I often have wondered about further studies of anti-mutagenic effects but have not done anything for the following reasons.
Chances are pretty good that the effect we studied is on the "repair" system, since it works so well against caffeine
mutagenesis, which appears to be on repair. So any meaningful study would quickly become one of the repair system--which
would likely be specific to Coli.
But maybe careful study of mammalian repair systems would give direction toward substances which would reduce spontaneous
rate in humans.
Another thought--perhaps reducing the rate for one kind of mutational event would increase the rate for another.
One other reason I have shied away is that so much nice work is being done--or should be done--on the molecular basis of mutational
events. George Streisinger[?] has some interesting information on the
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relation between frame shift rate and length of a series of repeating base pairs.
While I have your attention I want to show you the enclosed announcement from the NIH which outraged me.
When will you come up for a visit? Better make it before the California conquest turns this into LA-land.