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Reactive oxygen-mediated apoptosis

Colquhoun and Schumacher [98] have shown that y-linolcnic acid and eicosapentaenoic acid, which inhibit Walker tumor growth in vivo, decreased proliferation and apoptotic index in these cells. Development of apoptosis was characterized by the enhancement of the formation of reactive oxygen species and products of lipid peroxidation and was accompanied by a decrease in the activities of mitochondrial complexes I, III, and IV, and the release of cytochrome c and caspase 3-like activation of DNA fragmentation. Earlier, a similar apoptotic mechanism of antitumor activity has been shown for the flavonoid quercetin [99], Kamp et al. [100] suggested that the asbestos-induced apoptosis in alveolar epithelial cells was mediated by iron-derived oxygen species, although authors did not hypothesize about the nature of these species (hydroxyl radicals, hydrogen peroxide, or iron complexes ). [Pg.756]

Ko, S., Kwok, T.T., Eung, K.P., Choy, Y.M., Lee, C.Y., and Kong, S.K., 2000, Slow rise of Ca2-l- and slow release of reactive oxygen spedes are two cross-talked events important in tumour necrosis factor-alpha-mediated apoptosis. Free Radio. Res. 33 295-304. [Pg.145]

Reactive oxygen species (ROS) are a common mediator of apoptosis. Induction of apoptosis by bile acids appears to be caused, at least in part, by oxidative stress and consequent DNA damage. Unrepaired DNA damage can trigger apoptosis. Table 3.3 lists studies indicating that bile acids induce production of ROS and reactive nitrogen species (RNS) in cells of the GI tract. Table 3.4... [Pg.51]

Kluza, J., Mazinghien, R., Degardin, K., Lansiaux, A. and Badly, C. 2005. Induction of apoptosis by the plant alkaloid sampangine in human HL-60 leukemia cells is mediated by reactive oxygen species. European Journal of Pharmacology, 525(1-3) 32 0. [Pg.261]

Exposure to cigarette smoke increases apoptosis in the rat gastric mucosa through a reactive oxygen species-mediated and p53-independent pathway. Free Radic Biol Med 2000 28(7) 1125-1131. [Pg.351]

Jung EM, Lim JH, Lee TJ, Park JW, Choi KS, Kwon TK. 2005. Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5 (DR5). [Pg.390]

Nikolova S., Lee Y. S., Lee Y. S., and Kim J. A. (2005). Racl-NADPH oxidase-regulated generation of reactive oxygen species mediates glutamate-induced apoptosis in SH-S Y5 Y human neuroblastoma cells, free Radic. Res. 39 1295-1304. [Pg.158]

Bergamo, P., Luongo, D., and Rossi, M., Conjugated linoleic acid — mediated apoptosis in Jurkat T cells involves the production of reactive oxygen species, Cell. Physiol. Biochem., 14, 57, 2004. [Pg.339]

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]


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See also in sourсe #XX -- [ Pg.311 ]




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