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Re: Laymans questions on hormesis and LNT
Jim, ;-)
DSBs in and of themselves are not necessarily detrimental....
Essentially the hypothesis is that _improperly_repaired_DSBs_
are detrimental e.g. cancer -- unrepaired DSBs are fatal to the
cell (whether or not cell kill is detrimental depends on how many
cells are involved).
The study seemed to show that for low dose rates (I forget the
absolute number) cells do not repair DSBs, rather the cells usually
go on to die -- no big problem if a few cells die. If this is true in situ,
then there should be less risk of cancer induction for low doses.
Cary
>>> John Jacobus <crispy_bird@yahoo.com> 08/29/2003 15:01:53 >>>
Carl,
I think that this is part of the problem. We are able
to determine DS breaks and observe their repair or
non-repair. The arguement is the DS breaks are
precursors to cancer or other effects. I doubt that
in all cases this is true, whether or not repair takes
place. However, if you say that DS breaks are
detrimental, then we need to control does down to
those levels.
Note that hormesis does not even have to be invoked in
this arguement. Yet, it allows more flexibility in
establishing risk limits.
--- Cary Renquist <crenquis@med.umich.edu> wrote:
>
> It seems that experimental techniques are getting
> down to the level
> where DSB's and repair processes can be examined
> quite closely:
> Mentioned earlier in the year:
> Rothkamm, K. and M. Löbrich. 2003. Evidence for a
> lack of DNA double-strand break
> repair in human cells exposed to very low X-ray
> doses. Proc. Natl. Acad. Sci. USA,
>
> One speculation based on their research is: at low
> dose rates cells do not attempt to repair DSBs --
> thus
> eliminating the chance of an improper repair. Not
> exactly hormesis, but if that hypothesis stands up
> under
> further research it lends credence a dose-response
> model at variance to the LNT.
> . . .
=====
-- John
John Jacobus, MS
Certified Health Physicist
e-mail: crispy_bird@yahoo.com
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