The effect of boron on H+ extrusion and FeCN reduction in sunflower cell suspensions and on vanadate-sensitive H+-ATPase and NADH-FeCN reductase activities of isolated microsomes was investigated. Boron deficiency inhibited FeCN-dependent H+ extrusion and FeCN reduction in cells grown in darkness or at a light irradiance of 30 mumol . m-2 . s-1. In addition, an inhibition of FeCN-independent H+ extrusion by boron deficiency was detected when cells were maintained at a light irradiance of 30 mumol . m-2 . s-1. FeCN-dependent and FeCN-independent H+ extrusion were stimulated by FC and inhibited by vanadate and DCCD. However, FeCN reduction was not affected either by FC or by vanadate. In isolated microsomes, boron deficiency inhibited the vanadate-sensitive H+-ATPase and NADH-FeCN reductase activities. The presence of 2,4-D in the assay medium provoked an inhibition of H+ extrusion and FeCN reduction in cells grown with 0.1 mM H3BO3; in the same way, the addition of 2.4-D to the reaction medium inhibited the NADH-FeCN reductase activity of microsomes isolated from cells grown in media with boron. These data support the existence of a relationship between boron and auxins. Likewise, the present results suggest that boron could regulate H+ extrusion in sunflower cells through an effect on plasma membrane H+-ATPase and redox systems.