Figure 1.

Main mechanisms involved in PTE toxicity and plant responses. Upon metal excess, the cells undergo a variety of injuries that have been highlighted: 1. membrane damage, 2. oxidative burst, with production of ROS, 3. mitochondrial and chloroplast damage, 4. inhibition of enzymes activity, 5. DNA damage, 6. transcription inhibition, 7. protein synthesis inhibition, and 8. protein degradation and denaturation. Plants respond to the excess PTE by activating an array of strategies, both preventing metal entrance into cells (9. metal binding to cell wall and root exudates) and contrasting the metal stress (10. ROS scavenging mechanisms) and decreasing the metal concentration in the cytosol. The latter strategy starts with the sensing and signalling of the metal stress (11. hormone signalling and transduction pathways activation) that eventually promote transcription of stress responsive genes (12), encoding metal ions transporters (13), and proteins involved in PTE detoxification, such as metal chelation (14) and vacuolar sequestration (15).