Excised roots from aeroponic axenically 48 h darkgrown sunflower (Helianthus annuus L.) seedlings showed redox activities, being able to oxidize/reduce all the exogenously added electron donors/acceptors, that affected the H+/K+ net fluxes simultaneously measured in the medium. Trials were performed with in vivo and CN--poisoned roots; these showed null H+/K+ net flux activity but still oxidized/induced all the e(-) donors/acceptors tested except NADH. NADH enhanced the rate of H+ efflux by in vivo roots, otherwise nor changing any of the normal flux kinetic characteristics, suggesting that NADH donates e(-) and H+ to the exocellular NADH oxidoreductase activity of a CN--sensitive redox chain in the plasmalemma of the root cells. K+ influx was not affected, probably because the NADH concentration was not very high. The e- donor HFC(hexacyanoferrate)(II) activated the H+ efflux in a very different way: maximum H+ efflux rare was maintained, but both the maximum rare plateau and the optimal pH range were extended, and hence the total H+ efflux was significantly enhanced. Ar the same time, the K+ influx was doubled. The different H+-efflux kinetics, together with the small but significant HCF(II) oxidation by CN--poisoned roots, were taken as evidence that, besides the CN--sensitive redox chain, an alternative CN--resistant redox chain in the plasmalemma was involved in HCF(II) oxidation. The effect of the oxidized form HCF(III) on Hi and K+ fluxes was the opposite to that described for HCF(II), but the other H+ efflux kinetic characteristics were similar (the maximum rate plateau was extended so that total H+ efflux equaled that of the controls). It is proposed that HCF(III) accepts e(-) only from the alternative CN--resistant redox chain. We could not measure the effect of HCI(hexachloroiridate)(IV) on H+ efflux, as the pH electrodes alone quickly reduced the compound. HCI(IV) promoted a rapid transitory K+ efflux, followed by recovery of K+ influx. The HCI(TV) reduction by in vivo or CN--poisoned roots was extremely rapid, following similar kinetics. Thus, only the CN--resistant redox chain was involved in both cases. The redox chain inhibitor sis-platinum(II) annulled ion fluxes in the presence of both NADH and HCF(III), and later even inverted them (a small H+ influx down the gradient would induce K+ efflux). Cis-platinum(II) did nor affect HCF(III) reduction by in vivo roots, and only slightly depressed that by CN--poisoned roots. Overall, the effects of the exogenously added e(-) donors/accepters tested were consistent with the existence of a CN--resistant redox chain in the plasmalemma of the root cells which would donate/accept e(-) even when the H+ and K+ fluxes were annulled by CN- or even inverted by cis-platinum(II) treatments. Thus, in the plasmalemma of in vivo roots this chain would compete for electrons with the normal CN--sensitive one, as in plant mitochondria. The effects on the K+ flux were consistent with the current hypothesis that this contributes to counteracting the changes in membrane potential caused by redox activities and the Hi flux induced by the different redox compounds tested.
