THE EFFECT OF ASCORBATE AND UBIQUINONE SUPPLEMENTATION ON PLASMA AND CSF TOTAL ANTIOXIDANT CAPACITY

Citation
K. Lonnrot et al., THE EFFECT OF ASCORBATE AND UBIQUINONE SUPPLEMENTATION ON PLASMA AND CSF TOTAL ANTIOXIDANT CAPACITY, Free radical biology & medicine, 21(2), 1996, pp. 211-217
Citations number
36
Categorie Soggetti
Biology
ISSN journal
08915849
Volume
21
Issue
2
Year of publication
1996
Pages
211 - 217
Database
ISI
SICI code
0891-5849(1996)21:2<211:TEOAAU>2.0.ZU;2-N
Abstract
Free radicals are thought to be involved in the onset of neuronal dist urbances such as Alzheimer's disease, Parkinson's disease, and neurona l ceroid lipofuscinosis. It is also assumed that they play a role in c erebral injury caused by ischemia or trauma. Plasma and cerebrospinal fluid (CSF), Total (peroxyl) Radical-trapping Antioxidant Parameter (T RAP), and the known antioxidant components of TRAP, for instance, asco rbic acid, uric acid, protein sulfhydryl groups, tocopherol, and ubiqu inol were analyzed and the remaining unidentified fragment was calcula ted in five healthy volunteers before and after 4 weeks of ascorbate a nd ubiquinone (Q-10) supplementation. In CSF, TRAP was significantly l ower than in plasma. The major contributor to plasma's antioxidant cap acity was uric acid (UA), whereas in CSF it was ascorbic acid (AA). In CSF, AA concentrations were four times higher than in plasma. Oral su pplementation of AA (500 mg/d first 2 weeks, 1,000 mg/d following 2 we eks) and Q-10 (100 mg/d first 2 weeks, 300 mg/d following 2 weeks) ind uced a significant increase in plasma AA and Q-10. Surprisingly, in sp ite of the high lipophilicity of Q-10, its concentration did not chang e in CSF. The supplementation of AA increased its concentration in CSF by 28% (p < .05). However, the increase in AA did not result in an in crease in CSF TRAP. This indicates that AA had lost one-third of its r adical trapping capacity as compared to that in plasma. The facts that AA is the highest contributor to CSF TRAP and its effect on TRAP is c oncentration dependent could indicate that the peroxyl radical-trappin g capacity of CSF is buffered by AA.