[ RadSafe ] Two interesting papers on DNA repair mechanisms Interested in Hormesis advocates
parthasarathy k s
ksparth at yahoo.co.uk
Fri Jul 2 13:35:47 CDT 2010
Dear Dr Brennen,
One of the important observations in the papers is that when DSB repair occurs,
all repairs are not perfect. It leaves behind a trail of mutations.It may be so
whether DSB occurs due to ionizing radiation or action of chemicals.
There is some evidence that at very low doses of about one mGy, the DSB remains
unrepaired for a long time. There is also further claim that often such
unrepaired damage leads to the death of the cell and not to its proliferation
into cancer.
I am keen to get the views of those who strongly support hormesis at low doses.
Regards
Parthasarathy
________________________________
From: "Brennan, Mike (DOH)" <Mike.Brennan at DOH.WA.GOV>
To: radsafe at health.phys.iit.edu
Sent: Fri, 2 July, 2010 23:50:25
Subject: Re: [ RadSafe ] Two interesting papers on DNA repair mechanisms
Hi, Clayton.
While this is not my field of expertise, here is my understanding:
1) While we cannot (yet) say definitively, "This particular cancer was
caused by ionizing radiation.", we can say definitively, "This
particular cancer was NOT caused by ionizing radiation, because we know
that it was caused by (fill in the blank)." I would be greatly
surprised if our understanding of how various cancers start doesn't
improve, and that more specific viruses are linked with specific types
of cancer. I wouldn't rule out that in at least some cases of "cancer
causing chemicals", the chemicals actually interfere with a process that
limits a particular virus from causing a cancer.
2) I haven't seen anything on it, but if someone shows that the
disruption of the cell function by ionizing radiation (whether or not
DNA is damaged) increases the ability of viruses to successfully insert
their DNA into the host cell chromosome, I wouldn't be surprised (or
maybe the disruption interferes with the virus's ability to create new
copies of itself until it burst the cell, which spreads the virus, but
kills the cancer. Interesting thought.) If there is such an
interaction, it would be very difficult to separate the cause.
3) We will learn more about this: The millennium is still young. Of
course, if this follows the normal path of science, we won't so much
have the answers as have much more detailed questions.
-----Original Message-----
From: radsafe-bounces at health.phys.iit.edu
[mailto:radsafe-bounces at health.phys.iit.edu] On Behalf Of Clayton J
Bradt
Sent: Friday, July 02, 2010 10:44 AM
To: radsafe at health.phys.iit.edu
Subject: Re: [ RadSafe ] Two interesting papers on DNA repair mechanisms
I'll be eager to read these papers hopefully over the holiday weekend.
(That's the 4th of July for you non-US citizens on the list.)
What still puzzles me about the entire subject is the contradiction
between these two presumed facts:
1) Cancers caused by radiation are indistinguishable from non-radiogenic
cancers. 2) Human Papilloma Virus (HPV) causes cervical cancer.
The first statement can't be true, because cervical cancer cells caused
by
HPV have virus genes spliced into their DNA. These virus genes function
in specific ways to overcome some of the cells' control mechanisms and
allow for uncontrolled proliferation. It is hard to believe that random
radiogenic DNA damage and misrepair (no matter what the mechanisms)
could
duplicate these exact same virus genes in affected cells. So either
radiation can't cause cervical cancer, or it causes a different kind of
cervical cancer than HPV infection and there is a genetic marker that
can
distinguish the two.
How many other cancers are the result of the incorporation viral genetic
material? Are the mutations that result in oncogenesis ever the result
of
random damage and/or misrepair?
Clayton J. Bradt
Principal Radiophysicist
Laboratory for Inorganic & Nuclear Chemistry
NYS Dept. of Health
518-474-1993
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