Static magnetic field treatment enhanced photosynthetic performance in soybean under supplemental ultraviolet-B radiation.

The study was performed to analyze the impact of seed pretreatment by static magnetic field (SMF) of 200 mT for 1 h on photosynthetic performance of soybean (Glycine max) seedlings under ambient (aUV-B) and supplemental ultraviolet-B (a+sUV-B) stress. Ambient and supplemental UV-B were found to decrease the plant growth, chlorophyll concentration, PSII efficiency, selected JIP-test parameters such as Fv/Fm, φEo, ΔV(I-P), PIABS, PItotal, and rate of photosynthesis in the leaves of soybean seedlings emerged from untreated (UT) seeds. aUV-B and a+sUV-B were observed to increase the synthesis of UV-B-absorbing substances (UAS), reactive oxygen species (ROS) like superoxide radical (O2·-) and hydrogen peroxide (H2O2), antioxidants like ascorbic acid and α-tocopherol and decrease the nitrate reductase (NR) activity; subsequently, it results in a decreased rate of photosynthesis, biomass accumulation, and yield. However, our results provided evidence that SMF pretreatment increased the tolerance of soybean seedlings to UV-B radiation by increased NO content and NR activity; higher efficiency of PSII, higher values of φEo, ΔV(I-P), PIABS, and PItotal, decreased intercellular CO2 concentration, lower  amount of UAS, ROS, and antioxidants that consequently improve the yield of soybean plants under aUV-B as well as a+sUV-B stress. Thus, our results suggested that SMF pretreatment mitigates the adverse effects of UV-B stress by the enhancement in photosynthetic performance along with higher NO content which may be able to protect the plants from the deleterious effects of oxidative stress caused by UV-B irradiation.

Effect of cadmium on chlorophyll biosynthesis and enzymes of nitrogen assimilation in greening maize leaf segments: role of 2-oxoglutarate.

Supply of cadmium chloride (0.5 mM) inhibited chlorophyll formation in greening maize leaf segments, while lower concentration of Cd (0.01 mM) slightly enhanced it. Inclusion of 2-oxoglutarate (2-OG, 0.1-10 mM) in the incubation mixture increased chlorophyll content in the absence as well as presence of Cd. Substantial inhibition of chlorophyll formation by Cd was observed at longer treatment both in the absence and presence of 2-OG. When the tissue was pre-incubated with 2-OG or Cd, the inhibition (%) of chlorophyll formation by Cd was lowered in the presence of 2-OG. Treatment with Cd inhibited ALAD activity and ALA formation and the inhibition (%) of ALA formation by Cd was strongly reduced in the presence of 2-OG. Glutamate dehydrogenase (GDH) activity was increased by the supply of Cd both in the absence as well as presence of 2-OG. In the presence of 2-OG, Cd supply significantly increased glutamate synthase (GOGAT) activity and reduced inhibition (%) of glutamine synthetase (GS) activity. The results suggested the involvement of the glutamine synthetase/glutamate synthase (GS/GOGAT) pathway of ammonia assimilation to provide the precursor, glutamate, for ALA synthesis under Cd toxicity and 2-OG supplementation.

Inhibition of chlorophyll biosynthesis by mercury in excised etiolated maize leaf segments during greening: effect of 2-oxoglutarate.

Mercury (0.01-1.0 mM) inhibited chlorophyll formation in greening maize leaf segments. However, supplementing incubation medium with 2-oxoglutarate, maintained substantially higher level of chlorophyll in absence of metal after an initial period of 8 hr. On preincubation of leaf segments with HgCl2, per cent inhibition of chlorophyll synthesis by metal was same in the presence and absence of 2-oxoglutarate. Supply of 2-oxoglutarate (0.1-10.0 mM) exerted concentration dependent effect on chlorophyll formation in absence or presence of metal. Increase in delta-amino levulinic acid dehydratase as well as NADH-glutamate synthase activity and decrease in NADH-glutamate dehydrogenase activity by 2-oxoglutarate in the presence of Hg suggested that glutamate for delta-amino levulinic acid synthesis could be made available from NH4+ assimilation via., glutamine synthetase/glutamate synthase pathway during mercury toxicity.