Using germination of maize as a model, desiccation-induced free radical processes were studied with the object of understanding desiccation tolerance. Several significant elements of damage were observed in desiccated material associated with development of desiccation intolerance: increased lipid peroxidation, phospholipid de-esterification, build-up of a stable free radical, supression or repression of respiratory enzymes from complex I, II and IV. An EPR (electron paramagnetic resonance) response was also detected in isolated mitochondria following in vitro desiccation. The loss of desiccation tolerance appeared to be dependent on oxygen concentration. Two highly significant correlations were independently found between respiration rates and production of a stable free radical detected by EPR. These data suggest that respiration is an important factor in the loss of desiccation tolerance. We present a model suggesting that activated oxygen formation during desiccation originates in the disruption of the mitochondrial electron transport chain with increasing leakage to oxygen so generating irreversible and lethal peroxidative damage, leading to the development of desiccation intolerance.