Blossom-end rot of tomato (Lycopersicon esculentum Mill.) -: a calcium- or a stress-related disorder?

Many researchers have attributed the occurrence of blossom-end rot (BER) in tomato to a deficiency of Ca2+ in the fruit or parts of the fruit in connection with the uptake of nutrients by the roots, the transport of Ca2+ to and within the fruit or a varying demand for Ca2+ depending on the growth rate of fruits. However, a critical concentration of Ca2+ in the fruit has not yet been found, and the influence of favourable or unfavourable growing conditions on the development of BER is still poorly understood. The symptoms of BER are caused by a disintegration of the cell membranes and an increased ion permeability. It is proposed that not a single factor but the sequence of two equally important factors are involved: (1) a higher susceptibility to various stresses due to an increase in physiologically active gibberellins. (GAs) and a resulting decrease in Ca2+, causing the enhanced permeability of cell membranes, (2) some kind of stress, e.g. by soil water deficit, high salinity, or high NH4+ activity, causing the deterioration of cell membranes with subsequent loss of turgor and leakage of cell liquids. BER seems to occur when stress exceeds stress tolerance, most frequently in young fruit at the beginning of cell enlargement. At this stage, usually the highest amount of physiologically active GAs and the lowest amount of Ca2+ are found, i.e. stress tolerance is lowest. Ca2+ per se is considered neither a primary nor an independent factor in the development of BER. This hypothesis is advanced with the objective of stimulating further research into the causes of a physiological disorder that, as yet, remains stubbornly obscure. (C) 2001 Elsevier Science B.V. All rights reserved.