Influence of Gold Nanoparticle Tagged Snake Venom Protein Toxin NKCT1 on Ehrlich Ascites Carcinoma (EAC) and EAC Induced Solid Tumor Bearing Male Albino Mice

ISSN: 1875-5704 (Online)
ISSN: 1567-2018 (Print)


Volume 11, 6 Issues, 2014


Download PDF Flyer




Current Drug Delivery

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 126th of 254 in Pharmacology & Pharmacy

Submit Abstracts Online Submit Manuscripts Online

Editor-in-Chief:
Istvan Toth
School of Pharmacy,University of Queensland
Brisbane, 4072
Australia


View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 2.248

Influence of Gold Nanoparticle Tagged Snake Venom Protein Toxin NKCT1 on Ehrlich Ascites Carcinoma (EAC) and EAC Induced Solid Tumor Bearing Male Albino Mice

Author(s): Tanmoy Bhowmik, Partha Pratim Saha, Anjan Kumar DasGupta and Antony Gomes

Affiliation: Laboratory of Toxinology & Experimental Pharmacodynamics, Department of Physiology, University of Calcutta, 92, APC Road, Kolkata-700 009, India.

Abstract

Earlier the conjugation of gold nanoparticle (GNP) and snake venom protein toxin NKCT1 was reported and primary characterization was performed. In the present communication, further characterizations of GNP-NKCT1 were done with SEM, EDS, XRD and Raman spectra for its physio-chemical nature and bonding. SEM showed the formation of gold nanoparticles, whereas EDS and XRD confirmed 60-90% gold nanoparticles in the solution. Raman shift corresponding to (C=O), (N-H), (C-N) confirmed the proper conjugation of GNP with NKCT1. GNP-NKCT1 showed anticancer effect both in vivo and in vitro in EAC cell and antitumor effect in EAC induced mice. In in vivo studies, GNPNKCT1 increased MST 108.30% and decreased viable EAC cell count 51.39%. Fluorescent micrograph showed signs of apoptosis (membrane blebbing, membrane disruption). Decreased level of IL-10 and low incorporation of BrdU showed decreased proliferation of EAC induced by GNP-NKCT1. With upregulation of Bax, down regulation of Bcl2 and increased expression of caspase 3/9, it was confirmed that GNP-NKCT1 induced caspase dependent apoptosis pathway in EAC cell. In in vitro studies, GNP-NKCT1 increased the late apoptotic stage of cell and arrested cell cycle division at G0/G1 state. GNP-NKCT1 also decreased the tumor volume and tumor weight in EAC induced tumor in male albino mice. It inhibited angiogenesis, which was confirmed by lower percentage of expression of VEGF. This study indicated the capability of gold nanoparticles which enhanced the tumor uptake of NKCT1 and also suggested that GNP-NKCT1 might be a good source for anti-carcinoma and anti-tumor agents.

Keywords: Apoptosis, Caspase, Ehrlich ascites carcinoma, Gold nanoparticle, Snake venom, Tumor.

Purchase Online Rights and Permissions

  
  



Article Details

Volume: 11
Issue Number: 5
First Page: 652
Last Page: 664
Page Count: 13
DOI: 10.2174/1567201811666140515101130
Advertisement

Related Journals




Webmaster Contact: urooj@benthamscience.org Copyright © 2014 Bentham Science