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RISS 인기검색어
- 검색키워드
- 저자 : Dhasmana, A. (검색결과 3 건)
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Jamal, Qazi Mohammad Sajid,Dhasmana, Anupam,Lohani, Mohtashim,Firdaus, Sumbul,Ansari, Md Yousuf,Sahoo, Ganesh Chandra,Haque, Shafiul Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.13
Cigarette smoke derivatives like NNK (4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone) and NNAL (4-(methylnitrosamino)-1-(3-pyridyl)-1-butan-1-ol) are well-known carcinogens. We analyzed the interaction of enzymes involved in the NER (nucleotide excision repair) pathway with ligands (NNK and NNAL). Binding was characterized for the enzymes sharing equivalent or better interaction as compared to +Ve control. The highest obtained docking energy between NNK and enzymes RAD23A, CCNH, CDK7, and CETN2 were -7.13 kcal/mol, -7.27 kcal/mol, -8.05 kcal/mol and -7.58 kcal/mol respectively. Similarly the highest obtained docking energy between NNAL and enzymes RAD23A, CCNH, CDK7, and CETN2 were -7.46 kcal/mol, -7.94 kcal/mol, -7.83 kcal/mol and -7.67 kcal/mol respectively. In order to find out the effect of NNK and NNAL on enzymes involved in the NER pathway applying protein-protein interaction and protein-complex (i.e. enzymes docked with NNK/NNAL) interaction analysis. It was found that carcinogens are well capable to reduce the normal functioning of genes like RAD23A (HR23A), CCNH, CDK7 and CETN2. In silico analysis indicated loss of functions of these genes and their corresponding enzymes, which possibly might be a cause for alteration of DNA repair pathways leading to damage buildup and finally contributing to cancer formation.
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Crosstalk Between Co-Cultured 3T3-L1 and C2C12 Cells After the Exposure of Nano-Titanium Dioxide
Tripathi, Vinay Kumar,Sivakumar, Allur Subramaniyan,Dhasmana, Anupam,Hwang, Inho American Scientific Publishers 2018 Journal of Nanoscience and Nanotechnology Vol.18 No.6
<P>Nanotechnology is a promptly growing field in this century, and it have been extensively used in several solicitations. Reactive oxygen species (ROS) generation is one of the important mechanism of action of nanoparticles. The excess ROS generation can induce oxidative stress, so the cells are unable to sustain the normal biological redox-regulated tasks. The high oxidative stress and ROS formation condition, damage the biological macromolecules, cell signaling pathways and finally leads to cell death or cancer initiation. The objective of the present study is to reveal the effects of TiO2 nanoparticle on co-culture system. The cell viability, oxidative stress and apoptosis were evaluated in monolayer and co-culture 3T3-L1 cells after the exposure of TiO2. Our results indicated that TiO2 significantly induces the reactive oxygen species (ROS), lipid peroxidation and decrease in the level of glutathione. Additionally, real-time PCR data analysis shown an increased in the expression of p53, Bax, caspase-9, caspase-3 and decreased the level of Bcl-2, by this means specifying that apoptosis induced by TiO2 NPs occurs via the caspase-dependent pathway. This study analytically shows that oxidative stress is the fundamental mechanism by which TiO2 causes apoptosis in a co-culture system even at very low concentrations. In the future, the use of such nanoparticles should be cautiously scrutinized.</P>
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Tripathi, V. K.,Kumar, V.,Pandey, A.,Vatsa, P.,Dhasmana, A.,Singh, R. P.,Appikonda, S. H.,Hwang, I.,Lohani, M. Humana Press 2017 Molecular Neurobiology Vol. No.
<P>Expression of various cytochrome P450s (CYPs) in mammalian brain cells is well documented. However, such studies are hampered in neural/glial cells of human origin due to nonavailability of human brain cells. To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines. CPA induced significant expression of CYP2C8 and CYP3A4 in both types of cells in a time-dependent manner. Neural cell line exhibited relatively higher constitutive and inducible expression of CYPs than the glial cell line. MCP exposure alone could not induce the significant expression of CYPs, whereas the cells preexposed to CPA showed a significant response to MCP. Similar to the case of CPA induced expressions, neural cells were found to be more vulnerable than glial cells. Our data indicate differential expressions of CYPs in cultured human neural and glial cell lines. The findings were synchronized with protein ligand docking studies, which showed a significant modulatory capacity of MCP by strong interaction with CYP regulators-CAR and PXR. Similarly, the known CYP inducer CPA has also shown significant high docking scores with the two studied CYP regulators. We also observed a significant induction in reactive oxygen species (ROS), lipid peroxides (LPO), micronucleus (MN), chromosomal aberration (CA), and reduction in reduced glutathione (GSH) and catalase following the exposure of MCP. Moreover, the expressions of apoptotic markers such as caspase-3, caspase-9, Bax, and p53 were significantly upregulated, whereas the levels of antiapoptotic marker, Bcl2, was downregulated after the exposure of MCP in both cell lines. These findings confirm the involvement of ROS-mediated oxidative stress, which subsequently triggers apoptosis pathways in both human neural (SH-SY5Y) and glial (U373-MG) cell lines following the exposure of MCP.</P>
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