Zinc phosphodiesterase (ZiPD) participates in the maturation of tRNA precursors. The roles of metal ions in promoting phosphoryl transfer reaction on zinc phosphodiesterase (ZiPD) activity have not been fully characterized. Therefore, this study investigated the effects of some metal ions on phosphodiesterase activity of Escherichia coli ZiPD as well as the binding site and binding affinity of the metal ions. ZiPD activity was measured by monitoring the rate of hydrolysis of bis-para-nitrophenyl phosphate (bis-pNPP) in the presence of some selected divalent metal ions (Mn2+, Co2+, Mg2+ and Zn2+). The results obtained revealed that Mn2+ at 1 mM activated ZiPD activity by 4-fold with binding affinity score of 1.795. Co2+ at 0.5 mM activated ZiPD activity by 2-fold with binding affinity score of 1.773. Mg2+ at 0.5 mM enhanced the binding affinity of ZiPD for bis-pNPP but did not increase the turnover rate of ZiPD. Zn2+ at 1.5 mM activated ZiPD activity by 2-fold via increased affinity of ZiPD for bis-pNPP. In conclusion, the findings from this study showed that Mn2+ and Zn2+ are the most effective stimulatory ions of ZiPD for bis-pNPP while Zn2+ exerted the highest binding affinity of ZiPD for bis-pNPP.
In an effort at developing new filters and bio-packaging materials with antibacterial properties, nanocomposite fluorescence films of cellulose acetate reinforced with cellulose nanoparticles, methylcellulose nanoparticles, propylcellulose nanoparticles, toluene diisocyanate modified cellulose and cellulose acetate nanoparticles were prepared and characterized. The effects of the nanoparticles on the mechanical, crystallinity and morphology of the nanocomposite films was studied. The sensitivity of bacteria against the new nanocomposite films was experimented. Scanning electron microscopy showed the films to be well dispersed. Modulus increase was directly proportional to nanoparticle loading. Samples with maximum compatibility were cellulose nanoparticles (CNPs) loading of 40% with modulus of 113.3Mpa and toluene diisocyanate modified cellulose nanoparticles (TDI-CNPs) at 20% loading had 146.0Mpa. Others include cellulose acetate nanoparticles (CANPs) at 30% loading with 73.0Mpa; methylcellulose acetate nanoparticles (MCNPs) with 5% loading had a modulus of 87.3Mpa and pure cellulose acetate had 45.0Mpa. The films were applied as filters for the removal of cells of Bacillus; Enterococcus and Micrococcus sp. from the crude bacteriocin, with recoverability of 95.9% based on the bacteriocin produced. The films showed limited antibacterial properties against clinical Pseudomonas sp 1, Pseudomonas sp 2 and Proteus sp. It is concluded that the films showed limited antibacterial properties hence it has antibacterial potentials and capabilities.
The opening of mitochondrial permeability transition (mPT) pore is a well recognized important event in the execution of mitochondrial-mediated apoptosis. Some bioactive compounds induce apoptosis in tumour cells via the induction of mPT pore opening. This study therefore investigated the effect of 3-Para-fluorobenzoyl-propionic acid (3PFBPA), a metabolite of haloperidol on mPT pore, mitochondrial ATPase activity (mATPase), mitochondrial lipid peroxidation (mLPO) and cytochrome c release (CCR). Thirty-two male Wistar rats, were acclimatized for 14 days in clean cages. After 30 days of treatment, they were sacrificed and the liver mitochondria isolated using differential centrifugation. The mPT pore, mATPase, mLPO and CCR were determined by standard methods using a spectrophotometer. The mPT pore opening was induced by 3PFBPA by 1.4, 3.6, 5.6, 6.6 and 7.4 folds, when compared with the control. Also, there was release of cytochrome c and enhancement of mATPase activity by 3PFBPA. The results also show that 3PFBPA reduced lipid peroxidation. However, oral administration of 3PFBPA at 50, 100 and 200 mg/kg did not have any effect on mPT pore opening and mATPase activity when compared with the control but there was inhibition of mLPO. These findings suggested the pharmacological potential of 3PFBPA against the pathological processes related to insufficient apoptosis (based on the in vitro data) and oxidative stress due to its anti-lipidperoxidative effect.