Although some scientists suspected that radiation damage might spread from cell to cell—the so-called bystander effect—only the development of a technique for targeting individual cells allowed them to confirm the idea. The researchers were able to fire a single α particle at individual cells, so they knew exactly how many cells had absorbed hits. They used the absence of the CD59 antigen on the cell surface as an indicator of mutation. Zapping only 10% of the cells in a solution caused the same number of mutations as hitting 100% of the cells, the researchers found. “We had just assumed that, when you irradiated a population of cells, the damage was due to a direct hit by the α particles,” says James Trosko of Michigan State University (East Lansing, MI).The next step was to test the idea that some kind of damage signal spreads from the targeted cell to its neighbors through gap junctions, which chemically and electrically couple cells. When the authors doused the cells with octanol, which jams gap junctions, they found that the number of mutations fell by nearly 80%. Trosko says they have no idea what is spreading through the gap junctions to the bystanders, except that it must be smaller than 1,000 D to fit through the channel.
The study could force regulators to rethink radiation safety standards, says Trosko. Guidelines for low-level exposure are based mainly on extrapolations from studies of atomic bomb survivors and assume that risk declines linearly with dose. By revealing that small doses can have disproportionately large effects, the work suggests that current standards may not be formulated correctly, he says. But he cautions that further studies using additional markers for genetic damage are necessary, and that no one knows whether other sorts of radiation have similar effects. ▪