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Quantum dots (QDs), one of the fastest developing and most exciting fluorescent materials, have attracted increasing interest in bioimaging and biomedical applications. The long-term stability and emission in the visible region of QDs have proved their applicability as a significant fluorophore in cell labelling. In this study, an attempt has been made to explore the efficacy of l-cysteine as a capping agent for Mn-doped ZnS QD for intracellular imaging. A room temperature nucleation strategy was adopted to prepare non-toxic, water-dispersible and biocompatible Mn:ZnS QDs. Aqueous and room temperature QDs with l-cysteine as a capping agent were found to be non-toxic even at a concentration of 1500 µg/mL and have wide applications in intracellular imaging. Copyright © 2015 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

We demonstrate the role of molecular switching of TrkA/p75NTR signaling cascade in organophosphate pesticide-Monocrotophos (MCP) induced neurotoxicity in stem cell derived cholinergic neurons and in rat brain. Our in-silico studies reveal that MCP followed the similar pattern of binding as staurosporine and AG-879 (known inhibitors of TrkA) with TrkA protein (PDB ID: 4AOJ) at the ATP binding sites. This binding of MCP to TrkA led to the conformational change in this protein and triggers the cell death cascades. The in-silico findings are validated by observing the down regulated levels of phosphorylated TrkA and its downstream molecules viz., pERK1/2, pAkt and pCREB in MCP-exposed cells. We observe that these MCP induced alterations in pTrkA and downstream signaling molecules are found to be associated with apoptosis and injury to neurons. The down-regulation of TrkA could be linked to increased p75NTR. The in-vitro studies could be correlated in the rat model. The switching of TrkA/p75NTR signaling plays a central role in MCP-induced neural injury in rBNSCs and behavioral changes in exposed rats. Our studies significantly advance the understanding of the switching of TrkA/p75NTR that may pave the way for the application of TrkA inducer/p75NTR inhibitor for potential therapeutic intervention in various neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

Highlights: [•] Cypermethrin induces astrocyte injury via modulation in Ca++, ROS, JNK and P38 pathways. [•] Which affects permeability of BBB, TJ protein and MMP expression. [•] Finally causing astorcyte toxicity and up regulation of reelin signaling leading to deregulation of cellular migration. [Copyright &y& Elsevier]

Cobalt chloride (CoCl 2 ) is a well-known hypoxia mimetic mediator that induces hypoxia-like responses. CoCl 2 , a mediator confirmed to alleviate hypoxia-inducible factor-1 (HIF-1), has been associated with a variety of hypoxic responses. HIF-1 is the foremost transcriptionfactor that is particularly activated during hypoxia and regulates various genes. Therefore, this study aimed to investigate the cellular and molecular responses of the co-cultured cells under the influence of the CoCl 2 -induced hypoxic condition. Mono- and co-cultured C2C12 and 3T3-L1 cells were exposed to CoCl 2 , and a significant induction in HIF-1, reactive oxygen species and lipid peroxidase and a reduction in glutathione and catalase were observed. The expressions of proapoptotic genes like Bax, p53, caspase-9, and caspase-3 were notably increased, whereas the antiapoptotic gene, i.e., Bcl2, was downregulated during hypoxia in mono- as well as co-cultured C2C12 cells. However, the co-cultured C2C12 cells show significantly lower induction in oxidative stress and expression of apoptotic genes in comparison to monocultured C2C12 cells. Whereas, the co-cultured 3T3-L1 cells show comparatively higher oxidative stress and apoptotic event in comparison to monocultured 3T3-L1 cells. The reason may be the communication between the cells and some soluble factors that help in cell survival/death from hypoxia. Moreover, it may also be due to the fact that fat and muscle cells interact and communicate via proximity and mutual ability when growing together. Therefore, the co-culture system provides a unique approach to intercellular communication between the two different cell types., Competing Interests: The authors declare no competing financial interest., (Copyright © 2019 American Chemical Society.)

Quantum dots (QDs), one of the fastest developing and most exciting fluorescent materials, have attracted increasing interest in bioimaging and biomedical applications. The long-term stability and emission in the visible region of QDs have proved their applicability as a significant fluorophore in cell labelling. In this study, an attempt has been made to explore the efficacy of L-cysteine as a capping agent for Mn-doped ZnS QD for intracellular imaging. A room temperature nucleation strategy was adopted to prepare non-toxic, water-dispersible and biocompatible Mn:ZnS QDs. Aqueous and room temperature QDs with L-cysteine as a capping agent were found to be non-toxic even at a concentration of 1500 µg/mL and have wide applications in intracellular imaging., (Copyright © 2015 John Wiley & Sons, Ltd.)

Inducible expressions cytochrome P450s (CYPs) against environmental chemicals in brain tissues of experimental animals is well-documented. However, the precise role of specific brain cell type in the metabolism of different class of xenobiotics has not been explored adequately. We study the expression of selected CYPs (1A1/1A2, 2B1/2B2, 2E1) in primary cultures of rat brain neuronal and glial cell exposed to an organophosphate pesticide-monocrotophos (MCP), a known neurotoxicant. The cultured neurons and glial cells express significant expression of CYP1A1, 2B2 and 2E1 isoenzymes, where the levels were comparatively higher in neuronal cells. Neuronal cells exhibited greater induction of CYP2E1 against MCP exposure, while glial cells were having more vulnerability for CYP1A and 2B isoenzymes. Similarly, cells were showing substrate specific responses against the specific inducers of CYPs, that is, ethanol (2E1), cyclophosphamide (2B1/2B2), 3-methylcholanthrene (1A1/1A2). The altered expression and activity of selected CYPs in cultured neuronal and glial cells could be helpful in explaining the association between MCP-induced neurotoxicity/metabolism and synthesis or transport of the neurotransmitters. The induction of CYPs in glial cells may also have significance as these cells are thought to be involved in protecting the neurons from environmental insults and safeguard them from toxicity. The differential expression pattern of CYPs in neuronal and glial cells exposed to MCP also indicate the selective sensitivity of these cells against the xenobiotics, hence suggested their suitability as tool to screen neurotoxicity potential of variety of xenobiotics.