The present study prepared molybdenum trioxide (MoO3), the most important intermediate of molybdenum metal, by using a fluidized bed reactor for the thermal decomposition of ammonium molybdate (AM) in the presence of an air flow. During the process of fluidizing the sample inside the reactor, the reaction time and temperature were optimized with a close analysis of the X-ray diffraction (XRD) data and with thermogravimetric analysis (TGA). In particular, the temperature level, at which the AM decomposition is completed, is very important as a primary operating parameter. The analysis of the XRD and TGA data showed that the AM decomposition is almost completed at ~350 oC with a reaction time of 30 min. A shorter reaction time of 10 min. required a higher reaction temperature of ~500 oC with the same air flow rate to complete the AM decomposition. A sharp rise in the decomposition efficiency at a temperature ranging between 320 and 350 oC indicated a threshold for the AM decomposition. The operating conditions determined in this study can be used for future scale-ups of the process.

Molybdenum (Mo) in rhizosphere influences sulfate assimilation as well as a number of other physiological aspects. In this study, the activity of key enzymes in sulfate assimilatory pathways, such as ATP sulfurylase (ATPs), adenosine 5'-phosphosulphate reductase (APR), as well as the responses of reactive oxygen species (ROS), were analyzed to elucidate the metabolic and physiological effects of external Mo supply to detached leaves of Trifolium repens L. Mo supply with a range from 1 mM to 40 mM depressed the activity of ATPs throughout the entire time course. In the leaves exposed to 1 mM Mo, a continuous decrease in the activity of ATPs was confirmed by Native-PAGE. The APR activity was also declined by Mo treatment. The accumulation of H2O2 and O2 were not significant up to 10 mM Mo, whereas a remarked accumulation was detected under 40 mM Mo supply. The data suggest that an external supply of Mo has an inhibitory effect on sulfate assimilation, and induces oxidative stress only at an extremely high concentration.

The preventive effects of sodium molybdate on the acute toxicity of lead were studied by investigating tissue accumulation of lead, changes of nerve conduction velocity and concentrations of metabolites related to function of sciatic nerve in rats treated with lead, sodium molybdate and both, respectively. In lead-intoxicated rat, the conduction velocity, myo-inositol concentration and Na+/K+ ATPase activity of sciatic nerve were decreased by about 33 %, 48 % and 58 %, respectively. However, sodium molybdate treatment significantly normalized the conduction velocity, Na+/K+ ATPase activity and myo-inositol concentration of sciatic nerve in lead-intoxicated rat. Also, sodium molybdate treatment decreased the contents of lead in blood and sciatic nerve through promotion of urinary excretion of lead. But sodium molybdate treatment did not affect the glucose concentration in sciatic nerve. These results suggest that sodium molybdate prevented peripheral neuropathy not only by reducing lead contents in sciatic nerve and blood, but also by enhancing Na+/K+ ATPase activity in sciatic nerve.