[Investigating the synergic effect of Bee venom and aspirin on inhibition of glycation in diabetic conditions]

Background: Diabetes is one of the most common endocrine disorders. In this disease due to increased blood glucose levels, protein glycation increases. Protein glycation in diabetes leads to irreparable consequences. The aim of this study was to investigate the synergic effect of Bee venom and aspirin on human hemoglobin glycation in the presence of glucose.

Materials and Methods: In this experimental study, hemoglobin [10 mg/ml] was incubated in the presence and absence of glucose [40 mM], aspirin [2.5 mM] and Bee venom [in different concentrations of 10, 20 and 40 µg/ml] for 5 weeks. Amount of hemoglobin glycation was evaluated via investigation of changes in soret band, amount of hemoglobin heme degradation and alteration in secondary structure of protein using UV-visible spectroscopy, fluorometry and Circular Dichroism Spectropolarimetry methods. The data were analyzed using InStat 3 software and statistical tests including one way variance analysis and Tukey test. P values less than 0.05 were considered significant.

Results: Hemoglobin incubation in the presence of glucose led to reduction of soret band absorption, degradation of heme and increment of beta sheet value in secondary structure of hemoglobin. Simultaneous presence of Bee venom and aspirin reduced the rate of heme degradation [p< 0.001] up to 36%, and the beta sheet formation up to 54% [p< 0.001]. Also, the amount of structural alteration and hemoglobin glycation significantly decreased.

Conclusion: Bee venom and aspirin have significant antiglycation properties and simultaneous use of them can decrease protein glycation.

effects of extending of co-planarity in a series of structurally relative polypyridyl palladium[II] complexes on DNA-binding and cytotoxicity properties

In depth interaction studies between calf thymus deoxyribonucleic acid [CT-DNA] and a series of four structurally relative palladium[II] complexes [Pd[en][HB]][NO[3]][2] [a-d], where en is ethylenediamine and heterocyclic base [HB] is 2, 2›-bipyridine [bpy, a]; 1, 10-phenanthroline [phen, b]; dipyridoquinoxaline [dpq, c] and dipyridophenazine [dppz, d] [Figure 1], were performed. These studies have been investigated by utilizing the electronic absorption spectroscopy, fluorescence spectra and ethidium bromide [EBr] displacement and gel filtration techniques. a-d complexes cooperatively bind and denature the DNA at low concentrations. Their concentration at midpoint of transition, L1/2, follows the order a >> b > c > d. Also the g, the number of binding sites per 1000 nucleotides, follows the order a >> b c > d. EBr and Scatchard experiments for a-d complexes suggest efficient intercalative binding affinity to CT-DNA giving the order: d > c > b > a. Several binding and thermodynamic parameters are also described. The biological activity of these cationic and water soluble palladium complexes were tested against chronic myelogenous leukemia cell line, K562. b, c and d complexes show cytotoxic concentration [Cc[50]] values much lower than cisplatin