Abstract
When released in plant environment, strontium (Sr 2+) can be absorbed predominantly by the plant roots. As the plasma membrane of root cells is amongst the first barriers encountered by Sr 2+ during its soil/plant transfer and the main entry point of Sr 2+ into the roots, the main objective of this work aimed to enlighten on some of the Sr 2+-induced effects at this level in Zea mays L. cv. “Liberal”. Thus this study focused on the Sr 2+-induced changes on membrane potential of cortical root cells and on proton fluxes in maize roots, in order to determine whether the activity of some of the ion transport systems present in the plasma membrane of maize root cell could be among the first targets of Sr 2+. We focused in particular on the plasma membrane H +-ATPase, known to be one of the major transport systems found in the plasmalemma where it generates a proton motive force (contributing to membrane potential maintaining, and providing energy for ion transport through membrane). The data presented here showed that Sr 2+ triggered an early and transient membrane depolarisation whose magnitude and duration were dependent on the Sr 2+-concentration. The time course pattern of a second longer lasting depolarisation could be examined in perspective with the Sr 2+-induced decrease of the spontaneous proton extrusion observed in root tissues, suggesting a relationship between Sr 2+-effects on membrane potential and H + excretion. Furthermore, the inhibitory effect exerted by Sr 2+ on the fusicoccin (FC)-enhanced proton extrusion strongly suggested an inhibition of the plasma membrane H +-ATPase. This hypothesis was supported by the inhibition induced by Sr 2+ on proton pumping- and ATP hydrolysis-activities measured in plasma membrane vesicles (PMV) prepared from maize roots. Taken together the data reported here evidence that, with however a lower efficiency, Sr 2+ behaved in a quite similar way to Ca 2+ when inhibiting the H +-ATPase activity, and suggest that Sr 2+ could partially mimic Ca 2+ onto regulation of the H +-ATPase activity.
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