribeirão Preto, SP, Brazil. The composition of the habitual diet consumed by a sample of 2063 individuals aged 23-25 years was analyzed using a validated semi-quantitative food frequency questionnaire based on studies of prevention of non-communicable chronic diseases. The Dietsys software was used for dietary calculations. In terms of WHO/2003 recommendations, there was a high mean daily consumption of energy from fat (consumption: 35.4%; recommendation: 15-30%), a low mean intake of energy from carbohydrates (47.5%; 55-75%) and a low mean consumption of total fibers (15.2 g; >25 g). Mean intake of energy from fatty acids (10%; <10%) and protein (15.6%; 10-15%) was within recommended limits. When compared to the recommendations of the food pyramid adapted to the Brazilian population, adequate intake was observed only regarding the meat group (consumption: 1.9 portions; recommended: 1-2). There was a low consumption of vegetables (2.9; 4-5), fruits (1.2; 3-5), breads (3.6; 6-9), and dairy products (1.7; 3), with excessive fat and sugar intake (5.7; 1-2). We conclude that the inadequate food consumption observed in this young population may be associated with the development of excess weight and may contribute to the triggering of non-communicable chronic diseases.

We evaluated the porphyrinogenic ability of ethanol (20% in drinking water) per se, its effect on the development of sporadic porphyria cutanea tarda induced by hexachlorobenzene in female Wistar rats (170-190 g, N = 8/group), and the relationship with hepatic damage. Twenty-five percent of the animals receiving ethanol increased up to 14-, 25-, and 4.5-fold the urinary excretion of delta-aminolevulinate, porphobilinogen, and porphyrins, respectively. Ethanol exacerbated the precursor excretions elicited by hexachlorobenzene. Hepatic porphyrin levels increased by hexachlorobenzene treatment, while this parameter only increased (up to 90-fold) in some of the animals that received ethanol alone. Ethanol reduced the activities of uroporphyrinogen decarboxylase, delta-aminolevulinate dehydrase and ferrochelatase. In the ethanol group, many of the animals showed a 30% decrease in uroporphyrinogen activity; in the ethanol + hexachlorobenzene group, this decrease occurred before the one caused by hexachlorobenzene alone. Ethanol exacerbated the effects of hexachlorobenzene, among others, on the rate-limiting enzyme delta-aminolevulinate synthetase. The plasma activities of enzymes that are markers of hepatic damage were similar in all drug-treated groups. These results indicate that 1) ethanol exacerbates the biochemical manifestation of sporadic hexachlorobenzene-induced porphyria cutanea tarda; 2) ethanol per se affects several enzymatic and excretion parameters of the heme metabolic pathway; 3) since not all the animals were affected to the same extent, ethanol seems to be a porphyrinogenic agent only when there is a predisposition, and 4) hepatic damage showed no correlation with the development of porphyria cutanea tarda.

Immunoglobulins (Igs) from sera of Atlantic salmon (Salmo salar) were purified with 50% saturated ammonium sulphate followed by molecular sieving chromatography using Sephacryl S-300. The fraction of purified Igs was used as immunogen to generate a polyclonal antibody anti-salmon Igs. This antibody was affinity purified in a Sepharose-protein G column. By immunoradiometric assay against the immunogen, the rabbit IgG anti-salmon Igs showed a high specific titer (at least 1/100.000) for the antigen. This reagent offers the possibility of detection of salmon or trout (crossreactivity) humoral immune responses, both for diagnostic and research purposes

A partir de sueros de salmón del Atlántico (Salmo salar) se han purificado sus inmunoglobulinas (Igs) mediante precipitación con sulfato de amonio al 50% de saturación, seguido de cromatografía de exclusión por tamaño molecular en Sephacryl S-300. La fracción de Igs purificadas fue utilizada como inmunógeno para generar un anticuerpo policlonal anti-Igs de salmón, el cual fue purificado por afinidad usando Sefarosa-proteína G. Mediante ensayo inmunorradiométrico contra el inmunógeno, la IgG anti-Igs de salmón demostró un elevado título (a lo menos 1/100.000) específico para el antígeno. El anticuerpo generado ofrece la posibilidad de detectar respuestas humorales en salmón y trucha (reactividad cruzada), con fines diagnósticos o de investigación