A Model for Optimal Treatment of Cassava Wastewater Using Anaerobic Baffled Reactor

The major components of the effluents from cassava processing industries are cyanide and starch. However it is suspected that cyanide inhibits the treatment of cassava wastewater. The experimental data were successfully fitted to a polynomial model which was used to optimize the treatment processes at a laboratory scale. The Monod and Michealis-menten models for cassava wastewater treatment was successfully calibrated and validated in an ABR system. For Michealis-Menten model, the maximum substrate utilization rate is estimated in the range: 2866.88 to 1432.84 mgl-1 and for Monod’s model, it is estimated in the range: 493 to 1242 mgl-1, which is more realistic, hence validating the empirical model as more accurate than the former, which is theoretical. The result revealed that the inhibitor constant decreased from 9.9989 to 1.6101mgl-1 as the number of baffles increased from 3 to 10. To reach a maximum COD removal efficiency of 99%, it was found that the aspect ratio of 10, 20 baffles, cyanide inhibition constant of 30 mg/l and influent flow rate of 0.8 l/min, are the required optimum operating conditions of the anaerobic baffled reactors.

Cyanide degradation kinetics during anaerobic co-digestion of cassava pulp with pig manure

Anaerobic co-digestion of cassava pulp (CP) and pig manure (PM) under cyanide inhibition conditions was investigated and modeled. Batch experiments were performed with initial cyanide concentrations ranging from 1.5 to 10 mg/L. Cyanide acclimatized sludge from an anaerobic co-digester treating cyanide-containing CP and PM was used as the seed sludge (inoculum). Cyanide degradation during anaerobic digestion consisted of an initial lag phase, followed by a cyanide degradation phase. After a short sludge acclimatization period of less than 3 days, the anaerobic sludge was able to degrade cyanide, indicating that the sludge inhibition due to cyanide was reversible. Cyanide degradation during anaerobic co-digestion of CP and PM followed the first-order kinetics with a rate constant of 0.094 d−1. Gas evolution during batch anaerobic degradation was modeled using the modified Monod-type kinetics to incorporate cyanide inhibition. The model predicted results yielded a satisfactory fit with the experimental data.

Azide inhibition of urate oxidase

The inhibition of urate oxidase (UOX) by azide was investigated by X-ray diffraction techniques and compared with cyanide inhibition. Two well characterized sites for reagents are present in the enzyme: the dioxygen site and the substrate-binding site. To examine the selectivity of these sites towards azide inhibition, several crystallization conditions were developed. UOX was co-crystallized with azide (N3) in the presence or absence of either uric acid (UA, the natural substrate) or 8-azaxanthine (8AZA, a competitive inhibitor). In a second set of experiments, previously grown orthorhombic crystals of the UOX–UA or UOX–8AZA complexes were soaked in sodium azide solutions. In a third set of experiments, orthorhombic crystals of UOX with the exchangeable ligand 8-nitroxanthine (8NXN) were soaked in a solution containing uric acid and azide simultaneously (competitive soaking). In all assays, the soaking periods were either short (a few hours) or long (one or two months). These different experimental conditions showed that one or other of the sites, or the two sites together, could be inhibited. This also demonstrated that azide not only competes with dioxygen as cyanide does but also competes with the substrate for its enzymatic site. A model in agreement with experimental data would be an azide in equilibrium between two sites, kinetically in favour of the dioxygen site and thermodynamically in favour of the substrate-binding site.

Intracellular Na+ and metabolic modulation of Na/K pump and excitability in the rat suprachiasmatic nucleus neurons

Na/K pump activity and metabolic rate are both higher during the day in the suprachiasmatic nucleus (SCN) that houses the circadian clock. Here we investigated the role of intracellular Na+ and energy metabolism in regulating Na/K pump activity and neuronal excitability. Removal of extracellular K+ to block the Na/K pump excited SCN neurons to fire at higher rates and return to normal K+ to reactivate the pump produced rebound hyperpolarization to inhibit firing. In the presence of tetrodotoxin to block the action potentials, both zero K+-induced depolarization and rebound hyperpolarization were blocked by the cardiac glycoside strophanthidin. Ratiometric Na+ imaging with a Na+-sensitive fluorescent dye indicated saturating accumulation of intracellular Na+ in response to pump blockade with zero K+. The Na+ ionophore monensin also induced Na+ loading and hyperpolarized the membrane potential, with the hyperpolarizing effect of monensin abolished in zero Na+ or by pump blockade. Conversely, Na+ depletion with Na+-free pipette solution depolarized membrane potential but retained residual Na/K pump activity. Cyanide inhibition of oxidative phosphorylation blocked the Na/K pump to depolarize resting potential and increase spontaneous firing in most cells, and to raise intracellular Na+ levels in all cells. Nonetheless, the Na/K pump was incompletely blocked by cyanide but completely blocked by iodoacetate to inhibit glycolysis, indicating the involvement of both oxidative phosphorylation and glycolysis in fueling the Na/K pump. Together, the results indicate the importance of intracellular Na+ and energy metabolism in regulating Na/K pump activity as well as neuronal excitability in the SCN neurons.