Cellular, biological, and physicochemical basis for the hard‐to‐cook defect in legume seeds

Abstract

This review integrates current knowledge on the hard‐to‐cook (HTC) defect in legume seeds, with emphasis on the cellular and biological changes during storage and soaking, and the physicochemical changes during heating. Several postulated mechanisms, including the pectin‐cation‐phytate model, cell lignification, pectin β‐eliminative degradation, and protein denaturation in relation to starch gelatinization, are discussed in the context of current evidence. Subsequently, a developmental model of legume hardening is presented. It is held that the HTC defect develops during aging and soaking and is exhibited through cooking. During the process, there are many events involved. Free radical formation, lipid peroxidation, acid formation, membrane deterioration, protein denaturation, and leakage are events associated with aging and soaking, whereas pectin decomposition and solubilization, protein coagulation, and starch gelatinization are events that occur during cooking. Cooked HTC seeds are characterized by limited cell separation and restricted starch gelatinization. These defective features result from a restriction in pectin decomposition and solubilization as well as the protein coagulation that prevails over starch gelatinization during heating. This multichannel mechanism points to the direct involvement of two amphoteric colloids, cell wall pectin and storage protein, both of which are sensitive to pH and/or ion composition. The model also indicates the indirect involvement of cell membranes and starch granules. Except for events that occur during aging and soaking, it is likely that heat‐related textural problems in other plant tissues may proceed via a mechanism similar to legume hardening.