[An in vitro study of the effect of sodium selenite on telomere length and telomerase activity of bone marrow stromal cells in aged rats]

Background and Aim: the number and potential of proliferation and differentiation of bone marrow mesenchymal stromal cells decreases with age. These changes reduce efficacy of autologous transplantation in old people. The purpose of this study was to evaluate the effect of sodium selenite on telomere length and telomerase activity of bone marrow stromal cells [BMSCs] in aged rats

Material and Methods: the BMSCs collected from aged male rats were cultured and treated with different concentrations of sodium selenite for 72 h. We evaluated the effect of sodium selenite on the proliferation potential of these cells using trypan blue exclusion test. Then, we evaluated the efficacy of the effective concentration of sodium selenite on telomerase activity, telomere length and the related telomerase gene expression. Telomerase activity was assessed byPCR-ELSA method and telomere length, and its related gene expression was assessed by the real time PCR technique

Results: use of sodium selenite at the concentration of 100nM led to significant increase in the proliferation of BMSCs and decreased telomere length in the aged rats compared to the control group, although the difference was not significant. Telomerase activity and the related telomerase gene expression did not show any change

Conclusion: sodium selenite improved proliferation of BMSCs of the aged rats

G360t polymorphism in the APO AIV gene and its association with combined HDL/LDL-cholesterol phenotype: Tehran lipid and glucose study

Identifying genetic polymorphisms as risk factors for complex diseases can facilitate their prevention, diagnosis, and prognosis. The purpose of this study is to assess the association between Apo AIV polymorphism and lipid factors based on high density lipoprotein cholesterol [HDL-C] levels in a population of the Tehran Lipid and Glucose Study [TLGS]. A total of 181 elderly TLGS subjects with Combined HDLC/low density lipoprotein-Cholesterol [LDL-C] phenotype were investigated. The distributions of a polymorphic site in the apolipoprotein gene APO AIV and its relationship with total cholesterol, LDL-C, HDL-C, and triglycerides were investigated in subjects with LDL-C> 121 mg/dL and HDL-C< 40 mg/dL [case group] and those with LDL-C< 90 mg/dL and HDL-C> 50 [controls]. All the variables studied in the case and control groups were statistically different. At the APO AIV locus the G360T polymorphism at codon 360 showed a significant impact on total cholesterol [G: 211 +/- 1.16 vs, T: 228 +/- 1.20 mg/dL p 0.038] concentration in the case group and on Apo CIII [G: 157 +/- 66.9 vs, T: 83.18 +/- 17.1 mg/dL p <0001] level in the controls. These associations remained after adjustment for age, sex and smoking [P values: P Chol: 0.028 and P Apo CIII: 0.021]. Difference in the apolipoprotein AIV [G360T] polymorphism in the two groups with the combined HDL/LDL-C phenotype indicates that this phenotype can be a selective phenotype for genetic analysis in this field

[ role of 6-aminonicotinamide in the resistance of peritoneal macrophages against Leishmania major infection in BALB/c mouse]

The objective of this study was to investigate the relationship between glucose-6-phosphate dehydrogenase inhibition in macrophages treated with 6-Aminonicotinamide, the amount of nitric oxide [NO] production and the resistance of infected macrophages against Leishmania major infection. Peritoneal macrophages of BALB/c mice were isolated and treated with different concentrations [1.25, 2.5, 5, 10 mM] of 6-aminonicotinamide. After 24 hours, the viability of treated macrophages was measured by MTT assay at 540 nm. G6PD activity was measured in the cell extracts 24 hours later. Macrophages were then infected with leishmanial amastigotes and after 18 hours NO production was determined using Griess-reagent. In order to study the inhibition of macrophage activity, 5 mM concentration of 6-AN was used and number of leishmanial amastigotes was recorded in these cells from day 1 to7. Different concentrations of 6-AN were shown to cause a significant increase in cell death and decrease in G6PD activity and NO production in macrophages. Also, the number of amastigotes in macrophages was increased significantly [p < 0.05]. He concentration of 6-aminonicotinamide and G6PD activity affect the viability of BALB/c mice peritoneal macrophages through production of NO. Inhibition of G6PD activity leads to decreased leishmani-cidal activity of mouse peritoneal macrophages