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We established model systems for exploring the roles of symplastic and apoplastic ascorbate in heavy-metal-polluted dicot and monocot cells. Cell-suspension cultures of  Arabidopsis  and maize were treated with copper, cadmium or nickel; growth and ascorbate metabolism were measured. Growth was halved by ∼80 µM Cu 2+ , 90 µM Cd 2+  or 1200 µM Ni 2+  in  Arabidopsis , and ∼90 µM Cu 2+ , 650 µM Cd 2+  or 650 µM Ni 2+  in maize. Cu 2+  (128 µM) and Cd 2+  (512 µM) caused partial loss of symplastic ascorbate, especially in  Arabidopsis ; Ni 2+  (512 and 2048 µM) had moderate effects. Added apoplastic  l -ascorbate (1 mM) was consumed by the cultures (half-life ∼23 and 44 min in  Arabidopsis  and maize, respectively), consumption rate being 3–6-fold increased by Cu 2+ , Cd 2+  and Ni 2+  in  Arabidopsis , and by Cu 2+  in maize; Cd 2+  and Ni 2+  had relatively little effect on apoplastic ascorbate consumption in maize. Radioactivity from exogenous 1 mM  l -[1- 14 C]ascorbate remained extracellular; catabolites formed were dehydroascorbic acid, diketogulonate and oxalyl-threonates. In conclusion, suspension-cultured cells respond to heavy-metal stresses by maintaining symplastic ascorbate concentrations, which may beneficially scavenge symplastic reactive oxygen species (ROS). Apoplastic ascorbate is catabolised in metal-polluted cultures via several oxidative and non-oxidative reactions, the former potentially scavenging stress-related apoplastic ROS.

Copper, cadmium and nickel pollution inhibit growth and promote ascorbate catabolism in cell cultures of Arabidopsis thaliana and Zea mays