We investigated how salicylic acid (SA) enhances H2O2 and the relative
significance of SA-enhanced H2O2 in Arabidopsis thaliana. SA treatmen
ts enhanced H2O2 production, lipid peroxidation, and oxidative damage
to proteins, and resulted in the formation of chlorophyll and carotene
isomers. SA-enhanced H2O2 levels were related to increased activities
of Cu,Zn-superoxide dismutase and were independent of changes in cata
lase and ascorbate peroxidase activities. Prolonging SA treatments ina
ctivated catalase and ascorbate peroxidase and resulted in phytotoxic
symptoms, suggesting that inactivation of H2O2-degrading enzymes serve
s as an indicator of hypersensitive cell death. Treatment of leaves wi
th H2O2 alone failed to invoke SA-mediated events. Although leaves tre
ated with H2O2 accumulated in vivo H2O2 by 2-fold compared with leaves
treated with SA, the damage to membranes and proteins was significant
ly less, indicating that SA can cause greater damage than H2O2. Howeve
r, pretreatment of leaves with dimethylthiourea, a trap for H2O2, redu
ced SA-induced lipid peroxidation, indicating that SA requires H2O2 to
initiate oxidative damage. The relative significance of the interacti
on among SA, H2O2 and H2O2 metabolizing enzymes with oxidative damage
and cell death is discussed.