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Cancer oxygen species role

G. Waris et al., Reactive oxygen species Role in the development of cancer and various chronic conditions. J. Carcinog. 5, 14 (2006)... [Pg.438]

Marsh, J. P., and Mossman, B. L (1991) Role of asbestos and active oxygen species in. ictiva-rion. and expression of ornirhinc decarboxylase in hamster tracheal epithelial cells. Cancer Ra. 51(1), 167-173. [Pg.339]

Wiseman H, Halliwell B Damage to DNA by reactive oxygen and nitrogen species role In Inflammatory disease and progression to cancer. BlochemJ 1996 313 17. [Pg.497]

Cancer is one of the diseases in which a role has been implicated (see Table 13.1) for free radicals. Comprehensive accounts of the involvement of reactive oxygen species in human diseases may be found in Halliwell and Gutteridge (1989), Aruoma (1993) and in Cheeseman and Slater (1993). [Pg.199]

D. Washo-Stultz, C. L. Crowley-Weber, K. Dvorakova, C. Bernstein, H. Bernstein, K. Kunke, C. N. Waltmire, H. Garewal and C. M. Payne, Role of mitochondrial complexes I and II, reactive oxygen species and arachidonic acid metabolism in deoxycholate-induced apoptosis. Cancer Lett., 2002, 177(2), 129. [Pg.63]

Fenton-like reactions play an important role in a variety of catalytic and biological processes. In biology these reactions are believed to be the main source of reactive oxygen species (ROS) in the cell causing a variety of diseases, eg cancer, arteriosclerosis, essential hypertension, Alzheimer s disease, amyloidosis, osteoarthritis [9],... [Pg.362]

Free radicals may play a role in diseases and accelerate aging. In the course of everyday life, reactive oxygen species are encountered in the environment and produced in the body. These compounds break down into short-lived hydroxyl radicals, which can react with the body s proteins and DNA. The resulting damage accumulates and may result in heart disease, cancer, and premature aging. [Pg.134]

MK-2 induced apoptosis to a much lesser extent than GG. The major difference between MK-2 and GG is the u,(J>-unsaluraled ketone structure present in MK-2 but not in GG. The induction of cell death by MK-2 or GG was not coupled with radical generation. It has recently been reported that the induction of apoptosis by MK-4 in human ovary cancer cells is mediated by oxidative stress in mitochondria [70]. Since autophagy plays an important role in reducing mitochondrial damage and reactive oxygen species, there is a possibility that the apoptosis-inducing activity of MK-4 may be derived from the inhibition of autophagy. [Pg.196]

Unbalanced production of reactive oxygen species, first of aU superoxide and hydrogen peroxide, has been postulated as playing a role in the pathogenesis of a number of chnical disorders, such as acute respiratory distress syndrome, ischemia-reperfusion injury, atherosclerosis, neurodegenerative diseases and cancer. As the function of SOD and CAT is the protection against oxidative stress, their apphcation has been proposed in cases where oxidative stress is important in the mechanism of a disease. [Pg.140]

Mates, J. M. and Sanchez-Jimenez, F. M. 2000. Role of reactive oxygen species in apoptosis Implications for cancer therapy. Int. J. Biochem. Cell. Biol. 32 157-70. [Pg.187]


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See also in sourсe #XX -- [ Pg.705 ]




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