[Illustration: _Arrangement for long-term low-dose-rate irradiation of mice used for mutation-rate studies at Oak Ridge National Laboratory. The cages are arranged at equal distances from a cesium-137 gamma-ray source in the lead pot on the floor. The horizontal rod rotates the source._] This proved to be _not_ so in the case of mice. In male mice, a radiation dose delivered at the rate of 0.009 rad per minute produced only from one-quarter to one-third as many mutations as did the same total dose delivered at 90 rads per minute. In the male, cells in the gonads are constantly dividing to produce sex cells. The latter are produced by the billions. It might be, then, that at low radiation dose rates, a few of the gonad cells are damaged but that the undamaged ones produce a flood of sperm cells, “drowning out” the few produced by the damaged gonad cells. The same radiation dose delivered in a short time might, however, damage so many of the gonad cells as to make the damaged sex cells much more difficult to “flood out”. A second possible explanation is that there is present within the cells themselves some process that tends to repair damage to the genes and to counteract mutations. It might be a slow-working, laborious process that could keep up with the damage inflicted at low dosage rates but not at high ones. High dosage rates might even damage the repair mechanism itself. That, too, would account for the fewer mutations at low dosage rates than at high ones. To check which of the two possible explanations was nearer the truth, Russell performed similar tests on female mice. In the female mouse (or the female human being, for that matter) the egg cells have completed almost all their divisions before the female is born. There are only so many cells in the female gonads that can give rise to egg cells, and each one gives rise to only a single egg cell. There is no possibility of damaged egg cells being drowned out by floods of undamaged ones because there are no floods. Yet it was found that in the female mouse the mutation rate also dropped when the radiation dose rate was decreased. In fact, it dropped even more drastically than was the case in the male mouse. Apparently, then, there must be actual repair within the cell. There must be some chemical mechanism inside the cell capable of counteracting radiation damage to some extent. In the female mouse, the mutation rate drops very low as the radiation dose rate drops, so that it would seem that almost all mutations might be repaired, given enough time. In the male, the mutation rate drops only so far and no farther, so that some mutations (about one-third is the best estimate so far) cannot be repaired. If this is also true in the human being (and it is at least reasonably likely that it is), then the greater vulnerability of our genes as compared with those of fruit flies is at least partially made up for by our greater ability to repair the damage.