Medical/biological study (experimental study)

Exposure to 1950-MHz TD-SCDMA Electromagnetic Fields Affects the Apoptosis of Astrocytes via Caspase-3-Dependent Pathway med./bio.

By: Liu YX, Tai JL, Li GQ, Zhang ZW, Xue JH, Liu HS, Zhu H, Cheng JD, Liu YL, Li AM, Zhang Y

Published in: PLoS One 2012; 7 (8): e42332

Aim of study (acc. to author)

To investigate whether a radiofrequency field exposure alters the biology of glial cells and acts as a tumor-promoting agent.

Background/further details

Normal rat astrocytes and C6 glioma cells were exposed to a 1959 MHz TD-SCDMA (Time Division Synchronous Code Division Multiple Access) signal. Different endpoints were regarded: 1.) apoptosis, 2.) cell proliferation, 3.) morphological changes and ultrastructure, 4.) expression of the genes bax and bcl-2, 5.) expression of the protein caspase-3 and 6.) tumorigenicity assay in nude mice was conducted. Therefore, astrocytes and C6 cells, previously exposed, were injected into mice (n=3 per group). Mice were sacrificed 28 days later and examined.
In each experiment cells were divided into four groups: unexposed and exposed for 12, 24 or 48 hours.

Endpoint

cell viability/cell division/proliferation: apoptosis

Exposure

- 1,950 MHz
- microwaves
- mobile communications
- mobile phone

Exposure	Parameters
Exposure 1: 1,950 MHz Exposure duration: continuous for 12, 24, 48 h	power: 251.19 mW (24 dBm - nominal maximum power of TD-SCDMA mobile phones) SAR: 5.36 W/kg (according to the antenna calibration certificate)

Exposure 1

Main characteristics

Frequency	1,950 MHz
Type	electromagnetic field
Exposure duration	continuous for 12, 24, 48 h
Additional info	TD-SCDMA (Time Division Synchronous Code Division Multiple Access)

Exposure setup

Exposure source	dipole antenna
Setup	dipole antenna fixed under the cell plates; four bottles with cells exposed simultaneously; cell plates kept at a constant temperature of 37°C

Parameters

Measurand	Value	Type	Method	Mass	Remarks
power	251.19 mW	-	measured	-	24 dBm - nominal maximum power of TD-SCDMA mobile phones
SAR	5.36 W/kg	-	-	-	according to the antenna calibration certificate

Exposed system:

intact cell/cell culture
rat astrocytes, C6 cells (rat glioma cell line)

Methods Endpoint/measurement parameters/methodology

molecular biosynthesis: gene expression of bax and bcl-2 (RT-PCR and Real-time PCR), protein expression of caspase-3 (Western blot)
cell viability/cell division/proliferation: apoptosis (Annexin V and propidium iodide staining, flow cytometry), proliferation (commercial kit)
cancer: tumorigenicity assay in nude mice (weight and morphological changes of the tumors)
morphol./histopathol. changes: cell morphology (microscopy), ultrastructure (stained with uranyl acetate und lead citrate, transmission electron microscope)

Investigated system:

isolated bio./chem. substance
DNA/RNA
intact cell/cell culture
investigation on living organism

Time of investigation:

before exposure
after exposure

Main outcome of study (acc. to author)

Astrocytes: After 48 h exposure, the morphology and ultrastructure changed compared to the unexposed and 12 or 24 h exposed cells. Many cells became shorter and thicker and the mitochondria showed uneven distribution, irregular shapes, swelling, christa break and cavitation. Exposure for 48 h significantly inhibited the cell growth compared to the unexposed group. The percentage of apoptotic cells after 48 h of exposure was more than three times higher than that of other groups. A significant down-regulation of bcl-2 mRNA levels and up-regulation of bax mRNA levels was detected after 48 h of exposure in comparison to the unexposed group, while the gene expression was not influenced in 12 and 24 h exposed cells. A significant increase of the caspase-3 protein was detected after 48 h exposure, but not in the other groups. Tumor formation was not detected.
C6 cells: No differences occurred between unexposed, 12, 24 and 48 h exposed groups in all experiments.
The authors summarize that 48 h of exposure to a TD-SCDMA signal showed no evident effects on glial tumor formation, but damaged the mitochondria of astrocytes and induced apoptosis via a caspase-3-dependent pathway involving bax and bcl-2.

Study character:

medical/biological study
experimental study
full/main study

Study funded by

National Basic Research Program (Program 973), China

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