By C. W. Olanow, Peter Jenner, Moussa Youdim
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Additional info for Neurodegeneration and Neuroprotection in Parkinson's Disease (Neuroscience Perspectives)
E & Gores, G. (1991) Hepatology 14, 150-157. A. (1991) Proc. NatlAcad. Sci. USA 88, 3633-3636. L. & Sinet EM. (1991) Brain Res. 552, 198-214. E, Carlson, EJ. & Epstein, CJ. (1990) Stroke 21 (Suppl. III), 80-82. , Sies, H. & Boveris, A. (1979) Physiol. Rev. 59, 527-605. Cochrane, C. (1991) Mol. Aspects Med. 12, 137-147. Cohen, G. (1988) In Oxygen Radicals and Tissue Injury (ed. ), pp. 130-135, FASEB, Bethesda, Maryland. A. L. (1987) FEBS Lett. 223, 284-288. T. M. (1987) Adv. Hum. Genet. 16, 229-297.
1992). However, post-mortem studies may not provide a true indication of antioxidant activi~. First, the post-mortem stability of vitamin C and vitamin E, and the effect of post-mortem delay and freezing have not been studied. Second, the rate of conversion between the oxidized and reduced forms of these vitamins has not been measured and may be considerably increased in the presence of excess free radical formation. Changes in SOD activity in PD have been measured in two recent studies. , 1989).
These concepts are discussed in a later chapter. , 1987). Within the brain, MPTP is oxidized to MPP +, which is actively accumulated by mitochondria where it acts to inhibit mitochondrial respiratory activity at the level of complex I. , 1987). , 1995). These also inhibit complex I and ot-KGDH with potencies even greater than that of MPP +. Schapira and colleagues (1990a) and Mizuno et al. (1989) were the first to show that there was a specific decrease in the activity of complex I in homogenates of substantia nigra from patients with PD.
Neurodegeneration and Neuroprotection in Parkinson's Disease (Neuroscience Perspectives) by C. W. Olanow, Peter Jenner, Moussa Youdim