The curing or wound healing period immediately after harvest of potatoes is the period in which the wounds, that occur during harvest, are healed. This is an essential phase of potato storage since wounds are ideal entries for pathogens and because water can easily evaporate from the wounded tubers. S-carvone inhibits the process of wound healing temporarily (Figure 7a and b) by reduction of the suberization and the cambium layer formation. Suberization as a process is not impossible in the presence of S-carvone, since S-carvone-containing tissue develops clearly visible suberin layers after 10-14 days, i.e. after a delay of about 10 days. Initially, S-carvone inhibits the induction of phenylalanine ammonialyase
(PAL) (Oosterhaven et al. 1995c) but after about 10 days, the PAL activity increases and suberin is formed.
The inhibition of wound healing is coincided with a lack of induction of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR). Untreated wounded tissue showed an induction of HMGR whereas in S-carvone treated tissue no HMGR could be determined (Oosterhaven et al. 1995a). Western-blotting experiments revealed that this was caused by the fact that no HMGR-protein is synthesized in S-carvone containing tuber tissue (Oosterhaven 1995).
The inhibiting effect of S-carvone on wound healing implies that the application of S-carvone-containing sprout suppressants should not be performed at a high dosage before the end of the curing period, because this would lead to a delay of wound healing. In practical trials, a low dosage immediately after harvest has not shown a negative effect on wound healing, nor on pathogen attack or on weight losses (Hartmans et al. 1995).
12.6. ANTIFUNGAL ACTIVITY OF S-CARVONE 12.6.1. Mechanism of Antifungal Action of S-carvone
The antimicrobial activity of several essential oils and isolated compounds thereof, such as S-carvone, has been established for many different taxonomic groups of microorganism ranging from Gram-positive and Gram-negative bacteria to fungi including yeasts. Because essential oils contain a variety of compounds from different chemical classes, it is not possible to discriminate one single type of mechanism by which these compounds act on microorganisms. A prominent feature these compounds have in common, is their high degree of hydrophobicity. Due to this feature, these compounds partition preferentially into biological lipid bilayers as a function of their own lipophilicity and the fluidity of the membrane (Oosterhaven 1995b). Accumulation of lipophilic compounds into biological membranes enhances their availability to the cell and thus may cause toxic effects (Sikkema et al. 1992, Sikkema et al. 1994). This is exemplified by lipophilic hydrocarbons such as P-pinene and cyclohexane which have been shown to impair energy transducing processes in plasma and mitochondrial membranes of yeast cells (Uribe et al. 1985, Uribe et al. 1990). Inhibition of yeast mitochondrial respiration by P-pinene is most likely to be exerted on the level of NADH- and succinate oxidation (Uribe et al. 1985).
Despite the high degree of ordering of solutes in the lipid bilayer as compared to the bulk liquid phase (Simon et al. 1979), a good correlation has been observed between the partitioning coefficient of various lipophilic compounds in membrane/ buffer and octanol/ water two-phase systems (Sikkema et al. 1994, Sikkema et al. 1995). Therefore, octanol/ water partitioning coefficients, which are known for many different compounds present in essential oils, can be used to assess the potential antimicrobial activity of these compounds (Sikkema et al. 1994). However, the presence of specific reactive groups in such compounds, the variability in membrane composition and the differences in metabolic capacities of target organisms makes a reliable prediction of the antimicrobial activity of these compounds difficult, if not impossible when solely based on their hydrophobicity. Illustrative for this is the action of S-carvone and trans-cinnamaldehyde, two compounds with comparable hydrophobicity but a quite different antimicrobial mechanism. Both compounds inhibited in vitro growth of the fungus Penicillium hirsutum when administered via the gas phase (Smid et al. 1995). S-carvone caused full suppression of fungal growth only as long as the compound was present in the gas phase. Cinnamaldehyde, in contrast, caused irreversible inhibition of fungal growth, even after short term exposure. Comparable effects were observed when cell suspensions of the yeast Saccharomyces cerevisiae were exposed to different concentrations of S-carvone and trans-cinnamaldehyde (Smid et al. 1996). Exposure of washed yeast cells for 1 hour to 2mM trans-cinnamaldehyde resulted in 95% loss of viability, whereas S-carvone up to concentrations of 10mM did not significantly reduce viability of S. cerevisiae cells. Evidently, S-carvone acts predominantly as a fungistatic agent, whereas cinnamaldehyde is a fungicidal agent.
This difference between S-carvone and trans-cinnamaldehyde in mechanism of antifungal activity was studied in more detail using Saccharomyces cerevisiae (Smid et al. 1996). Cinnamaldehyde was found to cause a (partial) collapse of the integrity of the cytoplasmic membrane that eventually leads to an excessive leakage of metabolites and enzymes from the affected cells and finally loss of viability. Loss of membrane integrity was not observed with S-carvone which is in agreement with its fungistatic rather than fungicidal effect (Smid et al. 1996).
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