Abstract
Lipid peroxide-derived α,β-unsaturated aldehydes (2-alkenals) are potent electrophiles that can modify proteins and nucleic acids. Transgenic tobaccos overproducing the Arabidopsis 2-alkenal reductase (AER) are tolerant to photooxidative stress. This work aimed at the elucidation of their phototolerance mechanism. Upon illumination of strong light, leaves of wild type (SR1) tobacco accumulated 4-hydroxyhexenal and acrolein, but the AER-tobaccos did not, suggesting that these 2-alkenals were responsible for the damage. Because several enzymes in the Calvin cycle are vulnerable to 2-alkenals but thylakoid electron transport chain is much less sensitive, we infer that the tolerance was due to the larger electron sink capacity in the Calvin cycle that was protected from the toxicity of HHE and acrolein.
