Magnesium deficiency–induced impairment of photosynthesis in leaves of fruiting Citrus reticulata trees accompanied by up‐regulation of antioxidant metabolism to avoid photo‐oxidative damage

Limited data are available on the physiological responses of leaves from fruiting trees to magnesium (Mg) deficiency. Magnesium deficiency–induced effects on photosystem II (PSII) photochemistry in leaves of fruiting (Citrus reticulate cv. Ponkan) trees were assessed by the chlorophyll a fluorescence (OJIP) transient. Magnesium deficiency decreased leaf CO₂ assimilation and carbohydrates, but had no effect on intercellular CO₂ concentration. Activity of ribulose‐1,5‐bisphosphate carboxylase/oxygenase (Rubisco) and concentrations of Chlorophyll (Chl) and carotenoids (Car) decreased to a lesser extent than CO₂ assimilation. Chlorophyll a fluorescence transient from Mg‐deficient leaves had increased O step and decreased P step, accompanied by positive ΔL, ΔK, ΔJ, and ΔI bands. Magnesium deficiency decreased maximum quantum yield of primary photochemistry (F_v/F_m), quantum yield of electron transport from Q<$>_A^‐<$> to the photosystem I (PSI) end electron acceptors (φ_R0), maximum amplitude of IP phase and total performance index (PI_{tot, abs}), but increased deactiviation of oxygen‐evolving complex (OEC) and energy dissipation. Magnesium‐deficient leaves had higher or similar activities of antioxidant enzymes except for lower catalase (CAT) activity, higher or similar concentrations of antioxidant metabolites, and a higher ratio of Car : Chl. Magnesium‐deficiency did not affect concentration of malondialdehyde (MDA) and ratios of ascorbate (ASC) to ASC + dehydroascorbate (DHA) and reduced glutathione (GSH) to GSH + oxidized glutathione (GSSG). In conclusion, Mg deficiency–induced impairment of the whole photosynthetic electron transport chain may be the main factor contributing to decreased CO₂ assimilation. Enhanced energy dissipation and antioxidant metabolism provide sufficient protection to Mg‐deficient leaves against photo‐oxidative damage.