Disruption of calcium homoeostasis may be crucially important in damaging animal cells under oxidising conditions. In hepatocytes, oxidative stress causes an increase in cytosolic calcium, a process which is thought to be largely responsible for subsequent cell death. The oxidation of glutathione precedes a flux of calcium into the cytoplasm from internal and external sources. The possibility that similar events occur in plant cells has been tested using strips of epidermis taken from leaves of Commelina communis. The closure of stomata in response to many chemical or physical stimuli is thought to involve a transient rise in cytosolic calcium. Paraquat (10(-4) M) and hydrogen peroxide (10(-3) M) caused a marked reduction in stomatal aperture when included in the incubation medium of illuminated epidermal strips. The calcium channel blocker verapamil (10(-5) M) protected stomata from hydrogen peroxide-induced closure while the ion chelator EGTA (2 x 10(-3) M) protected stomata in both oxidising treatments. These results are discussed in so far as they support the hypothesis that a rise in cytosolic calcium may play a role in the pathology of oxidative stress in plant cells through a mechanism analogous to the liver cell system.