Submitted to: Journal of Agricultural and Food Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2000
Publication Date: N/A
Citation: N/A Interpretive Summary: Superficial scald is a serious, costly storage disorder of apple and pear fruits. The symptoms, mainly the appearance of brown or black patches on the skin, occur after long-term cold storage and worsen greatly when the fruit are rewarmed. It has long been thought that oxidation products of a natural oily compound called farnesene, which accumulate in the peel during storage, somehow trigger events resulting in death of cells just beneath the fruit skin. Recent evidence indicates that a gaseous breakdown product of farnesene referred to as "MHO" may be directly involved in the tissue damage that leads to scald symptoms. In this study, we purified the primary oxidation products of farnesene ("CTs") from apple peel and showed that in the test tube under air these compounds degrade to yield MHO. Moreover, it was found that production of MHO from CTs was much more rapid at warm than at cold temperature. These results could explain why scald becomes much worse after stored fruit are rewarmed, as the accumulated CTs are rapidly degraded to MHO and other volatiles. This kind of information is essential to develop an understanding of the biochemical basis of superficial scald, and ultimately will help scientists to devise safe postharvest treatments that prevent the disorder.
Technical Abstract: Accumulation of conjugated trienol (CTol) oxidation products of alpha- farnesene in apple peel during air storage at 0-1C is closely correlated with development of superficial scald, a serious physiological disorder. Recent studies indicated that a volatile product of alpha-farnesene oxidation, 6-methyl-5-hepten-2-one (MHO), may somehow initiate the tissue damage that leads to scald symptoms. Using HPLC-purified CTol products of alpha-farnesene oxidation from peel tissue of cold-stored 'Granny Smith' ('GS') and 'Red Delicious' ('RD') apples, we found that in vitro autoxidation of these compounds (two isomers) yields MHO as a major product. Furthermore, the rate of autoxidation was much more rapid at 20 than at 0C, and at 20C there was an initial lag phase of several hours typical of free radical-mediated reactions. These findings indicate that CTol is the precursor of MHO in the oxidative pathway leading from farnesene to MHO, and explain the burst of MHO production when apples are removed from cold storage, which coincides with a sharp decline in peel tissue levels of CTols and a rapid, marked intensification of scald symptoms. It is unclear why CTols from 'GS' apples autoxidized more readily than those from 'RD' apples. Possibly, small amounts of a natural lipophilic antioxidant coeluted with CTols in the 'RD' HPLC preparation.