Figure 1.

Scheme of copper-induced extracellular calcium entry through transient receptor potential (TRP) channels and voltage-dependent calcium channels (VDCCs) leading to the increases in intracellular calcium which crosstalk with increases in hydrogen peroxide and nitric oxide (NO). The increases in intracellular calcium activate CaMKs and CDPKs that, in turn, activate gene expression leading to enhance activities of antioxidant enzymes, ASC and GSH levels, proteins of photosystems (PSII and PSI) and proteins involved in protection and repair of PS, and enzymes involved in C, N, and S assimilation. The increase in photosynthesis enhances NADPH levels that coupled to the increase in ASC and GSH levels and in activities of antioxidant enzymes participate in the buffering of copper-induced oxidative stress. In addition, the binding of copper ions to UcMTs, the accumulation of copper-containing particles in chloroplasts, and the copper extrusion with GSH also participate in the buffering of oxidative stress. TRPs are indicated in red, green, and yellow; VDCCs are indicated in light and dark blue; red arrows indicate inhibitory processes; and black arrows indicate activation processes.