Many stresses are associated with increased accumulation of reactive oxygen species (ROS) and polyamines (PAs). PAs act as ROS scavengers, but export of putrescine and/or PAs to the apoplast and their catabolization by amine oxidases gives rise to H₂O₂ and other ROS, including hydroxyl radicals (^•OH). PA catabolization-based signalling in apoplast is implemented in plant development and programmed cell death and in plant responses to a variety of biotic and abiotic stresses. Central to ROS signalling is the induction of Ca²⁺ influx across the plasma membrane. Different ion conductances may be activated, depending on ROS, plant species, and tissue. Both H₂O₂ and ^•OH can activate hyperpolarization-activated Ca²⁺-permeable channels. ^•OH is also able to activate both outward K⁺ current and weakly voltage-dependent conductance (ROSIC), with a variable cation-to-anion selectivity and sensitive to a variety of cation and anion channel blockers. Unexpectedly, PAs potentiated ^•OH-induced K⁺ efflux in vivo, as well as ROSIC in isolated protoplasts. This synergistic effect is restricted to the mature root zone and is more pronounced in salt-sensitive cultivars compared with salt-tolerant ones. ROS and PAs suppress the activity of some constitutively expressed K⁺ and non-selective cation channels. In addition, both ^•OH and PAs activate plasma membrane Ca²⁺-ATPase and affect H⁺ pumping. Overall, ^•OH and PAs may provoke a substantial remodelling of cation and anion conductance at the plasma membrane and affect Ca²⁺ signalling.

Anticancer properties of non-psychoactive cannabinoid cannabidiol (CBD) have been demonstrated on tumors of different histogenesis. Different molecular targets for CBD were proposed, including cannabinoid receptors and some plasma membrane ion channels. Here we have shown that cell lines derived from acute lymphoblastic leukemia of T lineage (T-ALL), but not resting healthy T cells, are highly sensitive to CBD treatment. CBD effect does not depend on cannabinoid receptors or plasma membrane Ca²⁺-permeable channels. Instead, CBD directly targets mitochondria and alters their capacity to handle Ca²⁺. At lethal concentrations, CBD causes mitochondrial Ca²⁺ overload, stable mitochondrial transition pore formation and cell death. Our results suggest that CBD is an attractive candidate to be included into chemotherapeutic protocols for T-ALL treatment.