Submitted to: Postharvest Biology and Technology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/20/2000
Publication Date: N/A
Citation: N/A Interpretive Summary: Superficial scald is a serious, costly storage disorder of apples and pears. For some varieties in certain years it can cause fresh market losses of up to 80 percent, and commercial control of the problem involves chemical treatments that pose a potential human health risk. It is therefore important to understand the biochemical reactions that cause scald so that new resistant lines can be developed by genetic means. The prevailing theory for over 30 years has been that an oily compound, farnesene, which builds up in the fruit skin during cold storage, breaks down and yields toxic products that eventually kill the tissue. Our study showed that apple fruit from certain hybrid lines develop mild to moderate scald symptoms but accumulate only very low levels of farnesene breakdown products. These results support the conclusion that breakdown of farnesene is a secondary result of the main cause of scald. This knowledge will promote a reevaluation of the farnesene-scald theory and help scientists to determine the chemical mechanism that underlies scald development.
Technical Abstract: In a two-year study, fruit from 8 red- and 8 yellow-skinned White Angel x Rome Beauty hybrid apple selections were stored for 21 weeks at 0.5C plus 1 week at 20C and evaluated for scald incidence and severity. Peel-tissue samples taken from groups of fruit at 0, 7, 14, and 21 weeks of storage were analyzed for concentrations of alpha-farnesene and its conjugated trienol (CTol) oxidation products by HPLC with UV detection. Three red- and 5 yellow-fruited lines exhibited at least mild scald symptoms. The remaining 5 red- and 3 yellow-fruited lines were free of scald. Overall, production of alpha-farnesene and accumulation of CTols were not closely correlated with scald susceptibility. Data for the selections most prone to scald, Y-65, Y-40, & R-44, were consistent with the proposed role of farnesene oxidation products in scald induction, but for Y-55 and R-48, which developed mild to moderate scald and accumulated little CTols, the data contradicted the farnesene oxidation scald induction hypothesis. Also, scald-resistant lines Y-07 and R-22 produced high levels of alpha-farnesene and reached CTol levels comparable to those in several scald-susceptible lines. We conclude that if CTol do play a role in scald induction, there must be other mitigating factors of at least equal importance. Moreover, our findings support the proposal that oxidation products of farnesene are not essential for scald development in fruit with severely compromised antioxidative defenses, but free radicals and/or toxic volatiles generated by farnesene oxidation can exacerbate scald symptoms.