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Apoptosis hydrogen peroxide-induced

Hu Z, Guan W, Wang W, Huang L, Xing H, Zhu Z (2007a) Synthesis of [1-alanine C60 derivative and its protective effect on hydrogen peroxide-induced apoptosis in rat pheochromocytoma cells. Cell Biol Int. 31 798-804. [Pg.18]

Adams RR, Maiato H, Earnshaw WC, Carmena M (2001) Essential roles of Drosophila inner centromere protein (INCENP) and aurora B in histone H3 phosphorylation, metaphase chromosome ahgnment, kinetochore disjunction, chromosome segregation. J Cell Biol 153(4) 865-880 Ahn SH, Cheung WL, Hsu JY, Diaz RL, Smith MM, Alhs CD (2005a) Sterile 20 kinase phospho-rylates histone H2B at serine 10 during hydrogen peroxide-induced apoptosis in S. cerevisiae. Cell 120(l) 25-36... [Pg.329]

At a concentration of 700 pmol/L, hydrogen peroxide induced necrosis of immortalized rat embryo fibroblasts, while at a concentration of 150 pmol/L, it induced apoptosis (Guenal et al., 1997). In primary human diploid fibroblasts, low concentrations (50-100 (.unol/L) of hydrogen peroxide induced a senescence-like state, while higher concentrations (300-400 (imol/L) induced apoptosis (Bladier et al., 1997). Apoptosis was also observed in BHK-21 fibroblasts at hydrogen peroxide concentrations of... [Pg.675]

Wang, R. Xiao, X. Q. Tang, X. C. Huperzine A attenuates hydrogen peroxide-induced apoptosis by regulating expression of apoptosis-related genes in rat PC12 cells. Neuroreport, 2001, 12(12) 2629-2634. [Pg.176]

Whittemore, E.R., Loo, D.T. and Cotman, C.W. (1994) Exposure to hydrogen peroxide induces cell death via apoptosis in cultured rat cortical neurons. NeuroReport 5 1485-1488. [Pg.121]

Jang, J.H. andY.J. Surh. 2001. Protective effects of resveratrol on hydrogen peroxide-induced apoptosis in rat pheochromocytoma (PC12) cells. Mutation Research-Genetic Toxicology and Environmental Mutagenesis 496 181-190. [Pg.78]

While the role of the over activation of PARP-1 in DNA damage-induced necrotic cell death is now widely accepted, its role in apoptosis appears to hugely depend on the experimental conditions such as the cell type and nature of the stimulus. Nonetheless, Valina Dawson s group has shown that PARP activation is required for activation of the mitochondrial route of apoptosis, charaaerized by mitochondrial depolarization, release of AIF ftx>m the mitochondria to the cytosol and caspase-independent, AIF-mediated apoptosis. Notably, these findings are in line with our previous observation that PARP activation mediates mitochondrial alterations during peroxynitrite or hydrogen peroxide-induced necrotic thymocyte death. At the... [Pg.143]

Kanno, S., Shouji, A., Asou, K. and Ishikawa, M. (2003). Effects of naringin on hydrogen peroxide-induced cytotoxicity and apoptosis in P388 cells. Pharmacol Sci. Vol. 92 No. 2 pp. 166-170 ISSN 1347-8613... [Pg.355]

The flavonol quercetin has been the subject of much interest in terms of its beneficial properties against oxidative stress [62] and has been shown to exert a potent protective actions against hydrogen peroxide-induced apoptosis of rat thymocytes [63] and cell death in rat hepatocytes (BL-9) [60], as well as reducing oxidative stress and cell damage in fiver tumor cells induced by AAPH (2,2-azobis(2-aminopropane) dihydrochloride) [64]. Quercetin and another flavonol, kaempferol, as well as catechin and the flavone taxifolin, have been observed to suppress the cytotoxicity of 02 and H2O2 to Chinese hamster V79 cells, as assessed by the ability of the flavonoids to prevent the decrease in the number of cell colonies induced by the oxidants [65]. Furthermore, quercetin has been shown to protect cutaneous tissue-associated cells (human skin fibroblasts, keratinocytes, and endothelial cells) from oxidative injury induced by buthionine sulfoximine (BSO), an inhibitor of GSH synthesis [66]. [Pg.320]

Miyoshi N, Oubrahim H, Chock PB et al. (2006) Age-dependent cell death and the role of ATP in hydrogen peroxide-induced apoptosis and necrosis. Proc Natl AcadSci USA 103(6), 1727-1731. [Pg.96]

Certain natural compounds possess anti-apoptotic effects. For example, ascorbic acid and a-tocopherol prevent apoptosis caused by serum withdrawal in HL-60 cells with the antioxidative effects (76). Caffeic acid inhibits ceramide-induced apoptosis in U937 cells through the inhibition of protein tyrosine kinase activity 17). Quercetin inhibits hydrogen peroxide-induced apoptosis via intervention in the activator protein 1 (AP-1) -mediated apoptotic pathway 18). Epigallocatechin-3-gallate and theaflavins inhibits arsenite-induced apoptosis through the decrease in phosphorylation of Erks and JNKs (79). Therefore, it is important to know whether these natural compounds show inhibitory effects on Trp-P-1-induced apoptosis. In this study, we demonstrated that Trp-P-1 induced caspase-8-initiated apoptosis in rat MNCs, and that certain food components inhibited Trp-P-l-induced apoptosis. [Pg.129]

It has been shown in many studies that protective effects of carotenoids can be observed only at small carotenoid concentrations, whereas at high concentrations carotenoids exert pro-oxidant effects via propagation of free radical damage (Chucair et al., 2007 Lowe et al., 1999 Palozza, 1998, 2001 Young and Lowe, 2001). For example, supplementation of rat retinal photoreceptors with small concentrations of lutein and zeaxanthin reduces apoptosis in photoreceptors, preserves mitochondrial potential, and prevents cytochrome c release from mitochondria subjected to oxidative stress induced by paraquat or hydrogen peroxide (Chucair et al., 2007). However, this protective effect has been observed only at low concentrations of xanthophylls, of 0.14 and 0.17 pM for lutein and zeaxanthin, respectively. Higher concentrations of carotenoids have led to deleterious effects (Chucair et al., 2007). [Pg.328]

S. Tada-Oikawa, Y. Hiraku, M. Kawanishi, and S. Kawanishi, Mechanism for generation of hydrogen peroxide and change of mitochondrial membrane potential during rotenone-induced apoptosis. Life Sci. 73, 3277-3288 (2003). [Pg.458]

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]

Classic antioxidants, vitamin E, vitamin C, and others can suppress the activation of apoptosis. For example, ascorbic acid prevented cytochrome c release and caspase activation in human leukemia cells exposed to hydrogen peroxide [128], Pretreatment with A -acctylcystcinc, ascorbate, and vitamin E decreased homocysteine thiolactone-induced apoptosis in human promyelocytic leukemia HL-60 cells [129]. Resveratrol protected rat brain mitochondria from anoxia-reoxygenation damage by the inhibition of cytochrome c release and the reduction of superoxide production [130]. However, it should be mentioned that the proapoptotic effect of ascorbate, gallic acid, or epigallocatechin gallate has been shown in the same human promyelocytic leukemia cells [131]. [Pg.758]

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]


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