Extremely low frequency electromagnetic fields affect proliferation and mitochondrial activity of human cancer cell lines

• Published in: International journal of radiation biology Vol. 91; no. 12; pp. 964 - 972
• Main Authors: Destefanis, Michele, Viano, Marta, Leo, Christian, Gervino, Gianpiero, Ponzetto, Antonio, Silvagno, Francesca
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 02-12-2015
• Subjects: cancer cell proliferation; Cell Count; Cell Line, Tumor; Cell Proliferation - radiation effects; Electromagnetic Fields - adverse effects; Electron Transport - radiation effects; Extremely low-frequency electromagnetic fields; Gene Expression Regulation - radiation effects; Humans; Membrane Potential, Mitochondrial - radiation effects; Mitochondria - metabolism; Mitochondria - radiation effects; mitochondrial activity; mitochondrial protein expression; Mitochondrial Proteins - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; Space life sciences; Transcription, Genetic - radiation effects; mitochondrial protein expression; cancer cell proliferation; Extremely low-frequency electromagnetic fields; mitochondrial activity
• ISSN: 0955-3002; 1362-3095
• DOI: 10.3109/09553002.2015.1101648

Purpose: To date, the effects of electromagnetic fields on cell metabolism have been overlooked. The objective of the present study was to investigate the influence of extremely low frequency electromagnetic fields (ELF-EMF) over mitochondrial metabolism and the consequent impact on cancer cell growth.
Materials and methods: The effects of ELF-EMF on cancer growth were investigated in several human cancer cell lines by crystal violet assay. The modulation of mitochondrial activity was assessed by cytofluorimetric evaluation of membrane potential and by real-time quantification of mitochondrial transcription. Moreover the expression of several mitochondrial proteins and their levels in the organelle were evaluated.
Results: The long-term exposure to ELF-EMF reduced the proliferation of several cancer cell lines and the effect was associated to an increased mitochondrial activity without evident changes in ATP levels. The results of our experiments excluded a transcriptional modulation of mitochondrial respiratory complexes, rather suggesting that ELF-EMF increased the energy demand. The altered mitochondrial metabolism led to changes in mitochondrial protein profile. In fact we found a downregulated expression of mitochondrial phospho-ERK, p53 and cytochrome c.
Conclusion: The results of the present study indicate that ELF-EMF can negatively modulate cancer cell growth increasing respiratory activity of cells and altering mitochondrial protein expression.