Promotion of whole blood rheology after vitamin C supplementation: focus on red blood cells 1.

Hemorheological properties represent significant contributors in the pathogenesis of cardiovascular diseases. As plasma vitamin C is inversely associated with blood viscosity in humans, we aimed to characterize the effect of vitamin C supplementation on hemorheology with an emphasis on erythrocyte functions. Twenty young healthy volunteers were asked to take vitamin C (1000 mg per day) for 3 weeks. We observed beneficial effect of intervention on multiple hemorheological parameters: whole blood viscosity in the range of medium to high shear rates, Casson yield stress, complex viscosity, and storage and loss moduli. As erythrocyte properties play a significant role in hemorheology, we characterized their deformability, nitric oxide production, and sodium pump activity in erythrocyte membranes. We can conclude that observed promotion in whole blood rheology may be consequence of improved erythrocyte functionality as concerns their ability to pass through narrow capillaries of the microcirculation, nitric oxide production, and sodium pump activity. Parameters reflecting oxidative stress and antioxidant status in plasma were not affected by our intervention. As improvement in hemorheology may play an important role in cardioprotection, it would be challenging to investigate the vitamin C supplementation to patients suffering from microcirculatory disturbances and worsened organ perfusion in the case of cardiovascular diseases.

Multiple sclerosis: evaluation of purine nucleotide metabolism in central nervous system in association with serum levels of selected fat-soluble antioxidants.

In the pathogenesis of demyelinating diseases including multiple sclerosis (MS) an important role is played by oxidative stress. Increased energy requirements during remyelination of axons and mitochondria failure is one of the causes of axonal degeneration and disability in MS. In this context, we analyzed to what extent the increase in purine catabolism is associated with selected blood lipophilic antioxidants and if there is any association with alterations in serum levels of coenzyme Q10. Blood serum and cerebrospinal fluid (CSF) samples from 42 patients with diagnosed MS and 34 noninflammatory neurologic patients (control group) were analyzed. Compared to control group, MS patients had significantly elevated values of all purine nucleotide metabolites, except adenosine. Serum lipophilic antioxidants γ -tocopherol, ß -carotene, and coenzyme Q10 for the vast majority of MS patients were deficient or moved within the border of lower physiological values. Serum levels of TBARS, marker of lipid peroxidation, were increased by 81% in the MS patients. The results indicate that the deficit of lipophilic antioxidants in blood of MS patients may have a negative impact on bioenergetics of reparative remyelinating processes and promote neurodegeneration.

Uric acid and allantoin levels in Down syndrome: antioxidant and oxidative stress mechanisms?

BACKGROUND: Down syndrome (DS) is a chromosomal abnormality (trisomy 21) leading to mental retardation, to the characteristic change of individual's phenotype and to the pathological features of Alzheimer disease. Patients with DS have elevated ratio of superoxide dismutase to (catalase plus glutathione peroxidase) with respect to controls in all age categories suggesting that oxidative imbalance contributes to the clinical manifestation of accelerated aging. RESULTS: We report that persons with DS have elevated uric acid levels compared with controls, 348.56+/-22.78 versus 284.00+/-20.86 micromol/l (p=0.018). The levels of hypoxanthine and xanthine in DS children (6.35+/-0.31 and 1.02+/-0.23 micromol/l) were significantly lower than in controls (7.83+/-0.59 and 2.43+/-0.66 micromol/l). This result suggests increased conversion of hypoxanthine and xanthine to uric acid with subsequent free radical-dependent oxidation of uric acid to allantoin, mechanisms potentiated by the oxidative stress in DS. Allantoin is a nonenzymatic oxidative product of uric acid in human. In DS individuals, the levels of allantoin were significantly higher than those in healthy controls (18.58+/-2.27 and 14.07+/-1.07 micromol/l, respectively, p=0.03). CONCLUSIONS: Our data supported the presumption of increased oxidative stress in DS.