Central nervous system free radicals

Youdim, K.A., Shukitt-Hale, B. loseph, l.A. (2004). Flavonoids and the brain interactions at the blood-brain barrier and their physiological effects on the central nervous system. Free Radical Biology Medicine, 37,1683-1693. 

Braughler, J.M, and Hall, E.D. (1989). Central nervous system trauma and stroke. I. Biochemical considerations for oxygen radical formation and lipid peroxidation. Free Rad. Biol. Med. 6, 289-301. 

Sadrzadeh, S.M.H. and Eaton, J.W. (1992). Hemt obin-induced oxidant damage to the central nervous system. In Free Radical Mechanisms of Tissue Injury (eds. M.T. Moslen and C.V. Smith) pp. 24—32. CRC Press, Boca Baton. 

Demopoulos, H.B., Flam, E.S., Peitronigro, D.D. and Seligman, M. (1980). The free radical pathology and the micro-circulation in the major central nervous system disorders. Acta Physiol. Scand. 492, 91-119. 

Sparaco M, Gaeta LM, Tozzi G, Bertini E, Pastore A, Simonati A, Santorelli FM, Piemonte F. 2006. Protein glutathionylation in human central nervous system Potential role in redox regulation of neuronal defense against free radicals. J Neurosci Res 83 256-263. 

The 3-aminomethyl-l-pyrrolidinyl radical, which was considered to be bioiso-steric to piperazine [91], also produced highly active quinolones, which were however also found not to be tolerated. In trovafloxacin 16 [92], the 3-aminomethyl-l-pyrrolidinyl radical is integrated into a bicydic amine structural unit with a free amino group [(la,5a,6a)-6-amino-3-azabicyclo[3.1.0]hexane]. A correlation probably exists between the increased central nervous system (CNS) side effects obtained with this quinolone [93] and the 2,4-difluorophenyl radical in the 1-posi-tion. Severe hepatic intolerance reactions finally resulted in major restrictions on its use, which was then limited in the USA to severe clinical infections [68]. 

Free radicals in central nervous system injury... 

Floyd, R.A. (1997). Protective action of nitrone-based free radical traps against oxidative damage to the central nervous system. Adv. Pharmacol. 38 361-78. 

Orr (43) used dimethyl sulfoxide as a free radical sink to inhibit the effect of Cu and ascorbic acid on catalase and 8-glucuronidase as well as the degradation of hyaluronic acid. The formation of a radical from ascorbic acid and Cu in water was detected by EPR (44). Based on an EPR spectroscopic study of ascorbic acid during oxidation of methyl-arachidonate-enriched liposomes, ascorbic acid may be important in preventing free radical damage in the central nervous system (45). 

Harman D. Hendricks, S, Eddy DE. Seibold J. Free radical theory of aging effect of dietary fat on central nervous system function.. 1 Am Gerialr Soc 1976 24 301-307. 

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