The pressure microprobe was used to measure cell turgor (ψp) in tomato pericarp tissue, and also to sample vacuolar fluid for the measurement of cell osmotic potential (ψs) in a nanoleter freezing point osmometer. In fresh tissue, cell ψs agreed well with the ψs of frozen-thawed whole tissue measured with a vapor pressure osmometer. Under a wide range of ripeness conditions however, and for both intact fruit and discs of fruit tissue, fruit cell turgor was consistently lower than expected, based on the values of cell ψs. When tissue discs were hydrated in aerated distilled water, disc fresh weight increased substantially (20 - 50+%), and both cell turgor and tissue ψs increased. Cell ψs however, remained relatively constant. These and other observations suggest that the turgor increase during hydration was largely due to losses of solute from the apoplastic space, partly by direct losses from the tissue, and partly by cell solute accumulation.
Immature fruit of ‘French’ prune were treated in air or ethylene and mesocarp tissues incubated with crude cell wall degrading enzymes to release cells and protoplasts. Ethylene treatment substantially reduced the release of cells and protoplasts and increased the proportion of pectic polymers in the cell walls.
The pressure microprobe has been used to measure cell turgor and, in addition, to sample vacuolar tissues. In carrot, a rapid initial loss of tissue firmness (instron technique) occurred when the tissue was heater (cooked), and this could be entirely attributed to a loss in cell turgor. Turgor was well-correlated to firmness over the range of turgor measurements (0–0.8 MPa). In cherry and other fruits, turgor is typically 1 to 2 orders of magnitude lower than that expected based on cell osmotic potential, indicating the presence of apoplastic solutes. Cherry fruit firmness and cell turgor were well-correlated during the first 2 h of hydration at 20C, but, as fruit began to crack, tissue decreased, whereas turgor continued to increase.
Eight-one percent of the harvest firmness in kiwifruit (Actinidia chinensis Planch.) was lost during the first 8 weeks of storage in air at 0°C. As softening proceeded, a solubilization of uronic acids and the neutral sugar residues usually associated with pectic polymers (galactose, arabinose, and rhamnose) was detected. No consistent changes were noted in cellulose or the neutral sugars usually associated with hemicelluloses. Starch degradation also occurred coincident with softening. The amount of cell wall components soluble in water following fruit homogenization and the proportion of ethanol-precipitable pectic neutral sugars in this fraction increased during the first 8 weeks of storage. Once the rate of softening slowed (8 to 20 weeks), an equilibrium situation apparently was established between the amounts of the sugars formed in the ethanol-precipitable (i.e., polymeric) and ethanol-soluble fractions, suggesting that digestion of wall components continues after their excision from the insoluble wall matrix. Controlled atmosphere (2% O2+ 5% CO2; CA) storage retarded flesh softening relative to that measured in fruit held at 0° in air. A comparison of the changes in the cell wall components of air-stored and CA-stored kiwifruit suggests that, in addition to cell wall degrading processes contributing to fruit softening, starch degradation (possibly causing cell turgor changes) also may be involved in low-temperature softening of kiwifruit. The losses in water-insoluble cell wall pectic neutral sugars and uronic acids in air and CA storage were similar during the first 8 weeks of storage. Once softening slowed in CA, small but consistent reductions in the amount of cell wall turnover were observed as compared to air storage.