Effects of triacontanol on ascorbate-glutathione cycle in Brassica napus L. exposed to cadmium-induced oxidative stress

- TRIA could be considered as inducer tolerance of plants to heavy metal toxicity.
- Cd contamination decreases chlorophyll content, growth and activities of several enzymes in canola seedlings.
- The effect of TRIA on improving Cd toxicity was varied with modulating the antioxidant pathway AGC and GSH metabolic enzymes.

The ability of exogenous triacontanol (TRIA), a plant growth regulator, to reduce Cd toxicity was studied in canola (Brassica napus L.) plants. The following biological parameters were examined in canola seedlings to investigate TRIA-induced tolerance to Cd toxicity: seedling growth, chlorophyll damage and antioxidant response. In particular, TRIA application reduced Cd-induced oxidative damage, as shown by reduction of ROS content, lipoxygenase (LOX) activity and lipid peroxidation level. TRIA pretreatment increased non-enzymatic antioxidant contents (ascorbate, AsA, glutathione and GSH), phytochelatin content (PCs) and activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), guaiacol peroxidase (GPX), monodehydroascorbate reductase (MDHAR), dehydro ascorbate reductase (DHAR), and glutathione reductase (GR), so reducing the oxidative stress. These results clearly indicate the protective ability of TRIA to modulate the redox status through the antioxidant pathway AGC and GSH, so reducing Cd-induced oxidative stress.