Las aguas y sedimentos del río tunecino Hamdoun presentan riesgo de disrupción endocrina / Water and sediment waste rejected in Hamdoun’sriver are major endocrine disrupting system

Diversos estudios recientes sostienen que muchos productos químicos antropogénicos, presentes en el medio ambiente, imitan la acción de hormonas endógenas. Estos disruptores endocrinos pueden originar múltiples efectos adversos en la fauna, como la feminización de peces, la pérdida de capacidad reproductiva, defectos congénitos y, a veces, pueden estar en el origen de algunos tipos de cáncer en el ser humano. La aparición de intersexos en peces de varios ríos europeos se ha atribuido a la exposición a sustancias químicas estrogénicas presentes en los efluentes de estaciones de tratamiento de aguas residuales. Para profundizar en el efecto ambiental de estos contaminantes, hemos investigado la actividad estrogénica, de receptor de hidrocarburo arílico y de receptor X de pregnano, de muestras de agua y sedimentos del río Hamdoun, tomadas aguas arriba y aguas abajo de la zona de vertidos procedentes del área industrial de la región central de Túnez. Mediante un ensayo in vitro de células cancerosas bioluminiscentes que expresan el gen de la luciferasa bajo el control de ciertos elementos con acción hormonal, hemos detectado escasa actividad estrogénica en agua y sedimentos por encima de la zona de vertidos; sin embargo, encontram os fuerte actividad es trogénica, de receptor de hidrocarburo arílico y de receptor X de pregnano en agua y s edimentos río abajo. Con experimentos de com petición demostramos que, predominantemente, las muestras de agua y de sedimentos con actividad estrogénica contienen compuestos con alta y baja afinidad con el ER " recombinante, respectivamente. Estos resultados indican que el agua del río y los sedimentos constituyen un importante sumidero y pueden ser fuente potencial de contaminantes disruptores endocrinos(AU)

In recent years, many studies supported that anthropogenic chemicals occurring in the environment have been shown to mimic the action of endogenous hormones. These endocrine-disrupting chemicals can potentially lead to a host of adverse effects on wildlife, such as the feminization of fish, the lack of reproduction success, birth defects and sometimes they can be the origin of some kind of cancers in human. The occurrence of intersex fish in a number of European rivers has been attributed to the exposure to estrogenic chemicals present in sewage treatment work effluents. To further understand the environmental effect of these contaminants, the estrogenic, aryl hydrocarbon receptor and pregnane X receptor activities of water and sediments were investigated in this study. The water and sediment samples were obtained from upstream and downstream outfalls of the Hamdoun River located in proximity of the industrial area in the centre region of Tunisia. Using an in vitro assay with bioluminescent cancer cells expressing luciferase gene under different hormonal responsive element control, we detected a much lower level of estrogenic activity in water and sediment upstream, however, we found out a strong estrogenic, aryl hydrocarbon receptor and pregnane X receptor activities in water and sediment downstream this river. By using competition experiments, we demonstrated that estrogenic activity found contained mainly compounds with a strong and lower affinitiy in water and sediment respectively with the recombinant ER ". These results suggest that the river water and sediments are a major sink and could be a potential source of endocrine-disrupting chemicals contaminants(AU)

Adenoviral vector cytotoxicity depends in part on the transgene encoded.

First-generation adenoviral vectors induce G(2)/M arrest and cell death at high multiplicities of infection (m.o.i.'s) in vitro. It is unclear whether this cytotoxicity is entirely adenoviral gene related or influenced in part by the encoded transgene. We examined this question in epithelial cells using seven vectors at relatively low (50) or higher (200) m.o.i.'s. The vectors contained no transgene (+/-promoter), transgenes encoding a cytoplasmic reporter protein (two luciferase constructs; beta-galactosidase), or transgenes encoding a secretory protein (alpha1-antitrypsin; growth hormone). After 24 h with a m.o.i. of 50, vectors encoding cytoplasmic reporter proteins led to greatest cytotoxicity (approximately 35-40% cells in G(2)/M). Vectors without a transgene resulted in lower cytotoxicity (approximately 15%, minus, or 23%, plus promoter, cells in G(2)/M). Vectors encoding secretory proteins led to approximately 22-25% cells in G(2)/M. A similar pattern resulted when cell number was measured. Results were unrelated to the steady-state levels of transgene product. At the higher m.o.i., all vectors caused substantial growth retardation. This is the first demonstration that adenoviral vector-induced cytotoxic effects are in part related to the transgene encoded.