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The transformation of recalcitrant pharmaceutical pollutants into products with diminished concerns via heterogeneous photocatalysis has gained considerable momentum over the past several years. However, practical applications of most semiconductor-based photocatalysts are severely restricted, attributed to insufficient visible light response pertaining to their wide band gap, ultrafast recombination of the photogenerated charge carriers, and issues corresponding to retrieval for persistent usage. Herein, rosette-like molybdenum disulfide (MoS 2 ) nanoflowers are directly grown on the interpenetrating networks of graphene aerogels (GAs) through a facile one-step hydrothermal method, and the resulting lightweight, self-supporting composites are systematically assessed for the photocatalytic degradation of tetracycline (TC). Notably, after 120 min of exposure to visible light, ∼91% of TC is degraded over the MoS 2 /GAs, which is severalfold higher than pristine MoS 2 , standalone GA, and other contemporary photocatalysts. Based on the radical quenching assay, hydroxyl radicals and superoxide anions are the principal mediators of the photocatalytic dissociation of TC. Furthermore, the primary intermediates and residual products of the photocatalytic breakdown of TC are distinguished, and a conceivable disintegration pathway is proposed. Besides, these tailor-made hybrid aerogels can be recuperated easily and successfully reused over multiple cycles, suggesting their widespread consideration in photocatalytic wastewater treatment.

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Glucocorticoids (GCs) are rapidly released in response to stress and play an important role in the physiological adjustments to re-establish homeostasis. The mode of action of GCs for stress coping is mediated largely by the steroid binding to the glucocorticoid receptor (GR), a ligand-bound transcription factor, and modulating the expression of target genes. However, GCs also exert rapid actions that are independent of transcriptional regulation by modulating second messenger signaling. However, a membrane-specific protein that transduces rapid GCs signal is yet to be characterized. Here, using freshly isolated hepatocytes from rainbow trout (Oncorhynchus mykiss) and fura2 fluorescence microscopy, we report that stressed levels of cortisol rapidly stimulate the rise in cytosolic free calcium ([Ca2+]i). Pharmacological manipulations using specific extra- and intra-cellular calcium chelators, plasma membrane and endoplasmic reticulum channel blockers and receptors, indicated extracellular Ca2+ entry is required for the cortisol-mediated rise in ([Ca2+]i). Particularly, the calcium release-activated calcium (CRAC) channel gating appears to be a key target for the rapid action of cortisol in the ([Ca2+]i) rise in trout hepatocytes. To test this further, we carried out in silico molecular docking studies using the Drosophila CRAC channel modulator 1 (ORAI1) protein, the pore forming subunit of CRAC channel that is highly conserved. The result predicts a putative binding site on CRAC for cortisol to modulate channel gating, suggesting a direct, as well as an indirect regulation (by other membrane receptors) of CRAC channel gating by cortisol. Altogether, CRAC channel may be a novel cortisol-gated Ca2+ channel transducing rapid nongenomic signalling in hepatocytes during acute stress.

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Glucocorticoids (GCs) stimulate rapid cell signalling by activating the membrane-anchored intracellular glucocorticoid receptor (GR). However, the recruitment of the GR to the plasma membrane to facilitate nongenomic signalling is far from clear. As cytosolic free calcium ([Ca2+]i) is involved in intracellular protein dynamics, we tested the hypothesis that acute elevation in cortisol levels rapidly stimulates GR translocation to the plasma membrane via a calcium-dependent process in rainbow trout (Oncorhynchus mykiss) hepatocytes. To test this, we monitored temporal changes in intracellular GR distribution in response to cortisol exposure. Immunofluorescence labelling showed that the GR was present in cytosolic and nuclear compartments in trout hepatocytes. However, upon cortisol exposure, the GR rapidly (within 5 min) formed punctate and colocalized with caveolin-1, suggesting plasma membrane localization of the receptor. This redistribution of the GR to the plasma membrane was transient and lasted for 30 min and was evident even upon exposure to cortisol-BSA, a membrane-impermeable analogue of the steroid. The rapid cortisol-mediated GR translocation to the plasma membrane involved F-actin polymerization and was completely abolished in the presence of either EGTA or Cpd5J-4, a calcium release–activated calcium (CRAC) channel blocker. Additionally, the modulation of the biophysical properties of the plasma membrane by cholesterol or methyl β-cyclodextrin, which led to changes in ([Ca2+]i) levels, modified GR translocation to the plasma membrane. Altogether, acute cortisol-mediated rise in ([Ca2+]i) levels rapidly stimulated the translocation of intracellular GR to the plasma membrane, and we propose this as a mechanism promoting the nongenomic action of the GR for hepatocyte stress resistance.

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