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NADPH oxidase, an enzyme associated with the plasma membrane, constitutes one of the main sources of reactive oxygen species (ROS) which regulate different developmental and adaptive responses in plants. In this work, the involvement of NADPH oxidases in the regulation of photosynthesis and cell ionic homeostasis in response to short cadmium exposure was compared between wild type (WT) and three RBOHs (Respiratory Burst Oxidase Homologues) Arabidopsis mutants (AtrbohC, AtrbohD, and AtrbohF). Plants were grown under hydroponic conditions and supplemented with 50 µM CdCl2 for 24 h. Cadmium treatment differentially affected photosynthesis, stomatal conductance, transpiration, and antioxidative responses in WT and Atrbohs mutants. The loss of function of RBOH isoforms resulted in higher Cd2+ influx, mainly in the elongation zone of roots, which was more evident in AtrbohD and AtrbohF mutants. In the mature zone, the highest Cd2+ influx was observed in rbohC mutant. The lack of functional RBOH isoforms also resulted in altered patterns of net K+ transport across cellular membranes, both in the root epidermis and leaf mesophyll. The analysis of expression of metal transporters by qPCR demonstrated that a loss of functional RBOH isoforms has altered transcript levels for metal NRAMP3, NRAMP6 and IRT1 and the K+ transporters outward-rectifying K+ efflux GORK channel, while RBOHD specifically regulated transcripts for high-affinity K+ transporters KUP8 and HAK5, and IRT1 and RBOHD and F regulated the transcription factors TGA3 and TGA10. It is concluded that RBOH-dependent H2O2 regulation of ion homeostasis and Cd is a highly complex process involving multilevel regulation from transpirational water flow to transcriptional and posttranslational modifications of K/metals transporters.

Salt stress is one of the biggest environmental factors impacting plant growth and productivity in many parts of the world, particularly in irrigated lands of arid and semi‐arid regions. The involvement of glycolate oxidase (GOX), an enzyme that catalyzes the conversion of glycolate into glyoxylate during photorespiration with concomitant production of H₂O₂, in the regulation of photosynthesis and reactive oxygen species (ROS) metabolism was investigated in salt‐challenged Arabidopsis wild type and two gox Arabidopsis mutants (gox1 and gox2). Plants were grown under hydroponic conditions supplemented or not with 100 mM NaCl for 24 h. Under control conditions, pigments contents (chla, chlb, total chlorophyll) were higher in WT than gox mutants. However, a different behavior was observed following NaCl treatment. The same trend of pigment content was registered for gas exchange parameters. Under control conditions, as expected, leaf GOX activity was reduced in gox mutants compared to WT, while NaCl increased GOX activity only in gox mutants. Leaf H₂O₂ content was reduced in gox mutants compared to WT under control and stress conditions. NaCl‐induced oxidative stress, noticed by oncrease of malondialdehyde content, was observed only in WT and gox1 mutant. Modulation of catalase, guaiacol peroxidase, and glutathione reductase activitives in leaves were also registered in all genotypes and depending on the treatment. As a whole, data show the crucial role of GOX in regulating both photosynthetic activity and ROS metabolism under salinity conditions.

SUMMARY To verify a possible implication of lipids and some other compounds such as hydrogen peroxide (H2O2) and glyceraldehydes-3-phosphate dehydrogenase (G3PDH) in the response of Hordeum vulgare to an early potassium deprivation, plants were grown in hydroponics for 30 days with a modified Hewitt nutrient solution containing 3 mM K+ and then incubated for increasing time ranging from 2 h up to 36 h in the same medium deprived of K+. In contrast to leaves, root K+ concentration showed its greatest decrease after 6 h of treatment. The main lipids of the control barley roots were phospholipids (PL), representing more than 50% of the total lipids. PL did not change with treatment whereas free sterols (FS) amounts decreased following K+ deprivation, showing an about 17% reduction after 36 h. As regards the individual PL, 30 h K+ deprivation caused a reduction in phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylinositol (PI) levels whereas phosphatidylglycerol (PG), phosphatidylethanolamine (PE) and phosphatidic acid (PA) increased. The maximum PA accumulation as well as the highest phospholipase D (PLD) activation, estimated by an accumulation of phosphatidylbutanol (PtBut), were observed after 24 h of K+ starvation. At the root level, after 6 h of incubation in –K solution, H2O2 level showed the maximum value. At the same time G3PDH activity reached the minimum. On the basis of a concomitant stimulation of PLD activity and, consequently, PA accumulation, enhancement of H2O2 production, and inhibition of G3PDH activity we can suggest a possible involvement of these three compounds in an early response to K+ deprivation.