Antioxidative response patterns of Norway spruce bark to low-density Ceratocystis polonica inoculation

KEY MESSAGE : Based on time courses of individual antioxidant compounds, bark phenolic metabolism has been recognised to integrate ascorbate–glutathione system as a redox hub in Norway spruce defence against Ceratocystis polonica infection. Temporal courses of individual phenolics, thiols and ascorbate were studied in Norway spruce phloem over a 5-month period after inoculation at low density with Ceratocystis polonica. The initial reaction of Norway spruce 3 days after inoculation was characterised by significantly increased isorhapontin and taxifolin concentrations, accompanied by significantly lowered catechin contents. On later sampling dates, catechin concentrations within infected bark increased until September. The slightly accumulated astringin contents in April and May diminished at later sampling dates in response to infection. The isorhapontin levels strongly raised in April and were slightly lowered from June onwards. Compared to the controls, taxifolin concentrations were higher in the infected samples showing a double peak with maxima in April and June. The taxifolin values eased later but remained above the control levels. The initial response of the ascorbate–glutathione system to fungal infection was characterised by a significantly more oxidised glutathione pool, slightly more reduced ascorbate system and by higher glutathione reductase activity. Three weeks later an accumulation of thiols was observed, whereas total ascorbate was significantly lowered and the ascorbate redox state shifted towards more oxidised values. Until the middle of July a gradual increase of total glutathione was determined within the infected bark, which was accompanied by significantly increased cysteine contents, higher glutathione reductase activity, but significantly lowered total ascorbate contents. The increased pressure on the ascorbate system reflects its interaction with phenolics, as ascorbate is needed for reducing the phenoxyl radicals formed during pathogen defence.