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CRON4healthyfuture dug up this study ( 2004-02-10) which found the level of isothiocyanates, one of the healthy compounds in cabbage (and broccoli), was higher after eating raw rather than cooked cabbage.

Raw cabbage gets more ITCs in you than cooked; ATR, p53, and "replication stress"

1) If you think the isothiocyanates are what make cabbage and
broccoli good for you, than you are better off eating them raw.
14744743.

2) It has been determined that p53 exerts different effects in
different cell populations, and it has been implicated in mammalian
aging. ATR is a protein that turns on p53. Scientists have recently
figured out how ATR exerts its effects 14742437. They have
determined that it finds "stalled replication forks", and therefore
only shows up during "replication stress", which is primarily in
conditions where the cell is trying to copy damaged DNA. These
findings could have very broad implications encompassing everything
from why the WRN protein is associated with the progeroid syndrome of
Werner's Syndrome to the mechanism of lifespan prolongation
associated with IGF-1 antagonism. WRN is a DNA helicase which
unwinds the helix, and when it is damaged, it produces "stalled
replication forks" 14657243 12750383 11256630. Upon encountering
these types of forks, it is not unreasonable to expect that the
ATR-p53 axis may eventually be triggered. IGF-1 is a mitogenic
hormone that causes cells to replicate faster than they normally
would, and is therefore an agent that could plausibly be implicated
in generating "replication stress".

Quiescent cells that do not feel like dividing can apparently
downregulate their ATR-p53 activity. In 14755251, lymphocytes were
isolated that downregulate their ATR-p53 activity in association with
their quiescence. The authors of the study hypothesized that this
mechanism may have evolved to allow for the accomodation of
"endurable genotoxic stress" without the triggering of an overzealous
p53 "quality control" response. The authors of this study discuss
this effect as a pathological state that could promote malignancy,
but in certain other contexts, such as CR, it is not hard to imagine
that a downregulation of p53 would be beneficial. It will be
interesting to see if ATR downregulation is a mechanism operating in
special metabolic states.

So basically, the idea of "replication stress" triggering p53, a
protein that has been shown to accelerate aging, is advanced in this
research, and the effect can be mediated by ATR.