Anaerobic exposure before or after wounding reduces the production of wound-induced phenolic compounds in fresh-cut lettuce

Abstract

Wounding lettuce (Lactuca sativa L., Longifolia) leaves by excising 5-mm thick mid-rib segments increased phenylpropanoid metabolism with the synthesis and accumulation of wound-induced phenolic compounds (WIPC). Immersing freshly excised segments for 1h in 20°C water agitated with air or N2 produced a 45% or 65% reduction in wound-induced phenolic content, respectively, compared to non-immersed segments when measured after incubation for 48h at 10°C in air. In contrast, agitating the water with O2 produced a 23% increase in WIPC over the non-immersed controls. The enhanced reduction of WIPC in N2 versus air agitated water, and the increase in WIPC in O2 agitated water suggests that anaerobiosis, and not dilution of the wound signal, was the cause of the reduction in WIPC. Holding 5-mm segments in an anaerobic N2 atmosphere produced a similar reduction in WIPC as did holding the segments in water. Delaying the 1h anaerobic treatment for up to 3h had no significant effect on the ability of the anaerobic treatment to reduce WIPC. Exposing 8-cm long mid-rib sections to anaerobiosis for 2h before excision of the 5-mm segments reduced subsequent WIPC from the 5-mm segments. The previous anaerobic treatment of the 8-cm sections predisposed the tissue to have a reduced response to subsequent wounding. After a 2 d lag in WIPC accumulation, the rates of accumulation were similar for the air and 2h anaerobic treated 5-mm segments. Using vacuum treatments to facilitate the loss of volatile products of anaerobic metabolism (e.g., acetaldehyde and ethanol) did not have a significant effect on the accumulation of WIPC. Ion leakage from the symplastic volume of the tissue (i.e., across the cell membrane) was unaffected by the anaerobic treatments, but leakage from the apoplastic volume increased with increasing duration of the anaerobic treatment. Immersing fresh-cut lettuce in an aqueous solutions did not reduce the wound response because of dilution of the wound signal, but because of the anaerobic environment created within the tissue. Some remnant of the anaerobic treatment seems to persist in the tissue and delay the accumulation of WIPC.