Salicylic acid (SA) is one component of a complex signalling pathway that is induced by a number of biotic and abiotic stresses. Exposing seedling radicles to aqueous solutions of 0.5 mM salicylic acid for 24 h before chilling at 2.5°C for 1–4 days reduced the chilling‐induced increase in electrolyte leakage from maize and rice leaves, and cucumber hypocotyls, but not from their radicles. The SA treatments that induced chilling tolerance in the aerial portion of the seedlings did not induce chilling tolerance in the radicles, even though the SA treatments were applied to the radicles. A comparison of activity among five antioxidant enzymes showed that SA did not alter enzyme activities in the radicles, but that chilling tolerance induced by SA in the aerial portions of maize and cucumber plants was associated with an increase in the activity of glutathione reductase and guaiacol peroxidase.

Wounding induced the accumulation of phenolic compounds in Iceberg and Romaine lettuce leaf tissue. Phenolic concentrations were quantified after holding the leaf tissue at 10 degrees C for 48 h as the absorbance of a methanol extract at 320 nm, and by the Folin-Ciocalteu method. Heat-shock treatments applied by immersing tissue in 45 degrees C water for 2.5 min before or after wounding reduced the accumulation of phenolic compounds. Compared to the nonwounded, nonheat-shocked controls, these and other wounding and heat-shock treatments produced leaf tissue with a 4-fold range in phenolic content. The antioxidant capacity of the tissue, measured as DPPH (alpha,alpha-diphenyl-beta-picrylhydrazyl)-radical scavenging activity, or as ferric-reducing antioxidant power (FRAP), increased after wounding. The increase was linearly correlated with the increase in phenolic compounds in Iceberg (R(2) > 0.97) and in Romaine (R(2) > 0.95) lettuce leaf tissue. Increased consumption of diets rich in phenolic antioxidants may contribute to reducing human diseases. Treatments that reduce the browning of wounded lettuce leaf tissue by preventing the oxidation of the accumulated wound-induced phenolic compounds may produce a healthier fresh-cut product than treatments that prevent the wound-induced synthesis and accumulation of phenolic compounds with antioxidant properties.

A novel and facile marine mussel-inspired surface modification approach for microcrystalline celluloses (MCC) and enhanced interfacial adhesion with the soy protein isolate (SPI) matrix were demonstrated in an effort to develop renewable composite films. The surface composition and micromorphology of the poly­(dopamine) (PDA)-modified MCC (PDMCC) were characterized by X-ray photoelectron spectroscopy, attenuated total reflectance-Fourier transform infrared spectroscopy, thermogravimetric analysis, and scanning electron microscopy. The biomimetic adherent PDA layer was successfully coated onto the MCC surface via dopamine self-polymerization through a simple dip-coating method. As expected, the adlayer of PDA between the PDMCC and peptide chains greatly enhanced the mechanical properties of the resultant films. Because of the favorable interfacial adhesion between PDMCC and SPI, as certified by solid state 13C nuclear magnetic resonance and atomic force microscopy, the tensile strength of the PDMCC/SPI film was improved by 82.3%, and its water absorption was reduced by 31.3% in comparison to that of the unmodified SPI film.

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Chilling whole cucumber seedlings that had 10‐mm long radicles for 4 days at 2.5°C significantly inhibited subsequent radicle growth both by increasing the time it took the seedlings to recover from chilling and attain a linear rate of radicle growth, and by decreasing the subsequent rate of linear growth. Exposing cucumber seedlings to 45°C for up to 20 min had no effect on subsequent radicle growth, while longer exposures produced reductions in growth. A heat shock at 45°C for 10 min induced the optimal protection to 4 days of chilling at 2.5°C by reducing chilling inhibition from 60 to 42%. Two hours after being chilled, heat shocked or heat shocked and then chilled, there was no difference in protein content of the apical 1 cm of the seedling radicle among these treatments and the non‐heat shocked, non‐chilled control. Two days after treatment, the protein content was still similar in tissue that had been heat shocked or heat shocked and chilled, while it was significantly reduced in tissue that had been chilled. In general, 2 h after treatment, the activity of the 5 antioxidant enzymes examined in this study [superoxide dismutase (SOD; EC 1.15.1.1), catalase (CAT; EC 1.11.1.6), ascorbate peroxidase (APX; EC 1.11.1.11), guaiacol peroxidase (GPX; EC 1.11.1.7) and glutathione reductase (GR; EC 1.6.4.2)] were reduced by chilling and unaffected or increased by heat shock. When heat shock was followed by chilling, there was a consistent effect of the heat shock treatment on preventing the loss of enzyme activity following chilling. This protective effect of the heat shock treatment was even more pronounced after 2 days of recovery at 25°C for SOD, CAT and APX. In contrast, the activity of GR and GPX was substantially higher in chilled tissue than in tissue that had been heat shocked before being chilled. Elevated levels of GR and GPX therefore appear to be correlated with the development of chilling injury, while elevated levels of SOD, CAT and APX appear to be correlated with the development of heat shock‐induced chilling tolerance.