A panel of 20 to 27 screened judges was used to determine the threshold of pure limonin and naringin in distilled water, sucrose solutions, citric acid solutions adjusted to various pH values and in citrus juice model systems. Thresholds in distilled water were 1 and 20 mg/l for limonin and naringin, respectively. Sucrose, citric acid and combinations of these constituents in a model system increased the threshold of limonin and naringin several fold. The highest thresholds were obtained at low pH values in the absence of sugar. In a 1.2 % citric acid solution containing 5 % sucrose, 2.5 % dextrose and 2.5 % fructose the maximum limonin threshold of 1 1 mg/kg was obtained at pH 3.8. The maximum difference threshold for limonin in orange juice was 6.5 mg/kg and also occurred at pH 3.8. The optimum pH for limonin bitterness suppression (maximum threshold) was 3.8 in both model systems and natural orange juice. Thresholds on either side of this value were lower and limonin bitterness was more noticeable. No pH optimum was observed for naringin threshold in model systems. Individual thresholds showed a wide range of sensitivity to both limonin and naringin bitterness.
SUMMARY– Tissues of early‐season navel oranges and grapefruit were found by paper electrophoretic procedures to contain a nonbitter precursor of limonin, but no significant amounts of limonin. Limonin is the intensely bitter triterpenoid dilactone responsible for the bitterness which develops in certain navel orange juices on standing. The nonbitter precursor was identified as limonin monolactone by comparison with the authentic compound prepared by partial hydrolysis of limonin and by acid‐catalyzed conversion into limonin. Limonin monolactone is stable in the tissues of the intact fruit (which are not bitter) because it is apparently not in direct contact with the acidic juice. It is slowly converted into limonin (and the juice becomes bitter) when the fruit tissues come in contact with the juice, after the juice is expressed from the fruit. Limonin monolactone was not detected in late‐season navel oranges or grapefruit. This agrees with the fact that juice made from these fruits does not contain limonin. Work is in progress to determine whether the naturally occurring limonin monolactone is the A‐ring monolactone, the D‐ring monolactone, or a mixture of the two.
ABSTRACIThree plant growth regulators, paclobutrazol, ancymidol, and decylimidazole, which are putative inhibitors of gibberellin (GA) biosynthesis, were studied to determine their effect on abscisic acid (ABA) biosynthesis in the fungus Cercospora rosicola. All three compounds inhibited ABA biosynthesis, and paclobutrazol was the most effective, inhibiting ABA 33% at 0.1 micromolar concentrations. In studies using (E,E,)-l-"Cq farnesyl pyrophosphate, it was shown that ancymidol blocked biosynthesis prior to farnesyl pyrophosphate (FPP), whereas paclobutrazol and decylimidazole acted after FPP. The three inhibitors did not prevent 4'-oxidation of (2Z,4E)-a-ionylideneacetic acid. C. rosiciola metabolized ancymidol by demethylation to a-cyclopropyl-a-(p-hydroxyphenyl)-5-pyrimidine methyl alcohol. Paclobutrazol was not metabolized by the fungus. Information that these plant growth regulators inhibit ABA as well as GA biosynthesis should prove useful in determining the full range of action of these compounds.
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