Synthesis of Thiol Functionalized MOF-808 and its Efficiency for Mercury Removal.

A thiol-functionalized MOF-808 was produced and used to remove mercury by post-synthetic modification using 6-mercaponicotinic acid (6mna). Parent MOF-808 was impregnated for varied periods in the 6mna solution to create modified MOF-808 materials, known as MOF-808-6mna-x, where x refers to the impregnation time. Diffraction and several spectroscopic techniques were employed to quantify and confirm the coordination of 6mna into MOF-808 framework.

Ionic determinants of pH of acidic compartments under hypertonic conditions in trout hepatocytes.

Exposure of trout hepatocytes to hypertonicity induced a decrease in acridine orange (AO) fluorescence, indicating a corresponding decrease in pH inside the lumen of acidic compartments (pH(L)). Pre-exposure of cells to the specific V-ATPase inhibitor bafilomycin A1 (0.3 micromol l(-1)) increased AO fluorescence - unmasking H(+) leaks under steady-state conditions - and partially removed the hypertonicity-induced pH(L) decrease.

Interdependence of Ca2+ and proton movements in trout hepatocytes.

This study was undertaken to investigate possible interrelationships between Ca2+ homeostasis and pH regulation in trout hepatocytes. Exposure of cells to Ca2+ mobilizing agents ionomycin (0.5 micromol l(-1)) and thapsigargin (0.

Signalling pathways involved in hypertonicity- and acidification-induced activation of Na+/H+ exchange in trout hepatocytes.

In trout hepatocytes, hypertonicity and cytosolic acidification are known to stimulate Na+/H+ exchanger (NHE) activity, which contributes to recovery of cell volume and intracellular pH (pHi), respectively. The present study investigated the signalling mechanisms underlying NHE activation under these conditions. Exposing trout hepatocytes to cariporide, a specific inhibitor of NHE-1, decreased baseline pHi, completely blocked the hypertonicity-induced increase of pHi and reduced the hypertonicity-induced proton secretion by 80%.