John Budny wrote:
>Why would rodent models for dadmium nephrotoxicity be a "good model" for
the similar adverse effects in humans? If we can sort out why
toxicologists feel that the rodents are good models for cadmium toxicity
in humans, then I think we may have something substantial to contribute
to the discussion on animal models.
Well, frankly, I don't know why rodents would, a priori, provide a good model
for the nephrotoxicity of Cd. Perhaps there is an underlying rationale in
the anatomy/physiology/biochemistry of the respective kidneys which would
have told us to look at the rodent model. Of course there is always the
underlying postulate that mammals are more similar than different and the
practical excuse that rodents are easy. It just so happens in this case that
if you compare the human (autopsy) data and the rodent data, it turns out
that the rodent data is a pretty decent predcitor. I know that this is
somewhat backwards in that we only know in this case that the rodent is a
good model because we have the human data to which to compare it. The
questions remains though: If you didn't have the human data, what would you
do? And maybe more to the point, what wouldn't you do?
Alan Stern, Dr.P.H., D.A.B.T.