Study on the host-guest interactions during caffeine encapsulation into zeolite

The objective of this study was to investigate the equilibrium and kinetics behavior, sorption mechanism and host-guest interactions during caffeine (CAF) encapsulation in natural zeolite. The chemical, spectral and morphological properties of the newly obtained drug-carrier system were analyzed. Zeolite surface chemistry and morphology were characterized by determination of pH of zero charge, FT-IR and digital microscopy analyses. Equilibrium and kinetic sorption experiments and modeling were conducted to assess zeolite potential. Satisfactory extend of CAF encapsulation in the zeolite matrix (E 36.4%) was obtained. The probable host-quest interactions include Van der Waals interactions, H-bonds and chemical interactions between CAF functional groups and zeolite silanol groups, as well as parallel intraparticle diffusion of drug molecules in the mesopores of the mineral particles. The analyses of the experimental results indicated that natural zeolite could be successfully applied for encapsulating CAF

Evaluation of the role of glutathione in the lead-induced toxicity in Saccharomyces cerevisiae

The effect of intracellular reduced glutathione (GSH) in the lead stress response of Saccharomyces cerevisiae was investigated. Yeast cells exposed to Pb, for 3 h, lost the cell proliferation capacity (viability) and decreased intracellular GSH level. The Pb-induced loss of cell viability was compared among yeast cells deficient in GSH1 (∆gsh1) or GSH2 (∆gsh2) genes and wild-type (WT) cells. When exposed to Pb, ∆gsh1 and ∆gsh2 cells did not display an increased loss of viability, compared with WT cells. However, the depletion of cellular thiols, including GSH, by treatment of WT cells with iodoacetamide (an alkylating agent, which binds covalently to thiol group), increased the loss of viability in Pb-treated cells. In contrast, GSH enrichment, due to the incubation of WT cells with amino acids mixture constituting GSH (l-glutamic acid, l-cysteine and glycine), reduced the Pb-induced loss of proliferation capacity. The obtained results suggest that intracellular GSH is involved in the defence against the Pb-induced toxicity; however, at physiological concentration, GSH seems not to be sufficient to prevent the Pb-induced loss of cell viability