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Re: Laymans questions on hormesis and LNT
How are those mutations created? By improper
repair, perhaps...
A few possibities:
o DSB gets repaired properly -- yay!
o DSB gets repaired improperly -- boo!
o DSB doesn't get repaired and cell dies -- whatever, as
long as most its neighbors are viable...
o DSB doesn't get repaired and cell mutates -- is
this possible? I suppose that you can get those
goofy looking chromosomes, but don't they usually
lead to death at the next division?
Radiation is a weak mutagen.
I've been trying to remember more info from the
paper... I think that the threshold dose below
which DSB repair seemed to be inhibited was less
than 1 rad. There was sort of a "equilibrium level"
for the average # of DSBs/cell -- below the level no
repair took place above the level repair took place
until the "equilibrium level" was reached (the
level was less than 1 DSB/cell, but I don't recall
the exact #).
Cary
>>> John Jacobus <crispy_bird@yahoo.com> 08/29/03 17:43 PM >>>
Carl,
My impression from talking to some researchers is that
the determination of risk is not that the DS breaks
are or are not repaired, but that they are formed at
all. That lowers the threshold even more. The
concerns are not that cells die, but are mutated and
before focus points for cancers.
--- Cary Renquist <crenquis@med.umich.edu> wrote:
> 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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=====
-- John
John Jacobus, MS
Certified Health Physicist
e-mail: crispy_bird@yahoo.com
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