Synthesis, characterization and biological activities of cetirizine analogues

Cetirizine second generation H1-receptor antagonist is an acid metabolite of hydroxyzine. Present work was based on six new analogues of cetirizine having nucleophilic substitution reaction synthetic pathway. The reactions were proceeded by replacing the scaffold on the cetirizine moiety using nucleophilic substitution reaction. The structures of analogues were confirmed using UV, IR,1H NMR and mass spectroscopic techniques. The analogues were tested for the anti-inflammatory activities on cellular immune response. Oxidative burst response of phagocytes after exposure to the analogues was found to exhibit moderate to significant inhibitory activity (23 to <3.1). However, the compounds as MPC and PPC also showed remarkable inhibitory effect on PHA activated T-cells response and may prove to be lead compounds in therapeutic world.

The Effects of Iron Deficiency on Neutrophil/Monocyte Oxidative Burst Response in Children.

Background: Microbial killing killing of by phagocytic cells by iron containing myeloperoxidase pathway is part of the immune system. We aimed to investigate the effects of iron deficiency anemia (IDA) on oxidative burst response of phagocytic cells and understand if the effect is reversible after iron supplementation. Material and methods: There were 57 IDA patients and 31 healthy children as the control group that were aged between 6 months-12 years with similar demographic status. IDA patients were classified according to the severity of their anemia as follows; group 1 (Hb<8 gr/dl), group 2 (Hb≥8 gr/dl and Hb≤10 gr/dl), and group 3 (Hb>10 gr/dl). Neutrophil and monocyte oxidative burst response of each three groups of IDA and control group were compared by flow cytometry. IDA group were given oral iron supplementation (3 mg/kg-Ferrosanol) therapy. On day 15 of iron supplementation therapy neutrophil and monocyte oxidative burst response of each three groups of IDA were rechecked and compared to the control group. In order to minimize the discrepancies observed in functional studies, the oxidative burst index was calculated as the proportion of oxidative burst response in IDA group to the simultaneous oxidative burst response in the control group. Results: The number of infection episodes observed in the last three months was significantly higher in the IDA group (0–13 episodes) than the control group (1–2 episodes) (p=0.05). Neutrophil (p=0.1) and monocyte (p=0.02) oxidative burst responses in IDA group were found to be less than the control group. On day 15 of iron supplementation therapy, these values were observed to increase to the control group’s values. Evaluation of neutophil and monocyte burst indexes at the diagnosis of IDA revealed that the neutrophil burst indexes in the Hb ≤10 gr/dl group (p=0.006), and monocyte burst indexes in the Hb <8 gr/dl group (p=0.01) were significantly low. The initially observed significant differences in oxidative burst responses disappeared at day 15 of iron supplementation therapy in all hemoglobin groups. Conclusion: Correction of the differences in oxidative burst response after iron supplementation therapy implies the fact that IDA might be the reason for changes in neutophil and monocyte burst indexes.