Plant cell signaling relies on a multitude of primary and secondary messenger molecules. Exogenous L-ascorbic acid (ascorbate) has not been considered as a signaling molecule in plant cells. However we have shown that, in Arabidopsis thaliana L. root cells, exogenous ascorbate (>30 μM) induces a transient increase of the cytosolic free Ca2+ activity ([Ca2+]cyt.). This phenomenon is fundamental to plant signaling because it underlies transmission of most important plant signals, such as hormones and stress. Exogenous copper and iron stimulated the ascorbate-induced [Ca2+]cyt. elevation while cation channel blockers, free radical scavengers, low extracellular [Ca2+], transition metal chelators and removal of the cell wall inhibited this reaction. These data show that the apoplastic redox- active transition metals are involved in the ascorbate-induced [Ca2+]cyt. elevation. Exogenous ascorbate also induced moderate increase in programmed cell death symptoms in intact roots, but it did not activate Ca2+ influx currents in patch-clamped root protoplasts. Intriguingly, replacement of gluconate with ascorbate in the patch-clamp pipette revealed a large ascorbate efflux current, which showed sensitivity to anion channel blocker, anthracene-9-carboxylic acid (A9C), indicative of the ascorbate release via anion channels. EPR spectroscopy measurements demonstrated that salinity (NaCl) triggered accumulation of root apoplastic ascorbyl radicals in A9C-dependent manner, confirming that L-ascorbate leaks through anion channels under depolarisation. This mechanism can underlie ascorbate release, signaling phenomena, apoplastic redox reactions, iron acquisition and control of membrane ionic and electrical equilibrium (together K+ efflux via GORK channels). Financial support of the Russian Science Foundation (grant#15-14-30008 to VD) is gratefully acknowledged.