Glutathione homeostasis as an important and novel factor controlling blossom-end rot development in calcium-deficient tomato fruits.

Based on previous results in which oxidative metabolism was suggested as a possible inducer of blossom-end rot (BER), the main questions addressed here were whether calcium deficiency is the main factor that induces BER or whether this physiological disorder a general stress-related phenomenon? Tomato plants were grown under optimal or deficient calcium concentrations. Only the application of 0.1mM calcium resulted in BER induction, although only half of the fruits grown under this treatment had this disorder. Having fruits showing or not showing BER in the same plant and treatment provided us with a powerful tool that we used to investigate whether calcium deficiency operates alongside another mechanism in the induction of BER. Whether or not this other mechanism was the one controlling BER incidence was also investigated. We performed a complete study of the oxidative metabolism in the pericarp of healthy fruits and in the healthy portion of BER-affected fruits. Calcium deficiency led to an induction of NADPH oxidase, superoxide dismutase, dehydro- and monodehydroascorbate reductase, and to an inhibition of catalase, ascorbate peroxidase and glutathione reductase, with a concomitant accumulation of hydrogen peroxide and an increase in lipid peroxidation. While the ascorbate redox state was not affected by calcium deficiency, the glutathione redox state was markedly reduced. We conclude that calcium deficiency fundamentally affected the activity of the ascorbate-glutathione enzymes, with special importance to the inhibition of GR, which lead to a reduction of the glutathione redox state. This could cause the breakdown of cellular homeostasis, the inhibition of other enzymes responsible for H(2)O(2) detoxification, and ultimately an increase of lipid peroxidation. Therefore, BER is defined here as the visual symptom of a massive lipid peroxidation event caused by the breakdown of cellular glutathione homeostasis.