کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2146580 | 1548358 | 2011 | 9 صفحه PDF | دانلود رایگان |

The production of mitotic spindle disturbances and activation of the apoptosis pathway in V79 Chinese hamster cells by continuous 2.45 GHz microwaves exposure were studied, in order to investigate possible non-thermal cell damage. We demonstrated that microwave (MW) exposure at the water resonance frequency was able to induce alteration of the mitotic apparatus and apoptosis as a function of the applied power densities (5 and 10 mW/cm2), together with a moderate reduction in the rate of cell division. After an exposure time of 15 min the proportion of aberrant spindles and of apoptotic cells was significantly increased, while the mitotic index decreased as well, as compared to the untreated V79 cells. Additionally, in order to understand if the observed effects were due to RF exposure per se or to a thermal effect, V79 cells were also treated in thermostatic bath mimicking the same temperature increase recorded during microwave emission. The effect of temperature on the correct assembly of mitotic spindles was negligible up to 41 °C, while apoptosis was induced only when the medium temperature achieved 40 °C, thus exceeding the maximum value registered during MW exposure. We hypothesise that short-time MW exposures at the water resonance frequency cause, in V79 cells, reversible alterations of the mitotic spindle, this representing, in turn, a pro-apoptotic signal for the cell line.
► We study the effects of short-time microwave (MW) exposure at 2.45 GHz in V79 cells.
► We observe alteration of the mitotic apparatus and apoptosis.
► Both effects occur as a function of the applied power densities.
► We also expose cells to the temperatures recorded during MW exposure (T max = 39 °C).
► We exclude a thermal effect as damage is observed only if cells reach at least 40 °C.
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 716, Issues 1–2, 1 November 2011, Pages 1–9