North Eastern Hill University

About: North Eastern Hill University is a education organization based out in Shillong, Meghalaya, India. It is known for research contribution in the topics: Population & Catalysis. The organization has 2318 authors who have published 4476 publications receiving 48894 citations.

Theoretical study of the substituent effects on the S-H bond dissociation energy and ionization energy of 3-pyridinethiol: Prediction of novel antioxidant.

Abstract: The S-H bond dissociation enthalpies [BDE(S-H)] of a set of 5-X- and 6-X-3-pyridinethiols (X ) F, Cl, CH3, OCH3 ,N H 2, N(CH3)2 ,C F 3, CN, and NO2) have been computed using the density functional theory based (RO)B3LYP procedure with 6-311++G(2df,2p) basis set. The effects of substituents on the BDE(SH), proton affinity of the pyridinethiol anion [PA(S - )] and ionization energy (IE) are analyzed and their correlations with Hammett’s substituent constants are examined. Subsequently, a series of 6-substituted 3-pyridinethiols have been explored to find out their antioxidant potentials. Finally, a number of 3-pyridinethiol based compounds are theoretically proposed as novel antioxidants.

Validity of generalised second law in holographic DGP brane

Abstract: In this paper we study the validity of the generalised second law of thermodynamics (GSLT) of the universe bounded by the event horizon on the Dvali–Gabadadze–Porrati (DGP) brane world. The radius of the event horizon is calculated by establishing a correspondence between holographic dark energy and the effective energy density in the DGP brane world. It is shown that in the absence of cold dark matter (CDM), GSLT is always respected. In the presence of CDM, we take three different DGP models and find conditions under which GSLT holds.

N-Substituted Pyrido-1,4-Oxazin-3-Ones Induce Apoptosis of Hepatocellular Carcinoma Cells by Targeting NF-κB Signaling Pathway.

Abstract: Hepatocellular carcinoma (HCC) is a fatal disease and ranked fifth in cancer related mortality. Persistent activation of NF-κB is responsible for the oncogenesis, metastasis, tumor evasion, anti-apoptosis, angiogenesis and proliferation in HCC. Therefore, designing of chemically novel, biologically potent small molecules that target NF-κB signaling cascade have gained prominent clinical interest. Herein we synthesized a novel class of 4-(substituted)-2H-pyrido[3,2-b][1,4]oxazin-3(4H)-one by reacting 2H-pyrido[3,2-b][1,4]oxazin-3(4H)-one with various alkyl halides by using combustion derived bismuth oxide. We evaluated the antiproliferative efficacy of newly synthesized compounds against HCC cells and identified 4-(4-nitrobenzyl)-2H-pyrido[3,2-b][1,4]oxazin-3(4H)-one (NPO) as lead anticancer agent. In addition, we investigated the effect of NPO on the DNA binding ability of NF-κB and NF-κB regulated luciferase expression in HCC cells. The results demonstrated that NPO can induce significant growth inhibitory effects in HepG2, HCCLM3 and Huh-7 cells in dose and time-dependent manner. Interestingly, NPO induced significant downregulation in p65 DNA binding ability, p65 phosphorylation and subsequent expression of NF-κB dependent luciferase gene expression in diverse HCC cell lines. Further, in silico docking analysis suggested that NPO can show direct physical interaction with NF-κB. Finally, NPO was found to significantly abrogate tumor growth at a dose of 50 mg/kg in an orthotopic mouse model. Thus, we report the potential anticancer effects of NPO as a novel inhibitor of NF-κB signaling pathway in HCC.

Antiproliferative and cytotoxic effect of a novel organotin compound on mammalian cells both in vitro and in vivo.

Abstract: Organotin compounds are organometallic compounds showing various toxicological properties. Several organotin compounds also showed an antineoplastic effect. However, their relative mutagenic potential is not well established. In this study Et(2)SnCl(2).L [L=N-(2-pyridylmethylene)-4-toluidine] (OTC) has been subjected to investigation for its cytotoxic effect in mouse bone marrow cells (BMCs) and human peripheral blood lymphocyte cells (HPBLs). The Sn [bond] N bond in OTC is 2.46A which is greater than 2.39A and therefore, a better formation of tin-DNA complex can be expected. The present data indicate that OTC induced significant delay in cell kinetics and sister chromatid exchanges (SCEs) in both BMCs and HPBLs, whereas, induction of chromosome aberrations was found only in HPBLs. The presence of buthionine sulfoximine (BSO) modulated cellular sensitivity towards OTC in both cell systems. It may be inferred that the OTC could bind on DNA more easily owing to its structural advantage and this may explain the induction of DNA damage and the delay in cell proliferation. Since the cytotoxic effect of OTC is more in glutathione depleted cells, the concentration of OTC may be reduced to get an antitumour effect in GSH-depleted cells and thus minimizes its toxic side effect.