ABSTRACT
Synthesis of a metal-free carbon nitride (g-C3N4) photocatalyst in the form of nitrogen-rich g-C3-xN4+x derivatives is desirable for efficient solar to hydrogen conversion and remains a challenging task to achieve. Herein we report the development of homogeneous sheets of nitrogen-rich graphitic carbon nitride samples from melamine by a solid-gas interface approach. Using this method, pure g-C3N4 (CN), g-C3-xN4+x under ammonia flow (CN-NH3) and g-C3-xN4+x under nitrogen flow (CN-N2) are prepared. The g-C3-xN4+x (CN-NH3) sample shows better surface conductivity, wide optical absorbance in the visible region, reduced recombination and high electron donor density, and higher performance toward photoelectrochemical hydrogen evolution (HER). The g-C3-xN4+x (CN-NH3) generates a photocurrent of 2.06 µA cm-2, which is 2.5 times higher than that of the pure g-C3N4 (CN) sample (0.85 µA cm-2). It also shows higher photocatalytic water splitting ability compared to the CN and CN-N2 samples, generating 634 µmol g-1 hydrogen without cocatalyst and 1163 µmol g-1 of hydrogen with Pt cocatalyst. Density functional calculations suggest that the progressive band gap reduction with the increase in the N-dopant percentage can be attributed to the gradual increase in the partial π-occupations, which can lead to a significant stabilization of the conduction band minima. The theoretical modeling, however, indicates a saturation in the band gap effect after 75% of N-dopant. The onset potential of g-C3-xN4+x for HER appears at η = 0.43 V in dark and η = 0.34 V vs Ag/AgCl under solar light illumination of 1 sun.
ABSTRACT
ABC transporters have a significant role in drug disposition and response and various studies have implicated their involvement in epilepsy pharmacoresistance. Since genetic studies till now are inconclusive, we thought of investigating the role of xenobiotics as transcriptional modulators of ABC transporters. Here, we investigated the effect of six antiepileptic drugs (AEDs) viz. phenytoin, carbamazepine, valproate, lamotrigine, topiramate and levetiracetam, on the expression and function of ABCB1, ABCC1, ABCC2 and ABCG2 in Caco2 and HepG2 cell lines through real time PCR, western blot and functional activity assays. Further, the interaction of AEDs with maximally induced ABCC2 was studied. Carbamazepine caused a significant induction in expression of ABCB1 and ABCC2 in HepG2 and Caco2 cells, both at the transcript and protein level, together with increased functional activity. Valproate caused a significant increase in the expression and functional activity of ABCB1 in HepG2 only. No significant effect of phenytoin, lamotrigine, topiramate and levetiracetam on the transporters under study was observed in either of the cell lines. We demonstrated the interaction of carbamazepine and valproate with ABCC2 with ATPase and 5,6-carboxyfluorescein inhibition assays. Thus, altered functionality of ABCB1 and ABCC2 can affect the disposition and bioavailability of administered drugs, interfering with AED therapy.
