The day was opened with tutorial on genomic stability and signaling pathways.
The first talk by Robert Kanaar had some interesting statements and suggestions.
The spontaneously occurring DNA damage is very common in cells and it requires efficient repair mechanisms to continuously repair this damage. Some rough numbers were as follows:
- single strand breaks – 50,000/day
- abasic sites – 10,000/day
- deamination – 600/day
- oxidized bases – 2,000/day
- alkalized bases – 5,000/day
- replication errors – several tens/day
Sensitivity of different methods detecting DNA breaks varies dramatically:
- pulsed field electrophoresis – damage to be detected requires energy equal to energy of 10Gy
- comet assay – 1Gy
- focus formation by proteins in sites of damage – 0.4Gy
In the lab of the speaker has been developed more sensitive method relaying on transfection of cells with plasmids.
With none of the above methods was possible to confirm that RF induces DNA damage (breaks) more efficiently as compared with the spontaneous damage.
In case of ELF Primo Schär observed higher level of damaged DNA in exposed cells but it was not due to actual damage but rather due to inhibition of DNA repair processes by the ELF exposure.
In some studies saw suggested that there is higher level of DNA damage in exposed cells. It might be possible that similarly as with ELF exposures; the RF exposures might, in certain cell types affect the DNA repair process?
In the second talk Rony Seger presented effect of RF exposures on ERK kinase pathway and the “antenna” molecule was determined as NADH oxidase. How RF affects function of NADH oxidase remains undetermined (see my comment on classic heating at 43oC on the activity of ERK in earlier blog). These results were already published several years ago.
Interestingly, in pilot experiments with ELF exposure (50Hz, 1mT) there was only very weak effect on ERK pathway. This effect seemed to be cell type-dependent: observed in transformed cells but absent in non-transformed cells. In respect to the ELF exposures (Kuster set up) used in the ERK study, someone from the audience commented that in sham exposures there is low level of ELF = 6 microT what may mean that sham samples are also activated and therefore the difference between sham and exposed might be more difficult to detect.
Following the tutorial plenary session was session on anti-cancer clinical applications of EMF. In this session was presented the in vitro part of the clinical/animal study from Boris Pashe’s group. The presentation suggested that the IP3/DAG signaling pathway is activated what leads to an increase of cytoplasmic calcium. Unfortunately, the evidence concerning calcium level was poor and unconvincing. There was shown only a single sham exposed cell that looked not very healthy, with a couple of large vacuoles that absorbed green stain. In the other part of the cell was seen small diffuse area of green stain indicating area where calcium was located. To me this control cell looked “unhealthy”, in fact having appearance of apoptotic death. In the exposed sample were shown only 2 cells. The smaller one was clearly in advanced stage of apoptosis with extensive surface blebbing. The other cell, much larger in size, was clearly dying by necrosis and swollen by intake of water. There was clearly seen a very large bleb/vacuole. In both cells was seen diffuse green staining indicating location of calcium.
Unfortunately the evidence concerning IP3/DAG and calcium was absolutely unconvincing. Pashe needs a better qualified cell biologist to view the cell cultures and to determine which cells are alive and which are already dead or dying. Also, showing only 1-2 cells, without any numerical analysis is far too little.