CELLMED (셀메드)

Cellmed Orthocellular Medicine and Pharmaceutical Association (셀메드 세포교정의약학회)
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Homeopathic mother tincture of Conium initiates reactive oxygen species mediated DNA damage and makes HeLa cells prone to apoptosis

  • Bishayee, Kausik (Cytogenetics and Molecular Biology Laboratory, Department of Zoology, University of Kalyani) ;
  • Mukherjee, Avinaba (Cytogenetics and Molecular Biology Laboratory, Department of Zoology, University of Kalyani) ;
  • Paul, Avijit (Cytogenetics and Molecular Biology Laboratory, Department of Zoology, University of Kalyani) ;
  • Khuda-Bukhsh, Anisur Rahman (Cytogenetics and Molecular Biology Laboratory, Department of Zoology, University of Kalyani)
  • Received : 2012.05.16
  • Accepted : 2012.08.20
  • Published : 2012.08.31
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Abstract

Adverse side-effects and lack of scientific validation of some chemotherapeutic agents prevent the use of many traditional medicines claimed to have anti-cancer effects. Ethanolic extract of Conium maculatum has long been used in traditional and alternative systems of medicine including homeopathy for the treatment of glandular enlargements, cancerous tumours or hard lumps of testicles, prostate, ovaries, breasts and/ or uterus, particularly in the breast. However, if and how it acts still remains scientifically unknown. This study aims to test if Conium extract (CE), used as mother tincture of Conium in homeopathy, has demonstrable anti-cancer potentials without having much cytotoxicity in normal cells. Cytotoxicity of the drug was tested by conducting MTT assay on both normal (peripheral blood mononuclear cells) and HeLa cells. We also evaluated DNA fragmentation and DNA damage by DAPI and diphenylamine assay. The LDH activity assay was done to evaluate the percentages of apoptosis and necrosis. ROS accumulation also was evaluated to pin-point the actual events of apoptosis. Administration of drug clearly demonstrated its anti-cancer potentials as evidenced by the DNA damage analysis. The ROS activity also increased in case of the CE treated cells. LDH data revealed that the mode of cell death was mainly apoptotic and not necrotic. CE appears to induce apoptosis of cancer cells through ROS mediated pathway, and has negligible cytotoxicity against normal cells.

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References

  1. Ahemedin J, Bray F, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011;61:69-90. https://doi.org/10.3322/caac.20107
  2. Boericke W. Pocket manual of homeopathic material medica & repertory. reprint ed. (India: B. Jain Publishers (P) Ltd), 2002.
  3. Chakraborty D, Mukherjee A, Sikdar S, Paul A, Ghosh S, Khuda-Bukhsh AR. [6]-Gingerol isolated from ginger attenuates sodium arsenite induced oxidative stress and plays a corrective role in improving insulin signalling in mice. Toxicol Lett. 2012;210:34-43. https://doi.org/10.1016/j.toxlet.2012.01.002
  4. Fruehauf JP, Meyskens Jr FL. Reactive oxygen species: a breath of life or death? Clin Cancer Res. 2007;13:789-794. https://doi.org/10.1158/1078-0432.CCR-06-2082
  5. Fulda S, Debatin KM. Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy. Oncogene. 2006;25:4798-4811. https://doi.org/10.1038/sj.onc.1209608
  6. Green JA. Clinical trials in cancer. Br J Cancer. 2011;104:1521-1522. https://doi.org/10.1038/bjc.2011.137
  7. Ioannou YA, Chen FW. Quantitation of DNA fragmentation in apoptosis. Nucleic Acids Res. 1996;24:992-993. https://doi.org/10.1093/nar/24.5.992
  8. Khuda-Bukhsh AR. Towards understanding molecular mechanisms of action of homeopathic drugs: An overview. Mol Cell Biochem. 2003;253:339-345. https://doi.org/10.1023/A:1026048907739
  9. Kim JS, He L, Lemasters JJ. Mitochondrial permeability transition: a common pathway to necrosis and apoptosis. Biochem Biophy Res Commun. 2003;304:463-470. https://doi.org/10.1016/S0006-291X(03)00618-1
  10. Lemasters JJ, Nieminen AL, Qian T, Trost LC, Elmore SP, Nishimura Y, Crowe RA, Cascio WE, Bradham CA, Brenner DA, Herman B. The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy. Biochim Biophy Acta. 1998;1366:177-196. https://doi.org/10.1016/S0005-2728(98)00112-1
  11. Lopez-Lazaro M. Dual role of hydrogen peroxide in cancer: possible relevance to cancer chemoprevention and therapy. Cancer Lett. 2007;252:1-8. https://doi.org/10.1016/j.canlet.2006.10.029
  12. Lowe SW, Lin AW. Apoptosis in cancer. Carcinogenesis. 2000;21:485-495. https://doi.org/10.1093/carcin/21.3.485
  13. Mandal SK, Biswas R, Bhattacharyya SS, Paul S, Dutta S, Pathak S, Khuda-Bukhsh AR. Lycopodine from Licopodium clavatum extract inhibits proliferation on HeLa cells through induction of apoptosis via caspase-3 activation. Eur J Pharmacol. 2010;626:115-122. https://doi.org/10.1016/j.ejphar.2009.09.033
  14. Massague J. G1 cell-cycle control and cancer. Nature. 2004;432:298-306. https://doi.org/10.1038/nature03094
  15. Schep LJ, Slaughter RJ, Beasley DM. Nicotinic plant poisoning. Clin Toxicol. 2009;47:771-781. https://doi.org/10.1080/15563650903252186

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