Nanosecond pulsed electric fields induce apoptosis in p53-wildtype and p53-null HCT116 colon carcinoma cells

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09.12.2009, 04:17:3909.12.09
Subject:   Cancer  -  Review electric field interference with normal function of p53  - 
ElecFields (nanosec pulsed) ALTERNATIVE to IonizRadTrtmt...2007
Dear Olle:    An interesting study (re colon carcinoma) and another example of how non-ionizing radiation effects are similar, if not identical, to effects of ionizing radiaton (non-acute).....     Since p53 exists to prevent cells from becoming cancerous, it would seem reasonable to assume that the close, chronic, prolonged use of a cell phone for many hours a day, month-after-month and year-after-year, might promote malignant brain tumor formation in part by disruption of natural function of p53 protein.    Interesting to note "American Cancer Society" below also.       Take care  -  Joanne....   12-09-09

From: JCMPelican
To: JCMPelican
Sent: 12/9/2009 2:32:19 A.M. Central Standard Time
Subj: ElecFields (nanosec pulsed) ALTERNATIVE to IonizRadTrtmt...2007

Nanosecond pulsed electric fields induce apoptosis in p53-wildtype and p53-null HCT116 colon carcinoma cells

Journal Apoptosis
Publisher Springer Netherlands
ISSN 1360-8185 (Print) 1573-675X (Online)
Issue Volume 12, Number 9 / September, 2007
Category Original Paper
DOI 10.1007/s10495-007-0083-7
Pages 1721-1731
Subject Collection Medicine
SpringerLink Date Wednesday, May 23, 2007

Emily H. Hall1, 2, 3, Karl H. Schoenbach2 and Stephen J. Beebe1, 2

(1)  Center for Pediatric Research, Children’s Hospital of the King’s Daughters and Department of Physiological Sciences, Eastern Virginia Medical School, P.O. Box 1980, Norfolk, VA 23501-1980, USA
(2)  Center for Bioelectrics, Old Dominion University, Eastern Virginia Medical School, Norfolk, VA, USA
(3)  Present address: Department of Microbiology, University of Virginia, Charlottesville, VA, USA

Published online: 23 May 2007

Abstract  Non-ionizing radiation produced by nanosecond pulsed electric fields (nsPEFs) is an alternative to ionizing radiation for cancer treatment. NsPEFs are high power, low energy (non-thermal) pulses that, unlike plasma membrane electroporation, modulate intracellular structures and functions. To determine functions for p53 in nsPEF-induced apoptosis, HCT116p53+/+ and HCT116p53−/− colon carcinoma cells were exposed to multiple pulses of 60 kV/cm with either 60 ns or 300 ns durations and analyzed for apoptotic markers. Several apoptosis markers were observed including cell shrinkage and increased percentages of cells positive for cytochrome c, active caspases, fragmented DNA, and Bax, but not Bcl-2. Unlike nsPEF-induced apoptosis in Jurkat cells (Beebe et al. 2003a) active caspases were observed before increases in cytochrome c, which occurred in the presence and absence of Bax. Cell shrinkage occurred only in cells with increased levels of Bax or cytochrome c. NsPEFs induced apoptosis equally in HCT116p53+/+ and HCT116p53−/− cells. These results demonstrate that non-ionizing radiation produced by nsPEFs can act as a non-ligand agonist with therapeutic potential to induce apoptosis utilizing mitochondrial-independent mechanisms in HCT116 cells that lead to caspase activation and cell death in the presence or absence of p-53 and Bax.

Keywords  Non-ionizing radiation - Apoptosis - Caspases - Cytochrome c - Bcl-2 family - p53

This work was supported by the U.S. Air Force Office of Scientific Research/DOD MURI grant on Subcellular Responses to Narrow Band and Wide Band Radio Frequency Radiation, administered by Old Dominion University, and the American Cancer Society.
Contact Information Stephen J. Beebe
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