Shrinking factors of hyperbranched polysaccharide from fungus

The branched structure properties of hyperbranched polysaccharides (TM3a and TM3b), extracted from sclerotia of Pleurotus tuber-regium, were studied by using laser light scattering and viscometry. The configurational shrinking factor (g) and viscometric shrinking factor (g′) of TM3a and TM3b were discussed, where curdlan and pullulan were taken as the linear references for derivation of g and g′. The dependences of g factor, g′ factor, and Flory factor (Φ_branched) on weight average molecular weight (M_w) were established to be g = 1.07 × 10²$M_{\text{w}}^{-0.48\pm 0.09}$, g′ = 3.63 × 10¹$M_{\text{w}}^{-0.43\pm 0.01}$, and Φ_branched = 7.08 × 10²⁰$M_{\text{w}}^{0.39\pm 0.1}$ for TM3a in 0.25 M LiCl/DMSO at 25 °C, when curdlan acted as the linear reference. A power law relationship g′ = 2.71 × 10^?1g^?0.61±0.1 for TM3a was found, and the exponent was approximately same to 0.60 established by Kurata et al. for polystyrene star molecules. The dependence of g factor on M_w for TM3b was found to be g = 1.99 × 10²$M_{\text{w}}^{-0.53\pm 0.02}$, when pullulan was used as the linear reference. On the basis of Zimm–Stockmayer equation for tetrafunctional units, molecular weight of branching unit (M₀) deduced from nonlinear curve fitting of g versus M_w was 8739 ± 564 g/mol and 3961 ± 1245 g/mol for TM3a and TM3b, respectively. The effect of different linear reference curves and polydispersity was discussed. This work gave valuable information on branched structure characterization and insights into the biosynthetic pathways of the hyperbranched polysaccharide from fungus.     

Biological maturity at birth,the course of the subsequent ontogenetic stages and age at menarche

The main aim of the study was to assess the influence of biological maturity at birth on growth processes in the subsequent years and during puberty in girls. The material of this study comes from the outpatient clinic cards and cross-sectional research on girls from the province of Wielkopolska in Poland. It includes data of 527 girls. The influence of perinatal maturity on body weight in the later stages of ontogeny was determined with the use of the Kruskal–Wallis test and the Mann–Whitney U test. In order to determine the relationship between perinatal maturity and age at menarche, the survival analysis module was used.The results show a diverse influence of perinatal maturity on the values of body weight achieved in later years of life. The indicated predictive factors included both birth weight and gestational age. In the examined girls menarche occurred between the 10th year and the 17th year of life $(\overline{X}=12.87$, s = 1.26; Me = 13 years). The comparison showed a significant variation in age at menarche depending on the length of pregnancy (log-rank ${\chi }_2^2=27.068$, p < 0.0001) and birth weight (log-rank ${\chi }_2^2=23.241$, p < 0.0001). There was no variation in maturation of the examined girls conditioned by the occurrence of intra-uterine growth retardation (log-rank ${\chi }_2^2=2.046$, p > 0.05). Remote prognoses as to the postnatal development of preterm-born children and/or children with low birth weight indicate adverse influence of these variables on age at menarche. Perinatal biological maturity of a newborn conditions the course of postnatal development.     

Tocopheramine succinate and tocopheryl succinate: Mechanism of mitochondrial inhibition and superoxide radical production

Tocopherols (TOH) are lipophilic antioxidants which require the phenolic OH group for their redox activity. In contrast, non-redox active esters of α-TOH with succinate (α-TOS) were shown to possess proapoptotic activity in cancer cells. It was suggested that this activity is mediated via mitochondrial inhibition with subsequent ${\text{O}}_2^{\text{<mglyph src="https://sdfestaticassets-us-east-1.sciencedirectassets.com/shared-assets/16/entities/rad"></mglyph>}-}$ production triggering apoptosis and that the modification of the linker between the succinate and the lipophilic chroman may modulate this activity. However, the specific mechanism and the influence of the linker are not clear yet on the level of the mitochondrial respiratory chain. Therefore, this study systematically compared the effects of α-TOH acetate (α-TOA), α-TOS and α-tocopheramine succinate (α-TNS) in cells and submitochondrial particles (SMP). The results showed that not all cancer cell lines are highly sensitive to α-TOS and α-TNS. In HeLa cells α-TNS did more effectively reduce cell viability than α-TOS. The complex I activity of SMP was little affected by α-TNS and α-TOS while the complex II activity was much more inhibited (IC₅₀ = 42 ± 8 μM α-TOS, 106 ± 8 μM α-TNS, respectively) than by α-TOA (IC₅₀ >1000 μM). Also the complex III activity was inhibited by α-TNS (IC₅₀ = 137 ± 6 μM) and α-TOS (IC₅₀ = 315 ± 23 μM). Oxygen consumption of NADH- or succinate-respiring SMP, involving the whole electron transfer machinery, was dose-dependently decreased by α-TOS and α-TNS, but only marginal effects were observed in the presence of α-TOA. In contrast to the similar inhibition pattern of α-TOS and α-TNS, only α-TOS triggered ${\text{O}}_2^{\text{<mglyph src="https://sdfestaticassets-us-east-1.sciencedirectassets.com/shared-assets/16/entities/rad"></mglyph>}-}$ formation in succinate- and NADH-respiring SMP. Inhibitor studies excluded complex I as ${\text{O}}_2^{\text{<mglyph src="https://sdfestaticassets-us-east-1.sciencedirectassets.com/shared-assets/16/entities/rad"></mglyph>}-}$ source and suggested an involvement of complex III in ${\text{O}}_2^{\text{<mglyph src="https://sdfestaticassets-us-east-1.sciencedirectassets.com/shared-assets/16/entities/rad"></mglyph>}-}$ production. In cancer cells only α-TOS was reproducibly able to increase ${\text{O}}_2^{\text{<mglyph src="https://sdfestaticassets-us-east-1.sciencedirectassets.com/shared-assets/16/entities/rad"></mglyph>}-}$ levels above the background level but neither α-TNS nor α-TOA. Furthermore, the stability of α-TNS in liver homogenates was significantly lower than that of α-TOS. In conclusion, this suggests that α-TNS although it has a structure similar to α-TOS is not acting via the same mechanism and that for α-TOS not only complex II but also complex III interactions are involved.