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Oxidative stress hypothesis

Finally, there has been considerable interest in the use of vitamin E to combat EPS, including TD, based on the oxidative-stress hypothesis. A randomized trial of 12 patients receiving supplementary vitamin E and haloperidol versus 12 receiving haloperidol alone revealed that vitamin E had no prophylactic effect on acute drug-induced EPS, nor did it interfere with the antipsychotic s therapeutic efficacy ( 455). [Pg.83]

Markesbery WR. 1997. Oxidative stress hypothesis in Alzheimer s disease. Free Radic Biol Med 23 134-147. [Pg.468]

Fahn, S. and Cohen, G. 1992. The oxidant stress hypothesis in Parkinson s disease Evidence supporting it. Ann. Neurol. 32, 804-812. [Pg.153]

Luchsinger JA, Reitz C, Honig LS, Tang MX, Shea S, Mayeux R (2005) Aggregation of vascular risk factors and risk of incident Alzheimer disease. Neurology 65 545-551 Mark RJ, Lovell MA, Markesbery WR, Uchida K, Mattson MP (1997) A role for 4-hydroxynonenal, an aldehydic product of hpid peroxidation, in disruption of ion homeostasis and neuronal death induced by amyloid beta-peptide. J Neurochem 68 255-264 Markesbery WR (1997) Oxidative stress hypothesis in Alzheimer s disease. Free Radic Biol Med 23 134-147... [Pg.602]

Makin OS, Serpell LC (2005) Structures for amyloid fibrils. FEBS J 272 5950-5961 Malinchik SB, Inouye H, Szumowski KE, Kirschner DA (1998) Structural analysis of Alzheimer s beta(l O) amyloid protofilament assembly of tubular fibrils. Biophys J 74 537-545 Malisauskas M, Zamotin V, Jass J, Noppe W, Dobson CM, Morozova-Roche LA (2003) Amyloid protofilaments from the calcium-binding protein equine lysozyme formation of ring and linear structures depends on pH and metal ion concentration. J Mol Biol 330 879-890 Mantuano E, Veneziano L, Jodice C, ErontaU M (2003) Spinocerebellar ataxia type 6 and episodic ataxia type 2 differences and similarities between two allelic disorders. Cytogenet Genome Res 100 147-153 Markesbery WR(1997) Oxidative stress hypothesis in Alzheimer s disease. Free Radic Biol Med 23 134-147 Marks MS, Seabra MC (2001) The melanosome membrane dynamics in black and white. Nat Rev Mol Cell Biol 2 738-748... [Pg.70]

The cardioprotective role of n-3 PUFA as suggested by epidemiologic and clinical findings seems not to be in line with the prooxidant nature and the oxidant stress hypothesis of atherosclerosis formation. How can this paradox be reconciled ... [Pg.75]

As mentioned earlier, physiological concentrations of carotenoids in vivo are in the micromolar range, mainly because of limited bioavailabiUty. Also, the antioxidant efficiencies of carotenoids after absorption are probably limited. Concentrations before absorption are much higher and can justify possible antioxidant actions in vivo. To test this hypothesis, Vulcain et al. developed an in vitro system of lipid peroxidation in which the oxidative stress is of dietary origin (metmyoglobin from meat) and different types of antioxidants (carotenoids, phenols) are tested. [Pg.179]

Another peculiarity of the study is that the use of a biological system has allowed the authors to hypothesize a possible mechanism of action of the leachate as a mixture, hypothesis that could have been drafted on the basis of the only knowledge derived by chemical analysis. Researchers suggest that leachate inhibits cell proliferation at low doses probably inducing a reversible cell cycle arrest that becomes irreversible at high doses, probably due to leachate-induced oxidative stress. This activity is mainly due to the chemical compounds extracted in the aqueous phase. Similar effects were noticed by previous investigations on other human cells (human peripheral blood lymphocytes and a human breast cancer cell line, MCF-7) [31, 32], supporting the hypothesis that cells that survive the initial insult from leachate constituents maintains the potential to proliferate until the effects on cell metabolism lead to death. [Pg.180]

R. Rodrigo and G. Rivera, Renal damage mediated by oxidative stress a hypothesis of protective effects of red wine. Free Rad. Biol. Med. 33, 409—422 (2002). [Pg.458]

The mechanism responsible for releasing the contents of lysosomes is not yet known. According to one hypothesis (Ollinger and Brunk, 1995), the membranes of lysosomes are damaged during apoptosis induced by oxidative stress, possibly due to diffusion of intracellularly produced hydrogen peroxide into these organelles. Inside the lysosomal apparatus. [Pg.165]

Ghyczy M, Boros M (2001) Electrophilic methyl groups present in the diet ameliorate pathological states induced by reductive and oxidative stress a hypothesis. Br J Nutr 85 409-414 Gilbert BC, Silvester S (1997) EPR studies of the role of copper in bio-organic free radical reactions. Copper-catalyzed oxidations of thiols with peroxides, especially those involving glutathione. Nukleonika 42 307-322... [Pg.40]


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See also in sourсe #XX -- [ Pg.116 ]

See also in sourсe #XX -- [ Pg.323 ]




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