The aim of the present study was to assess the ABO blood group polymorphism association with prostate, bladder and kidney cancer, and longevity. The following data groups were analyzed: Prostate cancer (n=2,200), bladder cancer (n=1,530), renal cell cancer (n=2,650), oldest‑old (n=166) and blood donors (n=994) groups. The data on the ABO blood type frequency and odds ratio in prostate cancer patients revealed a significantly higher blood group B frequency (P<0.05); the pooled men and women, separate men bladder cancer risk was significantly associated with the blood group B (P<0.04); however, no such association was identified in the female patients. The blood group O was observed to have a significantly decreased risk of bladder cancer for females (P<0.05). No significance for the ABO blood group type in the studied kidney cancer patients was identified. A comparison of the oldest‑old and blood donor groups revealed that blood group A was significantly more frequent and blood type B was significantly rarer in the oldest‑olds (P<0.05). The results of the present study indicated that blood type B was associated with the risk of prostate and bladder cancer, and could be evaluated as a determinant in the negative assocation with longevity. Blood types O and A may be positive factors for increasing the oldest‑old age likelihood. The clustering analysis by the ABO type frequency demonstrated that the oldest‑olds comprised a separate cluster of the studied groups.

The aim of the study was to assess the effect of vitamin D-binding protein (DBP) polymorphism on coronary artery disease (CAD). DBP phenotypes were identified in the groups: control (n=306), men suffering from CAD (n=154), and long-lived individuals (n=108). Isoelectric focusing of DBP phenotypes in serum was performed on polyacrylamide gel. Distribution of DBP phenotypes in the study groups was found to be in Hardy-Weinberg equilibrium. Gc1s-1s phenotype and Gc1s allele frequency in CAD groups were significantly higher than in control, and Gc1s allele frequency was found significantly more often in CAD compared with long-lived group (p<0.05). The Gc2 allele frequency in control was higher as compared with Gc2 frequency in CAD group (p<0.05). The Gc2-2 phenotype was more frequent in long-lived survivors than in the CAD group (p<0.05). It was found that the Gc1s allele significantly increased the risk of CAD with the odds ratio (OR) equal to 1.45 (p<0.02) and showed Gc2 to be related with a decreased risk of CAD (OR = 0.69;p<0.03). Authors review the role of DBP in resistance to atherosclerosis and cancer as the main longevity determinants.

The study aim was to investigate the effect of dichloroacetate (DCA) on thymus and the thymocyte cycle in rats. Wistar male gonad-intact and castrated rats (4–5 weeks) were investigated in the following groups: (1) control; (2) treated with DCA; and (3) treated with the DCA and sodium valproate (NaVP) combination. Rats were treated for 4 weeks with DCA 200 mg/kg/day alone and 300 mg/kg/day of NaVP plus 200 mg/kg/day of DCA (every second week, beginning with NaVP). After the experiment, the thymus was weighted, and the thymus lobe was taken for thymocyte flow cytometry. In gonad-intact rats, the thymus weight of the control was higher than in rats treated with DCA ( P <0.001) or with the NaVP–DCA combination ( P <0.04); a comparison of thymus weight between DCA- and NaVP–DCA-treated groups revealed a higher thymus weight loss in the DCA-treated group ( P <0.03). Flow cytometry shows that DCA treatment increased the percentage of cells in the G₂–M phase ( P <0.03) and reduced in G₁–G₀( P <0.02). The DCA treatment effect was determined only in gonad-intact but not in castrated rats. The authors discuss the possible DCA and NaVP interaction mechanisms.

Sodium-dependent Cl⁻/HCO3-exchanger acts as a chloride (Cl⁻) efflux in lymphocytes. Its functional characterization had been described when Cl⁻efflux was measured upon substituting extracellular sodium (Na⁺) by N-methyl-D-glucamine (NMDG). For Na⁺and Cl⁻substitution, we have used D-mannitol or NMDG. Thymocytes of male Wistar rats aged 7–9 weeks were used and intracellular Cl⁻was measured by spectrofluorimetry using MQAE dye in bicarbonate buffers. Chloride efflux was measured in a Cl⁻-free buffer (Cl⁻substituted with isethionate acid) and in Na⁺and Cl⁻-free buffer with D-mannitol or with NMDG. The data have shown that Cl⁻efflux is mediated in the absence of Na⁺in a solution containing D-mannitol and is inhibited by H₂DIDS. Mathematical modelling has shown that Cl⁻efflux mathematical model parameters (relative membrane permeability, relative rate of exchanger transition, and exchanger efficacy) were the same in control and in the medium in which Na⁺had been substituted by D-mannitol. The net Cl⁻efflux was completely blocked in the NMDG buffer. The same blockage of Cl⁻efflux was caused by H₂DIDS. The study results allow concluding that Na⁺is not required for Cl⁻efflux via Cl⁻/HCO3-exchanger. NMDG in buffers cannot be used for substituting Na⁺because NMDG inhibits the exchanger.