Photodegradation behaviour of estriol: An insight on natural aquatic organic matter influence.

Estriol (E3) is one of the steroidal estrogens ubiquitously found in the aquatic environment, photodegradation being an important pathway for the elimination of such endocrine disrupting compounds. However, it is important to understand how environmentally important components present in aquatic matrices, such as organic matter, may affect their photodegradation. The main objective of this work was to investigate the photodegradation of E3 in water, under simulated solar radiation, as well as the effect of humic substances (HS - humic acids (HA), fulvic acids (FA) and XAD-4 fraction) in E3 photodegradation. Moreover, the photodegradation behaviour of E3 when present in different environmental aquatic matrices (fresh, estuarine and waste water samples) was also assessed. Results showed a completely different E3 degradation rate depending on the aquatic matrix. In ultrapure water the half-life obtained was about 50 h, while in presence of HS it varied between 5 and 10 h. Then, half-life times between 1.6 and 9.5 h were determined in environmental samples, in which it was observed that the matrix composition contributed up to 97% for the overall E3 photodegradation. Therefore, E3 photodegradation in the considered aquatic matrices was mostly caused by photosensitizing reactions (indirect photodegradation).

Dynamics of fast synaptic excitation during trains of stimulation in myenteric neurons of guinea-pig ileum.

Fast excitatory postsynaptic potentials (fEPSPs) occur in bursts in the myenteric plexus during evoked motor reflexes in the guinea-pig ileum in vitro. This study used electrophysiological methods to study fEPSPs during stimulus trains to mimic bursts of synaptic activity in vitro. The amplitude of fEPSPs or fast excitatory postsynaptic currents (EPSCs) declined (rundown) during stimulus trains at frequencies of 0.5, 5, 10 and 20 Hz. At 0.5 Hz, fEPSP or fEPSC amplitude declined by 50% after the first stimulus but remained constant for the remainder of the train. At 5, 10 and 20 Hz, synaptic responses ran down completely with time constants of 0.35, 0.21 and 0.11 s, respectively. Recovery from rundown occurred with a time constant of 7 s. Mecamylamine, a nicotinic cholinergic receptor antagonist, or PPADS, a P2X receptor antagonist, reduced fEPSP amplitude, but they had no effect on rundown. Responses caused by trains of ionophoretically applied ATP or ACh (to mimic fEPSPs) did not rundown. Blockade of presynaptic inhibitory muscarinic, adenosine A1, opioid, alpha2-adrenergic and 5-HT1A receptors or pertussis toxin (PTX) treatment did not alter rundown. Antidromic action potentials followed a 10-Hz stimulus train. Iberiotoxin (100 nM), a blocker of large conductance calcium activated K+ (BK) channels, did not alter rundown. These data suggest that synaptic rundown is not due to: (a) action potential failure; (b) nicotinic or P2X receptor desensitization; (c) presynaptic inhibition mediated by pertussis-toxin sensitive G-proteins, or (d) BK channel activation. Synaptic rundown is likely due to depletion of a readily releasable pool (RRP) of neurotransmitter.