Electron-affinic nitrofuran derivatives interfere with normal cellular metabolism by providing an electron shunt, apparently via free radical intermediates, between endogenous cellular reducing species and oxygen, in a manner analogous to that of vitamin K3. Pulse radiolysis was used to demonstrate the reactivity of nitrofuran radical anions with oxygen, as well as the NAD free radicals with nitrofurans. The reduction of nitrofurans under anaerobic conditions and the increased oxygen consumption (indicative of free radical formation) are enhanced by the addition of glucose and suppressed by the removal of endogenous reducing species, e.g. by the addition of diamide. Nitrofuran free radical production under aerobic conditions may result in the production of the Superoxide radical anion O2−. It is postulated that aerobic production of nitrofuran or oxygen free radicals or the resulting products may be responsible for the previously described cytotoxic effect of nitrofurans.