CONICET | Buscador de Institutos y Recursos Humanos

The luminal urinary bladder has developed an efficient permeability barrier of the uroepithelium, covering the organ-free surface, that protects it against the back-flow of toxics eliminated by the urine. We propose in this work that the permeability barrier may be vulnerable, allowing the urinary toxics exert some deleterious effect on the uroepithelium. We show that rats exposed to arsenic (As) by prolonged time of arseniccontaining water ingestion, not only induced pre-neoplasic morphological changes, but altered the permeability of the vesicle population beneath the plasma membrane allowing the passage of a endocytosed fluorescent marker HPTS (hydroxypyrene-1,3,6- trisulfonic acid) and its quencher DPX (p-xylene-bis-pyridinium bromide) out of the vesicular lumen. Using an induced endocytosis model and the fluorescence requenching technique it is shown that the vesicular leakage of the cationic DPX was almost complete while the release of the anionic HPTS molecule was fractional and higher in the arsenic-treated-rats in comparison with the control. The retention of As in the urinary bladder assessed by X-ray fluorescence spectrometry by synchrotron radiation (SR-mXRF) showed to be low compared with non-treated rats but was accompanied by altered concentration of K, Ca, Fe, Cu and Zn, all ions related to cellular metabolism. The results support the hypothesis that low amount of As can escape from the urinary bladder barrier by promoting an increased membrane permeability leading to early arsenic-associated toxicological processes.mXRF) showed to be low compared with non-treated rats but was accompanied by altered concentration of K, Ca, Fe, Cu and Zn, all ions related to cellular metabolism. The results support the hypothesis that low amount of As can escape from the urinary bladder barrier by promoting an increased membrane permeability leading to early arsenic-associated toxicological processes.