Author/Authors :
Mokarram P. نويسنده Department of Biochemistry, Shiraz University of Medical Sciences, Shiraz, Iran , Sheikhi M. نويسنده Department of Radiobiology, School of Paramedical Sciences, Shiraz, Iran , Mortazavi S. M. J. نويسنده Ionizing and Non-ionizing Radiation Protection Research Center (INIRPRC), Shiraz University of Medical Sciences, Shiraz, Iran , Saeb S. نويسنده Department of clinical biochemistry, school of medicine, Shiraz University of Medical Sciences, Shiraz, Iran , Shokrpour N. نويسنده Professor, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
Abstract :
Background: Over the past several years, the rapidly increasing use of mobile
phones has raised global concerns about the biological effects of exposure to radiofrequency
(RF) radiation. Numerous studies have shown that exposure to electromagnetic
fields (EMFs) can be associated with effects on the nervous, endocrine, immune,
cardiovascular, hematopoietic and ocular systems. In spite of genetic diversity, the
onset and progression of cancer can be controlled by epigenetic mechanisms such as
gene promoter methylation. There are extensive studies on the epigenetic changes of
the tumor suppressor genes as well as the identification of methylation biomarkers in
colorectal cancer. Some studies have revealed that genetic changes can be induced by
exposure to RF radiation. However, whether or not RF radiation is capable of inducing
epigenetic alteration has not been clarified yet. To date, no study has been conducted
on the effect of radiation on epigenetic alterations in colorectal cancer (CRC). Several
studies have also shown that methylation of estrogen receptor ? (ER?), MYOD,
MGMT, SFRP2 and P16 play an important role in CRC. It can be hypothesized that
RF exposure can be a reason for the high incidence of CRC in Iran. This study aimed
to investigate whether epigenetic pattern of ER? is susceptible to RF radiation and if
RF radiation can induce radioadaptive response as epigenetic changes after receiving
the challenge dose (?-ray).
Material and Method: 40 male Sprague-Dawley rats were divided into 4 equal
groups (Group I: exposure to RF radiation of a GSM cell phone for 4 hours and sacrificed
after 24 hours; Group II: RF exposure for 4 hours, exposure to Co-60 gamma
radiation (3 Gy) after 24 hours and sacrificed after 72 hrs; Group III: only 3Gy gamma
radiation; Group 4: control group). DNA from colon tissues was extracted to evaluate
the methylation status by methylation specific PCR.
Results: Our finding showed that exposure to GSM cell phone RF radiation was capable
of altering the pattern of ER? gene methylation compared to that of non-exposed
controls. Furthermore, no adaptive response phenomenon was induced in the pattern
of ER? gene methylation after exposure to the challenging dose of Co-60 ?-rays.
Conclusion: It can be concluded that exposure to RF radiation emitted by GSM
mobile phones can lead to epigenetic detrimental changes in ER? promoter methylation
pattern.