Evidence in the literature has generally supported either of two paraquat resistance mechanisms: an increase in activity of oxygen radical-scavenging enzymes in resistant plants which affords protection from active oxygen species formed by paraquat; and sequestration of paraquat away from its site of action in the chloroplast. Evidence for the first model relies primarily on measurement of increased enzyme activity and cross-resistance to other oxygen radical-generating stresses in resistant plants. The sequestration model is supported by data showing decreased translocation of paraquat and absence of paraquat injury in plant systems that do not have increased levels of protective enzymes. An alteration in paraquat transport at one of several plant cell membranes could confer resistance by modifying movement of paraquat into the compartment bounded by that membrane. Properties of the plasmalemma, chloroplast envelope, and tonoplast that may be important to paraquat transport are discussed and data supporting or discounting specific membrane alterations in resistant plants are presented. Finally, the possibility that both mechanisms may work in concert is addressed.