Spectroscopic Signature of Red Blood Cells in a D-Galactose-Induced Accelerated Aging Model.

This work presents a semi-quantitative spectroscopic approach, including FTIR-ATR and Raman spectroscopies, for the biochemical analysis of red blood cells (RBCs) supported by the biochemical, morphological and rheological reference techniques. This multi-modal approach provided the description of the RBC alterations at the molecular level in a model of accelerated aging induced by administration of D-galactose (D-gal), in comparison to natural aging. Such an approach allowed to conclude that most age-related biochemical RBC membrane changes (a decrease in lipid unsaturation and the level of phospholipids, or an increase in acyl chain shortening) as well as alterations in the morphological parameters and RBC deformability are well reflected in the D-gal model of accelerated aging. Similarly, as in natural aging, a decrease in LDL level in blood plasma and no changes in the fraction of glucose, creatinine, total cholesterol, HDL, iron, or triglycerides were observed during the course of accelerated aging. Contrary to natural aging, the D-gal model led to an increase in cholesterol esters and the fraction of total esterified lipids in RBC membranes, and evoked significant changes in the secondary structure of the membrane proteins. Moreover, a significant decrease in the phosphorous level of blood plasma was specific for the D-gal model. On the other hand, natural aging induced stronger changes in the secondary structures of the proteins of the RBCs' interior. This work proves that research on the aging mechanism, especially in circulation-related diseases, should employ the D-gal model with caution. Nonetheless, the D-gal model enables to imitate age-related rheological alterations in RBCs, although they are partially derived from different changes observed in the RBC membrane at the molecular level.

[Development of osteoporosis in prematurely aging OXYS rats].

The early osteoporosis in OXYS rats is the presentation of accelerated senescence and earlier positioned as senile. The present study shows the changes in metabolism detected in OXYS rats in the postnatal period. They lead to the development of osteoporosis in future and may underlie the formation of reduced peak bone mass. 90 males OXYS rats used in this study aged from 10 days to 24 months and the control group consisted of 90 male Wistar rats of the matched ages. No differences in BMD in OXYS and Wistar rats at the age of 10 days and 3 months was revealed. At the age of 10 days the OXYS rats showed the higher by 40% activity of ALH--the marker of osteoblast activity--than Wistar rats; but at the age of 3 months ALH activity in OXYS was lower than in Wistar rats. The peak bone mass and BMD in Wistar rats is formed by the age of 12 months, in OXYS rats already by 6, but it did not reach the level of Wistar. The content of Ca in the blood and bone tissue changes similarly: no difference in young age, but reduces in OXYS rats after 6 months to the background of enhanced Ca excretion in urine. However, changing the mineral composition of bone in OXYS rats did not affect the mechanical strength: the absolute strength of the long bones in OXYS at 12 months was lower than that of Wistar, but at the expense of decrease by 1,7 times the cross-sectional area. We suppose that genetically determined hypoplasia of the bone tissue in OXYS rats is the starts of pathogenetic mechanisms of idiopathic osteoporosis.

Protective role of salidroside against aging in a mouse model induced by D-galactose.

OBJECTIVE: To investigate the protective effects of putative AGEs (advanced glycation endproducts) inhibitor salidroside against aging in an accelerated mouse aging model induced by D-galactose. METHODS: A group of 5-month-old C57BL/6J mice were treated daily with D-galactose, D-galactose combined with salidroside, salidroside alone, and control buffer for 8 weeks. At the end of the treatment, serum AGEs levels, neurological activities, expression of glial fibrillary acidic protein (GFAP) and neurotrophin-3 (NT-3) in the cerebral cortex, as well as lymphocyte proliferation and IL-2 production were determined. RESULTS: D-galactose induced mouse aging model was developed as described before. As expected, salidroside blocked D-galactose induced increase of serum AGEs levels. It also reversed D-galactose induced aging effects in neural and immune system, as evidenced by improving motor activity, increasing memory latency time, and enhancing lymphocyte mitogenesis and interleukin-2 (IL-2) production. Furthermore, elevated expression of GFAP and NT-3 in the aged model mice was also reduced upon salidroside treatment. CONCLUSION: Salidroside inhibits AGEs formation in vivo, which at least partially contributes to its anti-aging effect in D-galactose induced aging model.