Re: NCRP 136 and 137 now available

["Bjorn Cedervall" <bcradsafers@HOTMAIL.COM>]

>Most of the material covered in Chapters 3 to 9 seemed to be irrelavent

to the overall subject and I really could not understand how the information 

discussed in the body of the report tracked to its conclusions. For example, 

how does the discussion of DNA repair, oncogenic transformation, etc. affect 

the question of whether LNT is a valid concept and/or reasonable basis for 

low-dose radiation exposure standards????

---

I haven't read the NCRP reports but the underlying mechanisms seems to be 

DNA damage->repair (including misrepair) ->Either chromosomal aberrations 

(with survival or cell death)



For low levels - work on micronucei (measuring chromosomal damage) may be 

the most relevant example (mGy level).



Chromosomal aberrations and/or DNA damage on a sequence level are known to 

be involved in carcinogenesis. For some tissues it seems to be enough with 

just one or very few hits to initiate a tumor. This year's Nobel Prize in 

medicine (cyclins and cyclin dependent kinases) gives some of the context 

about the cell cyle machinery - how the so called check points are related 

to DNA damage:

http://www.nobel.se/medicine/laureates/2001/index.html



This work relates more directly to about 10 genes and their products in 

humans but there are many other genes/gene products quite directly involved 

such as p53, MDM2, wee1, p21, and RB (retinoblastoma function involved in 

start of the S phase) as well as up- and downstream regulators of these. Due 

to the complexity of this biological system - a (hypothetical - used for 

modelling) system of differential equations does not seem useful in order to 

test predictions regarding the outcome of various functional damages.



My personal reflections only,



Bjorn Cedervall   bcradsafers@hotmail.com





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