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Expelling of dyestuff into water resource system causes major thread to the environment. Adsorption is the cost effective and potential method to remove the dyes from the effluents. Therefore, an attempt was made to study the adsorption of dyestuff (Methylene Blue (MB), Bromophenol Blue (BPB) and Coomassie Brilliant Blue (CBB)) by α-chitin nanoparticles (CNP) prepared from Penaeus monodon (Fabricius, 1798) shell waste. On contrary to the most recognizable adsorption studies using chitin, this is the first study using unique nanoparticles of ⩽50 nm used for the dye adsorption process. The results showed that the adsorption process increased with increase in the concentration of CNP, contact time and temperature with the dyestuff, whereas the adsorption process decreased with increase in the initial dye concentration and strong acidic pH. The results from Fourier transform infrared (FTIR) spectroscopy confirmed that the interaction between dyestuff and CNP involved physical adsorption. The adsorption process obeys Langmuir isotherm (R2 values were 0.992, 0.999 and 0.992 for MB, BPB and CBB, and RL value lies between 0 and 1 for all the three dyes) and pseudo second order kinetics (R2 values were 0.996, 0.999 and 0.996 for MB, BPB and CBB) more effectively. The isotherm and kinetic models confirmed that CNP can be used as a suitable adsorbent material for the removal of dyestuff from effluents.

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Herein, we report facile theranostic platinum nanoparticles (PtNPs) conjugated to an anticancer drug, doxorubicin (DOX), in unraveling the inhibition of a cell survival PI3K/AKT (phosphatidylinositol 3-kinase/protein kinase B) signaling pathway in MCF-7 and MDA-MB-231 human breast cancer cells. The significant features of our DOX@PtNPs as a theranostic platform are as follows: (i) drug release studies showed a progressive pH-dependent delivery; (ii) in vitro studies of DOX@PtNPs displayed a relatively higher cytotoxicity to breast cancer cells compared to unconjugated PtNPs and DOX; (iii) intracellular drug release studies showed a specific binding of DOX@PtNPs and their release within the cytoplasm and perinuclear region; (iv) DOX@PtNPs induced the apoptosis of cancer cells by DNA damage via the generation of elevated levels of reactive oxygen species and decreased mitochondrial membrane potential (ΔΨm), as evidenced by fluorescence microscopic studies; and (v) DOX@PtNPs inhibited the PI3K/AKT signaling pathway in breast cancer cells by activating PTEN, a tumor suppressor gene. The induced mitochondrial-dependent apoptotic pathway led to the activation of downstream caspases. Finally, our findings illustrate that DOX@PtNPs may serve as a better theranostic agent for cancer nanomedicine.