New directions for research on scald in apples (Malus x domestica Borkh.)
J.K. Fellman , D.S. Mattinson , J. Parrish , M.M. Haines and N.R. Natale
Proceedings of 26th International Horticultural Congress. Volume of Abstract . Toronto, Canada, 11-17 August, 2002. p. 260.
2002
บทคัดย่อ
Superficial scald, perhaps the most severe physiologic disorder known to occur in stored aples (Malus x domestica Borkh.) has been circumstantially associated with oxidative stress. The generally accepted hypothesis is that scald develops as a result of farnesene oxidation; farnesene is a nuturally-occurring sesquiterpene hydrocarbon present in apple peel. Farnesene oxidation products presumably cause death of surface cells resulting in discolored fruti unsuitable for release through marketing channels. Prevention of scald is commercially achieved by diphenylamine (DPA) treatment of fruit destined for longterm storge. DPA, an antioxidant compound, inhibits the oxidation of farnesene. Scald development is also associated with the harvest of immature fruit, resulting in a dilemma for producers, as fruit harvested before the onset of ripening has a much better storage life. We believe that the crucial events associated with scald development occur before or immediately after harvest. Exposure of apple fruit to certain environmental conditons before or immediately after harvest may result in the accumulation of chemical species that are able to persist in the peel tissue. Once is storage, these species can combine with oxygen to generate singlet oxygen which is a much more toxic from of O2. The use of spin-trapping reagents to identify intermediate chemical specles in the scald reaction revealed the preesence of reactive organic species associated with farnesene oxidation. Chemical identification of thse intermediates allow us conditions to mimic the naturally-occurring scald response to facilitate molecular investigations. Recent information from our laboratory as well as from other scald investigations suggest that oxidative stress associated with scald development attenuates a signal-tranducing mechanism that involves ethylene reception to induce apoptotic cell death.