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Wounding, as during excision and preparation of lettuce (Lactuca sativa L.) leaf tissue for salads, induces the synthesis and accumulation of phenolic compounds that participate in subsequent reactions that cause tissue browning. Exposure of excised 5-mm mid-rib segments of romaine lettuce leaf tissue to vapors of mono-carboxylic acids or aqueous solutions of mono-carboxylic acids or their salts inhibited wound-induced phenolic accumulation (WIPA) and subsequent tissue browning. The decline in phenolic content followed a quadratic curve with increasing concentration, reaching a maximum inhibition after 60 min of 74 ± 8% for 50 m M sodium acetate (2 carbons, C2) and 91 ± 4% for 20 m M sodium decanoate (capric acid, C10). Respiration (i.e. carbon dioxide production) was unaffected by concentrations of formic, acetic, or propionic acids that reduced wound-induced phenolic content or that increase ion leakage from the tissue into an isotonic mannitol solution. However, WIPA was suppressed up to 70% at concentrations (20 m M acetate) that did not increase ion leakage over that of water controls. Various acetate salts (i.e. ammonium, calcium, magnesium, and sodium) all produced the same level of inhibition. The effectiveness of the compounds increased with increasing number of carbons in the molecule from 1 to 10, and was unaffected by whether the carbons were a straight chain or branched or whether the treatment was delayed by up to 6 h. The effectiveness of butyrate (C4) in reducing WIPA (27% reduction at 20 m M) was less than that predicted from the response of the two adjacent mono-carboxylates similarly applied: propionate (C3) (62%) and valerate (C5) (73%). It appears that, unlike the n-alcohols, mono-carboxylates are not interfering with the synthesis or propagation of a wound signal but are interfering with subsequent steps in the production and accumulation of wound-induced phenolic compounds. [ABSTRACT FROM AUTHOR]

In plant tissue, a wound signal is produced at the site of injury and propagates or migrates into adjacent tissue where it induces increased phenylalanine ammonia lyase (PAL, EC 4.3.1.5) activity and phenylpropanoid metabolism. We used excised mid‐rib leaf tissue from Romaine lettuce (Lactuca sativa L., Longifolia) as a model system to examine the involvement of components of the phospholipid‐signaling pathway in wound‐induced phenolic metabolism. Exposure to 1‐butanol vapors or solutions inhibited wound‐induced increase in PAL activity and phenolic metabolism. Phospholipases D (EC 3.1.4.4), an enzyme involved in the phospholipid‐signaling pathway is specifically inhibited by 1‐butanol. Re‐wounding tissue, in which an effective 1‐butanol concentration had declined below active levels by evaporation, did not elicit the normal wound response. It appears the 1‐butanol‐treated tissue developed resistance to wound‐induced increases in phenylpropanoid metabolism that persisted even when active levels of 1‐butanol were no longer present. However, a metabolic product of 1‐butanol, rather than 1‐butanol itself, may be the active compound eliciting persistence resistance. Inhibiting a subsequent enzyme in the phospholipid‐signaling pathway, lipoxygenase (LOX; EC 1.13.11.12) with 1‐phenyl‐3‐pyrazolidinone (1P3P) or reducing the product of LOX activity with diethyldithio‐carbamic acid (DIECA) also inhibited wound‐induced PAL activity and phenolic accumulation. The effectiveness of 1‐butanol, DIECA, and 1P3P declined as the beginning of the 1‐h immersion period was delayed from 0 to 4 h after excision. This decline in effectiveness is consistent with involvement of the inhibitors in the production or propagation of a wound signal. The wound signal in lettuce moves into adjacent tissue at 0.5 cm h−1, so delaying application would allow the signal to move into and induce the wound response in adjacent tissue before the delayed application inhibited synthesis of the signal. Salicylic acid (SA) inhibits allene oxide synthase (AOS, EC 4.2.1.92), another enzyme in the phospholipid‐signaling pathway. Exposure to 1 or 10 mM SA for 60 min reduced wound‐induced phenolic accumulation by 26 or 56%, respectively. However, 1 mM SA lost its effectiveness if applied 3 h after excision, while 10 mM SA remained effective even when applied 4 h after excision. At 1 mM, SA may be perturbing the wound signal through inhibition of AOS, while at 10 mM it appears to have some generally inhibitory effect on subsequent phenolic metabolism. These data further implicate the phospholipid‐signaling pathway in the generation of a wound signal that induces phenolic metabolism in wounded leaf tissue. [ABSTRACT FROM AUTHOR]